The DOI matches its Crossref record; 4,084 of the 4,084 references it cites were found in a registry or an index; 285 of the 769 sources its claims cite were checked for support.
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
Open accessAbstract
autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Overview
AI snapshot
Written from a shortened version of the paper’s full text (it is longer than we read).
TL;DR
This 4th edition consensus guideline updates recommendations for selecting, performing, and interpreting assays that monitor autophagy and related processes in eukaryotes, emphasizing that no single assay is adequate and that autophagic flux—not just marker accumulation—must be measured. It is intended for researchers, clinicians, and reviewers evaluating autophagy-modulating therapies.
Key findings
- No individual assay is perfect for every situation; the guidelines call for multiple complementary techniques to properly monitor autophagy in each experimental setting, and state that "there are no absolute criteria for determining autophagic status that are applicable in every single biological or experimental context."
- Increases in LC3-II (or GFP-LC3 puncta, or autophagosome number by TEM) are not measures of autophagic flux per se; they can reflect either induction of sequestration or a block in autophagosome/amphisome clearance, so flux assays (e.g., LC3-II turnover with and without lysosomal inhibitors) are required.
- Because core autophagy components also regulate other pathways (e.g., apoptosis) and participate in canonical and noncanonical processes, genetic approaches to block autophagy should target two or more autophagy-related genes that ideally act at distinct steps.
- The document provides extensive cautionary notes across methods (TEM, Atg8-family protein detection, SQSTM1 turnover, TOR/AMPK/ULK1, PtdIns3K activity, transcriptional regulation, protein degradation, selective autophagy, model systems), including that LC3 can associate with nonautophagic structures and that LC3 puncta can appear in autophagy-deficient cells.
Methods
- Design: consensus guidelines (not primary experimental research), synthesizing and critically discussing current methods for assessing autophagy, with cautionary notes and conclusions for each method section.
- Scope: covers nomenclature; TEM; Atg8-family protein detection/quantification (western blotting, flux/turnover, GFP-Atg8 processing, HaloTag-LC3, tandem mRFP/mCherry-GFP, HiBiT reporter, in vitro lipidation); SQSTM1 and related receptor turnover; TOR/MTOR, AMPK and Atg1/ULK1; PtdIns3K (PIK3C3/VPS34) activity; additional markers (ATG9A, ATG12–ATG5, ATG14, ATG16L1, Atg18/WIPI, BECN1, STX17, TECPR1, ZFYVE1); sphingolipids; transcriptional/translational regulation; posttranslational modifications; autophagic protein degradation; and selective autophagy plus model systems.
- Analysis: qualitative critical appraisal with specific technical recommendations (e.g., inhibitor concentrations/timing such as 1–4 h bafilomycin A1 treatment, 10–20 µM E-64d for 1 h, CQ 10–40 µM, bafilomycin A1 1–100 nM; scoring ~50 or more cells across at least three fields; morphometric reporting as µm³ autophagic vacuole/µm³ cytoplasm).
Limitations
- Stated: the guidelines are "not meant to be a dogmatic set of rules," are likely to evolve as new methodologies are developed and current assays are superseded, and are not protocols—readers are referred to published protocols for experimental detail.
- Stated: the appropriateness of any assay largely depends on the question asked and the system used; some assays are unsuitable, problematic, or may not work at all in particular cells, tissues, or organisms.
- Evident from the text: many recommendations rest on context-dependent observations (e.g., LC3-II changes are tissue- and cell context-dependent; SQSTM1 changes can be cell-type, treatment, and transcription specific), and several areas lack consensus (e.g., "There is no consensus at the present time with regard to the best method for monitoring mitophagy in animal cells"; the specific ULK1 residues targeted by AMPK or MTOR remain unresolved).
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
215 Not checked yet · 90 Own interpretation · 87 No basis given · 72 Couldn’t confirm · 72 No full text of the sources · 62 Partly supported · 10 Sources not found · 6 Own method · 5 Supported so far · 5 Own result · 4 Mixed support · 2 Supported · 2 Not supported · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“However, being a nonspecific inhibitor of oxidative phosphorylation [674, 675]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [674] source
Checked before — its earlier verdict is held back until a new check runs.
- Disputedcites [675] sourceExperimental — accuracy not yet measured
The Results (p. 5) characterize compound C as a potent, selective AMPK inhibitor, not as a nonspecific inhibitor of oxidative phosphorylation. The discussion of impaired oxidative phosphorylation in the Results (p. 4) concerns metformin instead. (LLM, conf=0.84)
Checked by a reasoning model — may be wrong.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not checked yet
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“whereas it appears to stimulate autophagy in many other cell types, including fibroblasts, colon carcinoma cells and skeletal muscle [656-665]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Disputedcites [656] sourceExperimental — accuracy not yet measured
The Results section (‘AMPK phosphorylates and inhibits ULK1’; page unavailable) reports that activating AMPK inhibited the autophagy response in mouse embryonic fibroblasts, contrary to the claim’s fibroblast example. The Introduction describes AMPK stimulation of autophagy as a proposed model, but says its role remains controversial. The passages found do not establish stimulation in colon carcinoma cells or skeletal muscle. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
- Partly supportedcites [657] sourceExperimental — accuracy not yet measured
The Results section (“AMPK activity is critical for ACD in I(−) HCN cells”; page not provided) reports that inhibiting AMPK reduced autophagy in hippocampal neural stem cells. The paper also discusses AMPK-linked mitophagy in HepG2 cells, but our copy does not report the claimed effect in fibroblasts, colon carcinoma cells, or skeletal muscle. (LLM, conf=0.86)
- Partly supportedcites [658] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says AMPK is required for autophagy in yeast and Drosophila and reports that AMPK associates with human ULK1 and ULK2. It does not establish that AMPK stimulates autophagy in fibroblasts, colon carcinoma cells, or skeletal muscle; the authors say further work is needed to clarify the regulatory link. (LLM, conf=0.78)
- Supportedcites [659] source
The Discussion states that AMPK is required for autophagy induction in HT29 colorectal cancer cells. This supports the colon carcinoma example attributed to this paper within the sentence’s group of citations; the paper need not establish the fibroblast or skeletal-muscle examples. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [660] source
- Not checked — no full text of the sourcecites [661] source
- Not checked — no full text of the sourcecites [662] source
- Could not verifycites [663] sourceExperimental — accuracy not yet measured
The Introduction discusses AMPK in gluconeogenesis, and the Results discuss HDAC phosphorylation in hepatoma cells, but neither addresses autophagy in the named cell types. Searches for autophagy with AMPK and for fibroblasts, colon carcinoma cells, and skeletal muscle found no passage in our copy stating the claimed effect. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [664] source
- Could not verifycites [665] sourceExperimental — accuracy not yet measured
Section 2.2 (Skeletal and cardiac muscle; page unavailable) discusses AMPK activation of PGC-1α and mitochondrial function, but not autophagy. A search for autophagy found no passage addressing whether AMPK stimulates it in fibroblasts, colon carcinoma cells, or skeletal muscle. (LLM, conf=0.72)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Disputed
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“In liver cells, AMPK suppresses autophagy at the level of cargo sequestration, as indicated by the rapid sequestration-inhibitory effects of a variety of AMPK activators”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [656] sourceExperimental — accuracy not yet measured
The Results section, “AMPK phosphorylates and inhibits ULK1” (page unavailable), reports that AMPK activation inhibited autophagosome formation, consistent with suppression at an early sequestration stage. But the reported experiment used HEK293 cells and one AMPK activator, A769662; it does not establish rapid effects of a variety of activators in liver cells. The References list a hepatocyte study, but that listing does not supply those missing details. (LLM, conf=0.88)
- Disputedcites [657] sourceExperimental — accuracy not yet measured
The AMPK-p62 for autophagic cell death section reports the opposite direction in liver-derived HepG2 cells: activation of the AMPK-ULK1 pathway induces mitophagy. Our copy does not report rapid inhibition of cargo sequestration by AMPK activators in liver cells. Page numbers were not available in the indexed passages. (LLM, conf=0.82)
Checked by a reasoning model — may be wrong.
- Could not verifycites [658] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that AMPK associates with ULK1 and ULK2, but says further study is needed to establish regulatory links. Our copy does not address whether AMPK activators rapidly inhibit cargo sequestration in liver cells; searches for liver-cell suppression and sequestration-inhibitory effects found no such passage. (LLM, conf=0.76)
- Could not verifycites [659] sourceExperimental — accuracy not yet measured
The Discussion says AMPK is required for autophagy induction in HT29 colorectal cancer cells, not that it suppresses autophagy in liver cells. Searches for liver-cell cargo sequestration and rapid inhibitory effects of AMPK activators found no passage addressing those claims. The finding in a different cell type does not establish a contradiction. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [660] source
- Not checked — no full text of the sourcecites [661] source
- Not checked — no full text of the sourcecites [662] source
- Could not verifycites [663] sourceExperimental — accuracy not yet measured
The Introduction discusses AMPK as an inhibitor of gluconeogenesis, while the Results section on Class IIa HDAC phosphorylation describes effects of AMPK activators on HDACs in liver cells. Searches for autophagy and cargo sequestration found no passage addressing whether AMPK suppresses autophagy at that stage. (LLM, conf=0.74)
- Not checked — no full text of the sourcecites [664] source
- Could not verifycites [665] sourceExperimental — accuracy not yet measured
The Liver section discusses PGC-1α, SIRT1, and hepatic metabolic regulation, but not AMPK-mediated autophagy or cargo sequestration. Searches for AMPK, autophagy, and sequestration found no passage in our copy addressing the claim. (LLM, conf=0.73)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In theory, these nonautophagic processes can be assessed if degradation persists after blocking autophagic sequestration [14,16,29].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Not checked — no full text of the sourcecites [14] Kovács J, 1986, Biomed Biochim Acta
- Not checked — no full text of the sourcecites [16] source
- Could not verifycites [29] sourceExperimental — accuracy not yet measured
The Results section on autophagosome biogenesis reports reduced autophagosome formation in autophagy mutants, but does not assess whether degradation persists after sequestration is blocked. The Results section on selective autophagy discusses synaptic vesicle clustering, not a method for assessing nonautophagic degradation. Searches for the claim’s wording and for persistent degradation in autophagy-deficient mutants found no passage addressing that method. (LLM, conf=0.72)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In subsequent stages of the autophagic process the fusion of the autophagosome with an endosome and a lysosome results in increased density of IMPs in the membrane of the formed autophagic compartments (amphisomes, autolysosomes; Figure 6C) [6, 29, 137-140, 147, 148].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Partly supportedcites [6] sourceExperimental — accuracy not yet measured
In “The Discovery of Autophagy and its Identification as a Lysosomal Degradation Process” (page unavailable), the paper says autophagic vacuoles acquire intramembrane particles when autophagosomes fuse with endosomes. “Immunoelectron Microscopy Studies on the Origin of Autophagosome Membranes” (page unavailable) describes subsequent maturation into amphisomes and autolysosomes, but does not establish that lysosome fusion further increases particle density. (LLM, conf=0.86)
- Could not verifycites [29] sourceExperimental — accuracy not yet measured
The Results section on autophagosome biogenesis at AIY presynaptic sites reports where autophagosomes form and describes stalled maturation in mutants. Searches for IMP density, amphisomes, autolysosomes, and fusion with endosomes or lysosomes found no passage addressing the claimed membrane change; page numbers were not available in our copy. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [137] source
- Not checked — no full text of the sourcecites [138] source
- Could not verifycites [139] sourceExperimental — accuracy not yet measured
The Results section on anti-tumor effects describes autophagic vacuoles and autophagosome-mediated recycling, but not fusion with endosomes or lysosomes or membrane IMP density. Searches for amphisomes, autolysosomes, intramembrane particles, and fusion found no passage addressing the claimed increase in IMP density. Page numbers were not available in our copy. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [140] source
- Partly supportedcites [147] sourceExperimental — accuracy not yet measured
The Introduction (page not provided) says that an autophagosome’s outer membrane fuses with the vacuole in yeast, supporting the fusion aspect of the claim. It does not address fusion with an endosome, formation of amphisomes or autolysosomes, or any increase in membrane IMP density. (LLM, conf=0.84)
- Partly supportedcites [148] sourceExperimental — accuracy not yet measured
The Results (page not provided) describe fusion of an autophagosome with a vacuole in yeast. They do not report fusion with an endosome or an increased density of intramembrane particles in amphisomes or autolysosomes. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This is because some assays are unsuitable, problematic or may not work at all in particular cells, tissues or organisms [1][2][3][4].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Supportedcites [1] source
The Introduction states almost exactly the attributed claim: some assays are inappropriate, problematic, or may not work at all in particular cells, tissues, or organisms. The “Experimental systems” section likewise cautions that some techniques may not work in particular cell types or organisms. (LLM, conf=0.95)
- Supportedcites [2] source
The Introduction (p. 25) states that some assays are inappropriate, problematic, or may not work at all in particular cells, tissues, or organisms. The citing sentence closely paraphrases that statement. (LLM, conf=0.95)
- Supportedcites [3] source
The opening guidelines passage states almost exactly that some assays are inappropriate, problematic, or may not work in particular cells, tissues, or organisms. The “Experimental systems” section likewise says some techniques may not work in particular cell types or organisms. (LLM, conf=0.95)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Autophagosomes, also referred to as initial autophagic vacuoles (AVi), typically have a double membrane.This structure is usually distinctly visible by EM as two parallel membrane layers (bilayers) separated by a relatively narrower or wider electrontranslucent cleft, even when applying the simplest routine EM fixation procedure (Figure 3A) [67,68].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Partly supportedcites [67] sourceExperimental — accuracy not yet measured
In the main text (pp. 931–932), the paper says that autophagosomes are delimited by a double membrane, supporting the central claim. Our copy does not call them “initial autophagic vacuoles” or use the abbreviation “AVi,” so it does not verify that terminology. (LLM, conf=0.83)
- Partly supportedcites [68] sourceExperimental — accuracy not yet measured
The Discussion describes the phagophore membrane as two adjacent lipid bilayers, and the SB-EM and ET section describes double membranes in autophagosomes. Our copy does not use or establish the alternative name “initial autophagic vacuoles (AVi).” (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Additional identification problems may arise from damage caused by improper sample collection or fixation artefacts [67,68,155,156].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [67] sourceExperimental — accuracy not yet measured
The main text discusses misidentification of autophagic structures, particularly confusion between lipid bilayers and double membranes. It does not address damage from improper sample collection or fixation artefacts as a cause of identification problems; searches for those terms found no relevant passage. (LLM, conf=0.70)
- Partly supportedcites [68] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says that an apparent cleft between phagophore membranes has been suggested to be a fixation artifact, supporting the possibility that fixation can complicate morphological identification. Our copy does not link improper sample collection to damage or identification problems. (LLM, conf=0.83)
- Not checked yetcites [155] Müller-Reichert T, 2010
- Could not verifycites [156] sourceExperimental — accuracy not yet measured
The electron-microscopy methods describe sample collection and cryofixation, but do not say that improper collection or fixation artefacts cause identification problems. Searches for fixation artefacts and preparation-related damage found no passage addressing that claim; page numbers were not available in our copy. (LLM, conf=0.72)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“One approach to evaluate autophagic flux is to measure the rate of general protein breakdown by autophagy [6,25,26].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Supportedcites [6] source
In “Convergence of Biochemical and Ultrastructural Autophagy Studies” (page not supplied), the paper describes measuring overall protein degradation through amino-acid release. In “The Discovery of Autophagy and its Identification as a Lysosomal Degradation Process” (page not supplied), it says a selective inhibitor enabled quantitative measurement of autophagic protein degradation, supporting the described approach to evaluating flux. (LLM, conf=0.90)
- Not checked yetcites [25] source
Checked before — its earlier verdict is held back until a new check runs.
- Could not verifycites [26] sourceExperimental — accuracy not yet measured
The paper’s discussion of maturation times and LC3 measurements (section “What is the advantage of a transient precursor in autophagosome biogenesis?”, page unavailable) concerns autophagosome formation and disappearance, not general protein breakdown. Searches for protein breakdown, degradation assays, and autophagic flux found no passage describing the claimed approach. (LLM, conf=0.75)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“whereas decreased flux could also be due to inefficient degradation of the cargo once fusion has occurred [19].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Partly supportedcites [19] sourceExperimental — accuracy not yet measured
The paper’s Abstract says that autophagosomes fuse with lysosomes and that their cargo is then degraded in autolysosomes. This supports the claim’s sequence of events, but the passage does not explicitly say that inefficient degradation after fusion can decrease autophagic flux. (LLM, conf=0.78)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
- It may state two separate claims as one. 243
- Probably not a substantial claim. 140
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Moreover, GFP-LC3 puncta and LC3 lipidation can reflect the induction of a different/modified pathway such as LC3-associated phagocytosis (LAP) [20], or the noncanonical destruction pathway of paternal mitochondria after egg fertilization [21,22].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Disputedcites [20] sourceExperimental — accuracy not yet measured
The Results and Discussion report GFP-LC3 congregation near sperm mitochondria after fertilization, but conclude that this did not indicate their destruction through autophagy. The paper instead says sperm mitochondria persisted until the morula stage and that maternal mtDNA inheritance in mice was not achieved by postfertilization elimination of paternal mitochondria or mtDNA. It therefore does not support the cited example of a noncanonical destruction pathway. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Supportedcites [21] source
The Results describe Atg8-positive vesicles associated with the sperm flagellum and characterize paternal mitochondrial destruction as a common, nonorthodox endocytic and autophagic pathway. The Discussion likewise calls its role unconventional. This supports the noncanonical paternal-mitochondrial-destruction example to which this citation is attached. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [22] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Disputed
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Thus, induction of autophagy requires inhibition of MTORC1 and not of MTORC2 [771, 772].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [771] source
- Disputedcites [772] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says FOXO3 can activate autophagy independently of MTORC1 activity and reports no noticeable change in autophagy after MTOR inhibition in LPS-treated microglia. These statements contradict the claim that MTORC1 inhibition is required; the paper does not establish the claimed MTORC1-versus-MTORC2 distinction. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“Nutritional starvation suppresses TORC1-mediated Atg1 phosphorylation [423,509] while stimulating Atg1mediated Atg13 phosphorylation [586, 744, 745].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [423] source
- Could not verifycites [509] sourceExperimental — accuracy not yet measured
The Introduction and Discussion address Beclin 1 expression, autophagy, and lymphoma prognosis, but do not address how nutritional starvation affects Atg1 or Atg13 phosphorylation. Searches for both TORC1-mediated Atg1 phosphorylation and Atg1-mediated Atg13 phosphorylation found no relevant passage. Page numbers were not available in our copy. (LLM, conf=0.76)
- Could not verifycites [586] sourceExperimental — accuracy not yet measured
The Introduction and Results discuss autophagy in ARPE-19 cells, but the retrieved passages do not address nutritional starvation or phosphorylation of Atg1 and Atg13. Searches for “Atg1-mediated Atg13 phosphorylation” and “Atg13 TORC1 nutritional starvation phosphorylation” found no passage establishing the attributed mechanism. (LLM, conf=0.76)
- Partly supportedcites [744] sourceExperimental — accuracy not yet measured
The Results report that starvation increases Apg1 kinase activity, and the Discussion says starvation represses Tor activity and causes Apg13 dephosphorylation. The paper does not establish TORC1-mediated phosphorylation of Apg1 or show that starvation stimulates Apg1-mediated phosphorylation of Apg13; its reported change in Apg13 phosphorylation is a decrease. Page numbers are unavailable in our copy. (LLM, conf=0.85)
- Disputedcites [745] sourceExperimental — accuracy not yet measured
The citation is attached to the claim that starvation stimulates Atg1-mediated Atg13 phosphorylation. The paper reports instead that Apg13p is rapidly dephosphorylated under nitrogen starvation (Fig. 6B), and the Discussion states that phosphorylation persists in apg1-deletion cells, suggesting another kinase is involved. (LLM, conf=0.91)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“This electron-translucent cleft, however, is less visible in freeze-fixed samples, suggesting it may be an artefact of sample preparation (see Fig. S3 in ref. [69]).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Could not verifycites [69] sourceExperimental — accuracy not yet measured
The Experimental Procedures describe chemical fixation and electron microscopy, but no comparison with freeze-fixed samples. Searches for “cleft,” “freeze-fixed,” and preparation artefacts found no passage addressing whether the cleft is less visible or may be an artefact. Page numbers are unavailable in our copy. (LLM, conf=0.75)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“However, it has been observed that under special circumstances the potential exists for the formation of huge autophagosomes, which can even engulf a complete nucleus [29].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Could not verifycites [29] sourceExperimental — accuracy not yet measured
The Experimental Procedures (Electron Micrographs; page not provided) say that autophagosomes in C. elegans are relatively small. The Results discuss autophagosomes in developing neurons, but neither section addresses whether unusually large autophagosomes can engulf a complete nucleus. Searches for those terms found no supporting passage; the C. elegans size observation does not rule out the claim under other circumstances. (LLM, conf=0.76)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“The maturation from the phagophore through the autolysosome is a dynamic and continuous process [66], and, thus, the classification of compartments into discrete morphological subsets can be problematic; therefore, some basic guidelines are offered below.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Supportedcites [66] source
In “Identification of autophagic compartments in electron microscopy,” the paper describes autophagosomes maturing through fusion and shows that changes in their contents and membranes overlap rather than marking cleanly separated stages. It also says conventional TEM cannot always distinguish amphisomes from autolysosomes without specific markers. These passages support the cited point about maturation and the difficulty of discrete morphological classification. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Fourth, in mammalian cells LC3 is expressed as multiple isoforms (LC3A, LC3B, LC3B2 and LC3C [281,282]), which exhibit different tissue distributions and whose functions are still poorly understood.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Could not verifycites [281] sourceExperimental — accuracy not yet measured
The Autophagy section identifies LC3 as a mammalian homologue of Atg8, but does not discuss LC3 isoforms. Searches for LC3A, LC3B2, isoforms, and tissue distributions found no passage in our copy supporting the listed isoforms, their distributions, or the statement about their functions. (LLM, conf=0.72)
- Could not verifycites [282] sourceExperimental — accuracy not yet measured
The Editor’s Corner (p. 441) discusses a journal policy requiring reagent catalog numbers instead of company locations. Searches for LC3 isoforms, tissue distributions, and their functions found no passage addressing the cited claim. (LLM, conf=0.78)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“new evidence suggests that LC3 proteins have distinct subcellular distributions and mediate different types of selective autophagy [198,199].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Not checked — no full text of the sourcecites [198] source
- Partly supportedcites [199] sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says LC3 recruits p62 and NBR1, supporting a role in selective cargo recruitment. It does not show that different LC3 proteins have distinct subcellular distributions or mediate different types of selective autophagy; the paper instead compares the roles of the LC3 and GABARAP subfamilies in autophagosome formation. (LLM, conf=0.78)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Furthermore, commercial antibodies for GABARAPL1 also recognize GABARAP [33,195], which might lead to misinterpretation of experiments, in particular those using immunohistochemical techniques.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Could not verifycites [33] sourceExperimental — accuracy not yet measured
The discussion of GABARAP-family knockdowns and the Figure 1 caption mention GABARAPL1, GABARAP, and immunoblotting, but do not address whether commercial GABARAPL1 antibodies recognize GABARAP. Searches for antibody cross-reactivity and immunohistochemistry found no passage supporting the claimed risk of misinterpretation. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [195] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A dose-curve and timecourse standardization for the use of autophagic flux inhibitors is required for the initial optimization of the conditions to detect LC3-II accumulation and avoid nonspecific or secondary effects, and to exclude the possibility of a remaining residual flux, if inhibition is incomplete [314].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Turnover of LC3-II/Atg8-PE: Autophagic flux.
What the sources say
- Partly supportedcites [314] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“However, in human cells, pro-LC3B and LC3B-II are indistinguishable by western blotting [293], and a PLD cleavage assay may be required to discriminate between the two isoforms [289], which is particularly important under conditions where ATG4 activity is reduced.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Could not verifycites [293] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes LC3 cleavage and the electrophoretic migration of LC3-II, while Materials and methods describes immunoblotting. Neither passage says that pro-LC3B and LC3B-II are indistinguishable on western blots. Searches for those forms and for a PLD cleavage assay found no passage addressing the claimed distinction or assay. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [289] source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“This approach, however, is only valid when the knockdown of LAMP2 is directed against the mRNA region specific for the LAMP2B spliced variant, as targeting the region common to the three variants would also inhibit chaperone-mediated autophagy (CMA), which may result in the compensatory upregulation of autophagy [135,309,310].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Turnover of LC3-II/Atg8-PE: Autophagic flux.
What the sources say
- Could not verifycites [135] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [309] source
- Not checked — no full text of the sourcecites [310] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“However, estimation of the number of autophagic profiles per cell area is more reliable and correlates well with the volume fraction mentioned below [163].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [163] sourceExperimental — accuracy not yet measured
The Results and Discussion passages describe estimating autophagic-body sizes from electron-microscopy sections and correlating observed section-size distributions with original size distributions; no page number is available in our copy. Searches for profiles per cell area and volume fraction found no passage comparing their reliability or reporting a correlation between them. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LC3 proteins are involved in autophagosome formation, with participation of GABARAP subfamily members in later stages of autophagosome formation [201].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Partly supportedcites [201] sourceExperimental — accuracy not yet measured
The Results section (‘Rotenone elicits increased autophagy and mitophagy’; page unavailable) describes LC3 binding to autophagic membranes and identifies LC3 puncta as autophagosome markers. The Results section on LC3–cardiolipin interactions mentions GABARAP as a related protein, but does not say that GABARAP subfamily members participate in later stages of autophagosome formation. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“To avoid this socalled”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [160] Williams MA., 1977
- Could not verifycites [168] sourceExperimental — accuracy not yet measured
The available indexed passages are bibliographic metadata and keywords for the pexophagy paper, not a discussion of reference-space measurement. Searches for “reference trap,” “reference space volume,” and stereological methods returned no passage addressing the claim. The printed citing sentence is also incomplete, so the attributed point cannot be checked more narrowly. (LLM, conf=0.72)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Some evidence, however, suggests that, at least in certain cell types, the LC3 subfamily may be dispensable for bulk autophagic sequestration of cytosolic proteins, whereas the GABARAP subfamily is absolutely required [33].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Partly supportedcites [33] sourceExperimental — accuracy not yet measured
The paper’s main text (indexed under Abstract; page unavailable) reports that LC3-family knockdown did not impair bulk cargo sequestration in LNCaP cells. It also reports that GABARAP-family knockdown strongly suppressed sequestration, but notes that some starvation-induced activity remained. That supports a strong GABARAP requirement, not the claim that the subfamily is absolutely required. (LLM, conf=0.87)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Both starvation-induced autophagy and PINK1-PRKN-dependent mitophagy, as noted above, predominantly require the GABARAP subfamily over the LC3 subfamily [33,35,36].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Partly supportedcites [33] sourceExperimental — accuracy not yet measured
The Abstract reports that GABARAP-family knockdown strongly suppressed starvation-induced bulk cargo sequestration, whereas LC3-family knockdown did not. It does not address PINK1–PRKN-dependent mitophagy, so that half of the attributed claim is unsupported by this paper. (LLM, conf=0.90)
- Supportedcites [35] source
The Discussion reports that GABARAPs are key drivers of autophagic flux following starvation and that parkin-dependent mitophagy strongly relies on GABARAP-dependent flux. The Results identify the mitophagy pathway as PINK1-dependent and show substantially less mitochondrial clearance in GABARAP-deficient cells than in LC3-deficient cells. (LLM, conf=0.92)
- Could not verifycites [36] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes LC3 conjugation, and the section on metabolic restriction describes starvation-induced autophagy, but neither compares LC3 with GABARAP. Searches for GABARAP and PINK1/PRKN-dependent mitophagy found no passage addressing the claimed preferential requirement. (LLM, conf=0.73)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Accordingly, an enzymatic assay such as the Pho8∆60 assay may be preferred (see Autophagic protein degradation) [357,358], especially when the differences in autophagic activity need to be determined precisely (note that an equivalent assay has not been developed for more complex eukaryotic cells); however, as with any enzyme assay, appropriate caution must be used regarding, for example, sub”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [357] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
- Could not verifycites [358] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“An additional caveat when using the photoactivatable construct PA-GFP [303] is that the process of activation by photons may induce DNA damage, which could, in turn, induce autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [303] sourceExperimental — accuracy not yet measured
The Methods (Histology and imaging; Image analysis, pages unavailable) describe GFP-based fluorescent markers, but not PA-GFP or photoactivation. The Results (Vesicle acidification is impaired in V-ATPase-depleted cells, page unavailable) discuss autophagic vesicles, not photon-induced DNA damage. Searches for PA-GFP, photoactivation, and DNA damage found no passage addressing the proposed caveat. (LLM, conf=0.76)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“GFP-SQSTM1 displays the largest magnitude change following the induction of autophagy by amino acid deprivation or rapamycin treatment, and may thus be a better marker for following autophagic flux by this method (confirmed in SH-SY5Y neuronal cell lines stably expressing GFP-SQSTM1; E.M.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Partly supportedcites [497] sourceExperimental — accuracy not yet measured
The Abstract and Results and Discussion report that GFP-p62 had the strongest response to amino acid starvation and was the most suitable of the tested flow-cytometry reporters. For rapamycin, however, Results and Discussion says degradation of both GFP-p62 and GFP-NBR1 increased by 30%, so the claimed largest change is not established for that treatment. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In vitro reconstitutions of autophagosome-vacuole and autophagosome-lysosome fusion have partially overcome this problem and made it possible to identify relevant proteins and their functions in this specific step of autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Partly supportedcites [506] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [507] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Partly supportedcites [508] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Immunodetection of ATG and related proteins (particularly LC3 and BECN1) has been reported as a prognostic factor in various human carcinomas, including lymphoma [267, 509], breast carcinoma [510, 511], endometrial adenocarcinoma [512, 513], head and neck squamous cell carcinoma [514-516], hepatocellular”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [267] sourceExperimental — accuracy not yet measured
The Western immunoblotting Methods describe detecting LC3 to measure autophagic flux in lupus T cells. Neither that passage nor the Introduction addresses whether LC3 or BECN1 immunodetection is prognostic in lymphoma or other human carcinomas (searched: lymphoma, carcinoma, prognostic factor). (LLM, conf=0.76)
- Supportedcites [509] source
The Introduction reports that Beclin 1 (BECN1) was measured by immunohistochemistry in extranodal NK/T-cell lymphoma specimens and that its expression independently predicted survival. This supports the lymphoma example for which this paper is cited. (LLM, conf=0.93)
- Supportedcites [510] source
This citation supports the breast-carcinoma example in the multi-citation sentence. In the section “LC3B protein is a marker of poor prognosis for TN BC patients,” the authors report that LC3B measured by immunohistochemistry was associated with poor prognosis in triple-negative breast cancer, with the finding validated in an independent cohort. (LLM, conf=0.93)
- Partly supportedcites [511] sourceExperimental — accuracy not yet measured
The ‘Investigating Autophagy in Tissues’ section reports that LC3A staining patterns were associated with prognosis in breast carcinoma, with comparable results in colorectal adenocarcinoma. The ‘Expansion of the Study’ section includes endometrial adenocarcinoma among tumors examined for staining patterns, but does not report an endometrial prognostic finding; the cited passages also do not address BECN1. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [512] source
- Supportedcites [513] source
The paper supports the endometrial-carcinoma example to which this citation is attached. Its Discussion reports that high counts of LC3A-stained stone-like structures were associated with poorer five-year survival, including within endometrioid carcinomas. The citation need not establish the other cancer types or BECN1 findings covered by other citations in the sentence. (LLM, conf=0.92)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Along these lines, a caution concerning the use of the EGFP fluorescent protein for microscopy is that this fluorophore has a relatively neutral pH optimum for fluorescence [263], and its signal diminishes quickly during live cell imaging due to the acidic environment of the lysosome.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [263] sourceExperimental — accuracy not yet measured
The cited paper’s Experimental Procedures and Characterization of in Vitro Atg8p sections describe Atg8 conjugation and antibody-based detection, not EGFP fluorescence. Searches for EGFP’s pH optimum and for fluorescence loss in acidic lysosomes found no passage addressing the cited claim; page numbers were unavailable in our copy. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Therefore, the appearance of free GFP on western blots can be used to monitor lysis of the inner autophagosome membrane and breakdown of the cargo in metazoans (Figure 12A) [326,347,348], or the delivery of autophagosomes to, and the breakdown of autophagic bodies within, the fungal [349-351] and plant vacuole [291,292,326,352].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [326] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked yetcites [347] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [348] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [349] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [350] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [351] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [291] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked — no full text of the sourcecites [292] source
- Partly supportedcites [352] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Indeed, there is a reciprocal crosstalk between the UPS and autophagy, with SQSTM1 being a key link between them [595,596].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [595] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes p62/SQSTM1 as a cargo receptor that links ubiquitinated substrates to autophagic degradation. It also discusses proteasomal degradation of Nrf2, but does not establish reciprocal crosstalk between the ubiquitin–proteasome system and autophagy or identify p62 as the key link between those two systems. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [596] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“SQSTM1 may be transcriptionally upregulated under some conditions [421, 565-568], as observed in several C. elegans longevity models [569, 570], further complicating the interpretation of results.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [421] source
- Could not verifycites [565] sourceExperimental — accuracy not yet measured
The cited paper’s Results section reports transcriptional changes in several autophagy-related genes, but does not identify SQSTM1 as transcriptionally upregulated. Its Discussion cautions that SQSTM1 protein levels can be affected by autophagy-independent degradation; that does not establish the transcriptional-upregulation claim. The C. elegans observation is attached to different citations in the citing sentence. (LLM, conf=0.72)
- Could not verifycites [566] sourceExperimental — accuracy not yet measured
The Results and Discussion report increased SQST-1::GFP protein and aggregates in rpl-43 mutant larvae, not transcriptional upregulation of SQST-1 in longevity models. The Sma TGFβ and mitochondrial-stress sections describe increased transcription of other autophagy genes. Searches for SQST-1 transcription and longevity did not find a passage addressing the attributed observation. (LLM, conf=0.75)
- Could not verifycites [567] sourceExperimental — accuracy not yet measured
The Results section (‘Adriamycin induces autophagy in MMC’; page unavailable) discusses p62/SQSTM1 protein degradation as a marker of autophagic flux, not transcriptional upregulation. Searches for SQSTM1 transcriptional upregulation and C. elegans longevity models found no passage addressing either point. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [568] source
- Not checked — no full text of the sourcecites [569] source
- Supportedcites [570] source
The Results section reports increased p62/SQSTM1 transcription after leucine starvation in mammalian cells, with mRNA induction also observed after withdrawal of other essential amino acids. The C. elegans longevity-model observation is attached to different citations, not attributed to this paper. (LLM, conf=0.92)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Similarly, decreased SQSTM1 levels are associated with autophagy activation; however, similar to LC3-II, lysosomal inhibitors (such as CQ) can be used to assess increased autophagy flux based on an accumulation of SQSTM1 [87,561].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [87] sourceExperimental — accuracy not yet measured
The paper’s introduction (p. 897) describes using SOD and CAIII to monitor autophagy in rat hepatocytes, not SQSTM1. Searches for SQSTM1/p62, chloroquine/CQ, and lysosomal-inhibitor-based flux assessment found no passage addressing the cited claim. (LLM, conf=0.75)
- Partly supportedcites [561] sourceExperimental — accuracy not yet measured
In the Results sections describing Figures 5E and 6A, rapamycin-induced autophagy decreased p62/SQSTM1, while bafilomycin A1 treatment increased it. The paper uses SQSTM1 accumulation to assay autophagy inhibition or deficiency; it does not describe CQ treatment or establish that accumulation under an inhibitor demonstrates increased autophagic flux. Page numbers are not available in our copy. (LLM, conf=0.85)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In mouse platelets, endogenous PtdIns3P, the product of the BECN1-PIK3C3/VPS34 protein complex-mediated enzymatic reaction, can be detected using recombinant GST-2×FYVE followed by anti-GST immunofluorescence [391].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [391] sourceExperimental — accuracy not yet measured
The Methods section describes immunohistochemistry on human myocardial cryosections using antibodies to ubiquitin, proteasome subunit α5, and complement-9. Searches for mouse platelets, PtdIns3P, GST-2×FYVE, and anti-GST immunofluorescence found no passage addressing the claimed detection method. Page numbers were unavailable in our copy. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“First, SQSTM1 participates in proteasomal degradation, and its level may also increase when the proteasome is inhibited [597].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [597] sourceExperimental — accuracy not yet measured
The background passage in the paper’s Abstract says p62/SQSTM1 is induced at the mRNA and protein levels by proteasomal inhibitors, supporting the claim that its level may increase when the proteasome is inhibited. The Discussion describes p62 as a cargo receptor for degradation by autophagy, not proteasomal degradation; that part of the claim is not supported by our copy. Page numbers are unavailable. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of interest, SQSTM1 overexpression at both the gene and protein levels can be observed in muscle atrophy induced by cancer, though not by glucocorticoids, suggesting that the stimulus inducing autophagy may also be relevant to the differential regulation of autophagy-related proteins [584].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [584] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In the brain of hypoxic-ischemic encephalopathy dead human newborns, LC3 immunostaining on paraffin sections has been used to quantify increased autophagosome presence in dying neurons as shown by increased LC3-positive dots [534,535].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Supportedcites [534] source
The Immunohistochemistry section says the human samples were paraffin-embedded sections. The Quantification of autophagic and lysosomal labeling section describes counting LC3-positive dots per neuron, and the results report increased counts in human HIE cases compared with controls. The Enhanced autophagy in relation to neuronal death section concludes that autophagy is enhanced in dying neurons. (LLM, conf=0.93)
- Partly supportedcites [535] sourceExperimental — accuracy not yet measured
The human-newborn results (pp. 4–5) report increased LC3B-positive dots per neuron in the lentiform nuclei of HIE cases, and the specimen methods (p. 8) describe paraffin-embedded autopsy tissue. Histology (p. 4) identifies dying neurons in that region, but the LC3B quantification is reported for neurons generally, not specifically for neurons identified as dying. (LLM, conf=0.83)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Nonetheless, it would be prudent to keep in mind that SQSTM1 contains domains that interact with several signaling molecules [590], and SQSTM1 may be part of MTORC1 [591].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [590] sourceExperimental — accuracy not yet measured
The Discussion discusses Beclin 1, LC3, and PI3K in autophagy, but does not address SQSTM1. Searches for SQSTM1’s signaling domains and its possible membership in MTORC1 found no passage in our copy supporting either point. (LLM, conf=0.76)
- Could not verifycites [591] sourceExperimental — accuracy not yet measured
Citation [591] is attached to the claim that SQSTM1 may be part of MTORC1. The Discussion passage addresses doxycycline-induced mitochondrial effects, and searches of our copy for SQSTM1, p62, and MTORC1 found no passage addressing that claim. Page numbers were not available. (LLM, conf=0.76)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Another issue is that some phosphatidylinositol 3-kinase (PtdIns3K) inhibitors such as LY294002, and to a lesser extent wortmannin (but apparently not 3-MA) [437], can inhibit protein synthesis [609]; this might in turn affect the turnover of SQSTM1 and LC3, which could influence conclusions that are drawn from the status of these proteins regarding autophagic flux or ALIS formation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [437] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked yetcites [609] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“One such case is seen during retinoic acid-induced differentiation of AML cells where SQSTM1 is upregulated [566] with concomitant increased autophagic flux [574].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [566] sourceExperimental — accuracy not yet measured
The section “SQST1 aggregates in rpl43 mutants are degraded by elevated autophagy activity” describes autophagy in C. elegans intestines after starvation or Tor inhibition, not during retinoic acid-induced differentiation of AML cells. Searches for retinoic acid, AML, and differentiation found no passage addressing the cited claim of increased autophagic flux in that setting. (LLM, conf=0.76)
- Partly supportedcites [574] sourceExperimental — accuracy not yet measured
The citation to this paper [574] is attached to the increased-autophagic-flux portion of the sentence. The paper reports that PMA plus SB202190 appears to increase autophagic flux during differentiation of K562 chronic myelogenous leukemia cells, while also causing some autophagic degradation blockage (Introduction; Results and Discussion). It does not establish increased flux during retinoic acid-induced differentiation of AML cells. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, SQSTM1 upregulation, and at least transient increases in the amount of SQSTM1, is seen in some situations where there is an increase in autophagic flux [571-573].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [571] sourceExperimental — accuracy not yet measured
The 'Proteasomal Function and Autophagy' section reports impaired autophagic flux with palmitate and increased autophagosome clearance with carbamazepine, but does not mention SQSTM1. Searches for SQSTM1, p62, and sequestosome found no passage linking an increase in SQSTM1 to increased autophagic flux. No page number was available in our copy. (LLM, conf=0.75)
- Partly supportedcites [572] sourceExperimental — accuracy not yet measured
The Results sections on autophagy gene expression and hormetic heat shock report that heat shock induced a transcriptional reporter for sqst-1, the C. elegans SQSTM1/p62 orthologue, and that autophagy remained active in the heat-shocked animals. The paper does not report an increase, transient or otherwise, in the amount of SQSTM1 protein; reporter induction cannot establish that part of the claim. Page numbers are unavailable in our copy. (LLM, conf=0.86)
- Partly supportedcites [573] sourceExperimental — accuracy not yet measured
The Results sections on TFEB targets and autophagy report increased expression of the worm SQSTM1 orthologue, sqst-1, and modestly more SQST-1::GFP foci in certain tissues of glp-1 mutants. The authors say the foci may reflect increased autophagic flux, but they do not establish an increase in total SQST-1 protein or show that it is transient. (LLM, conf=0.86)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“GCA (grancalcin) inhibits K48-linked ubiquitination and activates TRAF6dependent K63-linked ubiquitination of ULK1 to induce autophagy [647].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [647] sourceExperimental — accuracy not yet measured
The Results section ('Hsp90 Regulates Starvation-Induced Autophagy'; page unavailable) supports a role for ULK1 in inducing autophagy, and the Discussion says Hsp90–Cdc37 stabilizes ULK1 against proteasome-mediated degradation. The copy does not support the attributed mechanism: it does not identify GCA as the regulator or describe K48-linked inhibition or TRAF6-dependent K63-linked ubiquitination of ULK1. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“they may have both similar and distinct functions that are tissue-or cell-type specific [637-641]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [637] source
- Partly supportedcites [638] sourceExperimental — accuracy not yet measured
In Results and Discussion (page unavailable), the paper groups ULK1/2 as showing a punctate pattern during autophagy activation and reports that ULK1, but not ULK2, was among the homologs consistently up-regulated in senescent cells. These observations offer limited support for similarity and difference, but the paper does not establish that ULK1 and ULK2 have distinct functions or that their functions are tissue- or cell-type specific. (LLM, conf=0.76)
- Not checked yetcites [639] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [640] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [641] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“ULK2 has a higher degree of identity with ULK1 than any of the other homologs”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [637] source
- Could not verifycites [638] sourceExperimental — accuracy not yet measured
The Results and Discussion section identifies ULK1 and ULK3 as human Atg1 homologs and mentions prior findings on ULK1/2 localization. It does not compare ULK2’s sequence identity with ULK1 or rank the homologs by identity (searched for the quoted claim and for sequence identity and closest-homolog terms). (LLM, conf=0.76)
- Supportedcites [639] source
In “A Family of Atg1 Proteins in Vertebrates,” the paper states that ULK1 and ULK2 are the most closely related mammalian family members. It reports 78% identity between their kinase domains, higher than the identities reported for ULK3, ULK4, and Fused relative to ULK1. (LLM, conf=0.93)
- Could not verifycites [640] sourceExperimental — accuracy not yet measured
The ‘Modulation of Autophagic Protein’ section says that ULK1 and ULK2 both share homology with yeast Atg1p. The Discussion likewise describes both as close homologs of Atg1p, but neither passage compares ULK2’s sequence identity with ULK1 against that of other homologs. Searches for sequence identity, similarity, and a closest homolog found no such comparison in our copy; page numbers were not available. (LLM, conf=0.72)
- Partly supportedcites [641] sourceExperimental — accuracy not yet measured
The Results section identifies ULK2 as a paralog of ULK1, and the Discussion calls them the closest mammalian homologs of Atg1. Neither passage compares their sequence identity with other homologs, so the claimed ranking is not established by our copy (page numbers unavailable). (LLM, conf=0.77)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“MTORC1-mediated autophagy is negatively regulated by SHOC2, a scaffold protein that activates the RAS-RAF-MAPK signaling pathway [682, 683].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [682] sourceExperimental — accuracy not yet measured
The Discussion section (‘Metabolic consequences of TBCK defects’; page unavailable) identifies mTORC1 as an inhibitor of autophagy initiation, supporting a connection between mTORC1 and autophagy. It does not mention SHOC2 or establish that SHOC2 negatively regulates autophagy or activates the RAS-RAF-MAPK pathway. (LLM, conf=0.82)
- Could not verifycites [683] sourceExperimental — accuracy not yet measured
The Introduction describes mTORC1 as involved in autophagy, and the Discussion reports that TBC1D7 depletion increases mTORC1 signaling and delays autophagy. Neither passage addresses SHOC2 or its proposed effect on autophagy; searches for SHOC2 and the RAS–RAF–MAPK pathway found no supporting passage in our copy. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Under glucose starvation, AMPK apparently promotes autophagy by directly activating ULK1 through phosphorylation, although the exact AMPK-mediated ULK1 phosphorylation site(s) remains controversial (Table 2) [665, 669-671].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [665] sourceExperimental — accuracy not yet measured
Section 1.1 says AMPK phosphorylates PGC-1α, not ULK1. A search of our copy for ULK1, autophagy, glucose starvation, and disputed phosphorylation sites found no passage addressing the attributed mechanism; section 2.1 discusses a different fasting response. (LLM, conf=0.75)
- Partly supportedcites [669] sourceExperimental — accuracy not yet measured
The Results section (‘Amino acid-activated AMPK keeps ULK1 and autophagy active’; page unavailable) states that AMPK activates ULK1 by phosphorylating S317 and reports that S317 phosphorylation was detected in starved cells. It does not establish that those cells were glucose-starved, and it does not describe the AMPK-mediated phosphorylation site as controversial. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [670] source
- Partly supportedcites [671] sourceExperimental — accuracy not yet measured
The main text (page unavailable) says ULK1 activity increases in an AMPK-dependent manner after glucose deprivation and that AMPK directly phosphorylates and activates ULK1. It identifies six phosphorylation sites and says further work is needed to annotate all sites, but it does not say the identified sites are controversial. (LLM, conf=0.82)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Another recent study demonstrated a functional link between CLEC16A and disrupted mitophagy in murine splenic immune cells and showed that incomplete mitophagy predisposes clec16a knockout mice to a cascade of altered immune signaling functions resulting in pathogenic inflammation [321,322].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [321] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
- Could not verifycites [322] sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“AMPK inhibits MTORC1 by phosphorylating and activating TSC2 [687], as well as by phosphorylating the MTOR binding partner RPTOR [688].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [687] sourceExperimental — accuracy not yet measured
Citation [688] is attached to the claim that AMPK inhibits mTORC1 by phosphorylating RPTOR. The Introduction identifies Raptor as an mTORC1 component, and the Discussion describes its binding to mTOR, but neither passage addresses AMPK phosphorylation. Searches for AMPK and TSC2 phosphorylation found no passage supporting the attributed mechanism; the TSC2 clause is cited separately to [687]. (LLM, conf=0.72)
- Not checked — no full text of the sourcecites [688] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Finally, there are several ULK1 substrates that exhibit no, or at least no apparent, function in autophagy, or that have additional cellular functions separate from autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [720] sourceExperimental — accuracy not yet measured
The Results section identifies SEC16A as a ULK1/2-phosphorylated protein, and the Discussion describes its role in ER-to-Golgi trafficking as independent of other autophagy proteins. This supports an example of a ULK1 substrate with a function separate from autophagy, but the paper does not establish the claim that several substrates have such functions. (LLM, conf=0.85)
- Partly supportedcites [721] sourceExperimental — accuracy not yet measured
The Results section identifies STING as a ULK1 substrate and reports that ULK1 phosphorylation of STING regulates innate immune signaling, while loss of ULK1 did not affect STING-dependent autophagy. This supports an example of a substrate with a function beyond autophagy, but the paper does not establish the claim about several ULK1 substrates. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [722] source
- Supportedcites [723] source
The Discussion (page unavailable) reports ULK1-mediated phosphorylation of SEC16A in COPII assembly at ER exit sites and of SEC23B in autophagic vesicle formation. It also describes effects on the secretory pathway, supporting the claim that ULK1 substrates can have cellular roles beyond autophagy. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [724] source
- Partly supportedcites [725] sourceExperimental — accuracy not yet measured
The Discussion identifies syntenin-1 as a ULK1 substrate involved in trafficking, a function separate from autophagy. It does not establish that several ULK1 substrates have nonautophagic functions or no apparent function in autophagy; the other substrates it names, FIP200 and mAtg13, are mentioned only in connection with a lack of reports on their involvement in endocytic trafficking. (LLM, conf=0.84)
- Supportedcites [726] source
The Introduction (page unavailable) identifies AMPK, mTOR, and raptor as ULK1 phosphorylation targets involved in mTOR/p70S6k signaling, and reports that ULK1 phosphorylation of PDK1 affects its activity toward Akt and p70S6k. This supports the claim that several ULK1 substrates have cellular signaling functions beyond their roles in autophagy; the paper does not establish that any lack an autophagic function. (LLM, conf=0.84)
- Partly supportedcites [727] sourceExperimental — accuracy not yet measured
The Results (ULK1 mediates Type I IFN-dependent activation of p38 MAPK; page unavailable) report p38α MAPK phosphorylation in a ULK1 kinase assay, and another Results section finds that ULK1 promotes IFN-dependent gene transcription independently of autophagy. The Discussion (page unavailable) cautions that p38 phosphorylation may occur directly or through intermediate kinases. The paper therefore supports a non-autophagic role for ULK1, but does not establish that several ULK1 substrates have no apparent autophagy function or separate cellular functions. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites [728] source
- Partly supportedcites [729] sourceExperimental — accuracy not yet measured
The Results sections on VCP phosphorylation and stress-granule dynamics show that VCP is a ULK1/2 substrate involved in a process that does not require canonical autophagy machinery. That supports the claim's point about an additional function separate from autophagy, but the paper does not establish that several ULK1 substrates have such functions or lack an apparent role in autophagy. Page numbers are unavailable in our copy. (LLM, conf=0.86)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In yeast, the AMPK ortholog Snf1 shows autophagy inhibitory functions dependent on its ability to inhibit cytosolic Acc1 (acetyl-CoA carboxylase)-mediated lipogenesis, which is required for autophagy in stationary phase cells [653].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [653] sourceExperimental — accuracy not yet measured
The Results section reports that AMPK activation supports cannabinoid-induced autophagy in pancreatic cancer cells, but does not address Snf1 in yeast. Searches for Snf1, Acc1, lipogenesis, and stationary-phase autophagy found no passage supporting the attributed mechanism. The different cell type and conditions mean the pancreatic-cell finding does not contradict the yeast claim. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“ULK1 is ubiquitinated for its activation through TRAF6-dependent K63-linked ubiquitination [501], or for degradation through CUL3-KLHL20-dependent K48-linked ubiquitination [646].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [501] sourceExperimental — accuracy not yet measured
Citation [646] is attached to the claim that CUL3-KLHL20-dependent K48-linked ubiquitination targets ULK1 for degradation; the TRAF6 clause has a separate citation. The Results discuss degradation of autophagic cargo, and the Discussion addresses autophagosome–lysosome fusion, but neither addresses ULK1 ubiquitination. Searches for ULK1, CUL3-KLHL20, and K48-linked ubiquitination found no supporting passage in our copy. (LLM, conf=0.76)
- Could not verifycites [646] sourceExperimental — accuracy not yet measured
The cited paper is attached to the CUL3-KLHL20/K48-linked degradation clause [646]. Its Results discuss kinase-inactivated ULK1, autophosphorylation, and autophagic protein degradation, but the passages found for CUL3-KLHL20 and K48-linked ubiquitination do not address ubiquitination or degradation of ULK1 itself. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Compound C is an effective and widely used inhibitor of activated (phosphorylated) AMPK [672, 673].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [672] sourceExperimental — accuracy not yet measured
The supplied passages discuss AMPK activation, phosphorylation of ULK1, and AMPK-deficient cells, but do not address Compound C. Searches for “Compound C” and “dorsomorphin” found no passage establishing that it inhibits activated AMPK or is widely used. (LLM, conf=0.72)
- Partly supportedcites [673] sourceExperimental — accuracy not yet measured
In the Results section (page not specified), the paper calls compound C an AMPK inhibitor and reports that it prevented AMPK from activating Ulk1 in an assay. It does not establish that compound C is widely used or specifically characterize its inhibition of phosphorylated AMPK. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“pharmacological inhibition of ULK1 and ULK2, with the compound MRT68921, blocks the process, and expression of a drugresistant ULK1 mutant is sufficient to rescue this block [457]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [457] sourceExperimental — accuracy not yet measured
The Autophagy regulation by phototransduction section reports reduced autophagy after GNAT1 knockout, not after treatment with MRT68921. Searches of our copy for MRT68921, ULK1/ULK2 inhibition, and a drug-resistant ULK1 rescue found no passage addressing either part of the claim. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“ULK1 activity can also be inhibited by the highly selective inhibitor SBI-0206965 [642] and the expression of a dominant-negative ULK1 mutant [643, 644].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Supportedcites [642] source
The Introduction (page unavailable) states that dominant-negative ULK1 mutants block autophagy, supporting the mutant-related part of the citing sentence attributed to this paper [643, 644]. The SBI-0206965 claim has a separate citation [642] and is not being judged against this source. (LLM, conf=0.86)
- Could not verifycites [643] sourceExperimental — accuracy not yet measured
The citation to this paper is attached to the dominant-negative ULK1 mutant, not to SBI-0206965. The section ‘Ulk1 is dispensable for adipogenesis in 3T3-L1 cells’ describes shRNA knockdown of Ulk1, but our copy does not say that expression of a dominant-negative mutant inhibits ULK1 activity (searched: dominant-negative ULK1, kinase-dead mutant, mutant kinase activity). (LLM, conf=0.74)
- Could not verifycites [644] sourceExperimental — accuracy not yet measured
The citation to this paper is attached to the dominant-negative ULK1 mutant, not to SBI-0206965. The “Methylation Silencing of ULK2 and Glioma Development” section describes a kinase mutant of ULK2, but the passages found for “dominant-negative ULK1 mutant” and “ULK1 kinase mutant” do not describe a dominant-negative ULK1 mutant or show that its expression inhibits ULK1 activity. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In cells with excess sphingomyelin, ATG9A is trapped in juxtanuclear recycling endosomes, and its failure to be recruited to autophagic membranes results in defective phagophore closure [807].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Partly supportedcites [807] sourceExperimental — accuracy not yet measured
The paper’s Discussion reports Atg9 cycling between mitochondria and the pre-autophagosomal structure in yeast, and its phagophore model links Atg9-containing membranes to autophagosome formation (pages not given). It does not report excess sphingomyelin, ATG9A trapping in juxtanuclear recycling endosomes, or defective phagophore closure. (LLM, conf=0.80)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Along these lines, both TORC1 and autophagy can be active in specific cell subpopulations of yeast colonies [757].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [757] sourceExperimental — accuracy not yet measured
The Introduction mentions yeast only as a source of genetic screens for autophagy genes. The Results and discussion concern apoptotic cell clearance in C. elegans. Searches for TORC1 and yeast-colony subpopulations found no passage addressing whether TORC1 and autophagy can be active in those cells; page numbers were not available in our copy. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“During mycobacterial infection of macrophages, MTOR induces the expression of MIR155 and MIR31 to sustain the activation of the WNT5A and SHH/sonic hedgehog pathways.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [777] sourceExperimental — accuracy not yet measured
The Introduction (p. 3) and results (p. 8) address mTORC1 regulation of autophagy in skeletal muscle, not mycobacterial infection of macrophages. Searches for MIR155, MIR31, WNT5A, SHH, and macrophage infection found no passage in our copy addressing the claimed pathway. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“ATG5, ATG12 and ATG16L1 associate with the phagophore and have been detected by fluorescence and immunofluorescence (Figure 24) [808,809].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [808] sourceExperimental — accuracy not yet measured
The Results section on Atg9 localization (Fig. 1) describes fluorescence detection of Atg9-GFP at the PAS, and Materials and methods describes fluorescence imaging of Atg9-positive puncta. Searches for Atg5, Atg12, and Atg16L1 found no passage in our copy addressing whether those proteins associate with the phagophore or were detected by fluorescence or immunofluorescence. (LLM, conf=0.74)
- Could not verifycites [809] sourceExperimental — accuracy not yet measured
The Results describe fluorescent localization of Atg9, Atg23 and Atg18 at the pre-autophagosomal structure (Figures 2A and 5A), not localization of ATG5, ATG12 or ATG16L1 at the phagophore. Searches for those proteins and immunofluorescence found no passage addressing the attributed claim. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Furthermore, free ATG12 can be detected in some cell lines and tissues and has ATG5-independent roles in cell signaling [814-816].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [814] sourceExperimental — accuracy not yet measured
The Results section on production of Apg5-deficient cells reports that Apg5 is almost completely conjugated with Apg12 in wild-type mouse embryonic stem cells. The Results and Discussion address the conjugate’s role in autophagosome formation, but the passages found do not address detectable free Apg12 in other cell lines or tissues, or Apg5-independent cell-signaling roles (searched for both). (LLM, conf=0.76)
- Could not verifycites [815] sourceExperimental — accuracy not yet measured
The Introduction describes ATG12 conjugated to ATG5, and the Results discuss ATG12–ATG5 puncta. Searches for free or unconjugated ATG12 and ATG5-independent signaling found no passage addressing its detection in cell lines or tissues or its proposed signaling roles. Page numbers were not available in our copy. (LLM, conf=0.76)
- Could not verifycites [816] sourceExperimental — accuracy not yet measured
The Results and Discussion passages describe free ATG5 and the ATG12–ATG5 conjugate in Arabidopsis seedlings, not detectable free ATG12. Searches for free ATG12 and ATG5-independent signaling found no passage addressing either part of the claim. (LLM, conf=0.75)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
None of the sources cited for this claim have been checked yet.
In the paper
“TORC1 activity does not necessarily preclude autophagy induction because there are TOR-independent mechanisms that induce autophagy both in mammals and yeast [757-761]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [757] sourceExperimental — accuracy not yet measured
The Introduction discusses conserved autophagy genes, and the Conclusion discusses their role in apoptotic cell clearance in C. elegans, but neither addresses TORC1 activity or TOR-independent autophagy induction. Searches for TORC1, TOR-independent mechanisms, and rapamycin did not locate a passage supporting the claim about mammals and yeast. (LLM, conf=0.70)
- Not checked yetcites [758] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [759] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [760] source
Checked before — its earlier verdict is held back until a new check runs.
- Could not verifycites [761] sourceExperimental — accuracy not yet measured
The Introduction (page not available) describes LC3-associated phagocytosis as a noncanonical function of autophagy proteins, but does not say it is induced independently of TORC1 activity. Searches for TORC1, TOR-independent autophagy induction, and yeast found no passage in our copy addressing the claim. (LLM, conf=0.75)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Accordingly, the ULK activity state may thus reflect its role in these processes [780-786].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [780] sourceExperimental — accuracy not yet measured
The Results section on autophagy and MTORC2 signaling measures AKT phosphorylation, not ULK activity. A ULK1-related work appears in the References, but the paper’s text does not say that ULK’s activity state reflects its role in these processes (searched: ULK1, ULK activity, and phosphorylation). (LLM, conf=0.72)
- Could not verifycites [781] sourceExperimental — accuracy not yet measured
The paper’s Abstract passages describe changes in mTOR activity during autophagy and lysosome reformation, but do not address ULK activity or what its activity state reflects. Searches for ULK activity and ULK1 kinase phosphorylation returned no passage addressing that point. (LLM, conf=0.75)
- Partly supportedcites [782] sourceExperimental — accuracy not yet measured
The passage on mTORC1 and developing autophagosomes (section labeled Abstract; page not provided) says that mTORC1 regulates autophagy upstream of the ULK complex and that ULK plays an essential role in early autophagosome formation. It does not assess ULK’s activity state or establish that this state reflects its role in the processes discussed. (LLM, conf=0.78)
- Supportedcites [783] source
The Introduction (page unavailable) describes ULK activation as required to initiate autophagy. The section “MTOR-dependent WNT-SHH signaling regulates autophagy” (page unavailable) reports activating and inhibitory ULK1 phosphorylation states during mycobacterial infection and uses them to infer that MTOR regulates autophagy independently of ULK. This supports the hedged claim that ULK’s activity state may indicate its role in the processes studied. (LLM, conf=0.82)
- Supportedcites [784] source
The ‘ULK1 interacts with PARP1’ section (page unavailable) reports that ULK1 catalytic activity is required for nuclear localization and interaction with PARP1, and that an activity-impaired mutant does not restore sensitivity to oxidative-stress-induced cell death. This supports the hedged claim that ULK activity may reflect its role in these processes. (LLM, conf=0.86)
- Partly supportedcites [785] sourceExperimental — accuracy not yet measured
In “Hypothesis-Based RNAi Screening for Effectors of α-Syn Misfolding” (page not provided), the paper identifies a kinase related to ULK2 and describes roles in autophagy and axon elongation. It does not discuss ULK’s activity state or suggest that the state reflects those roles. (LLM, conf=0.78)
- Not checked — no full text of the sourcecites [786] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Complex I is composed of PIK3C3/VPS34, PIK3R4/VPS15/p150, BECN1, ATG14 and NRBF2 for mammals, or Vps34, Vps15, Vps30/Atg6, Atg14 and Atg38 for yeast.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [789] sourceExperimental — accuracy not yet measured
The Introduction discusses Unc-51 and kinesin-mediated vesicle transport, while the References mention a Drosophila PI3K-pathway study; neither gives the composition of mammalian or yeast Complex I. Searches for PIK3C3/VPS34, NRBF2, Atg38, and the claimed subunit lists found no passage addressing that composition. (LLM, conf=0.76)
- Could not verifycites [790] sourceExperimental — accuracy not yet measured
The Results passage on Drosophila Unc-51 discusses synaptic organization, while the References mention autophagy studies but do not describe Complex I composition. Searches for PIK3C3/VPS34, NRBF2, Atg38, and the mammalian and yeast Complex I subunits found no passage in our copy addressing the claimed composition. (LLM, conf=0.78)
- Could not verifycites [791] sourceExperimental — accuracy not yet measured
The Abstract and Results discuss Ulk1/2-mediated endocytosis and NGF/TrkA signaling, not the composition of complex I. Searches for the named mammalian subunits and the yeast terms Atg38 and Vps30 found no passage addressing the claimed subunit lists. (LLM, conf=0.76)
- Could not verifycites [792] sourceExperimental — accuracy not yet measured
The Introduction describes autophagy machinery involving ULK1, Atg5, Atg7 and Beclin1, but does not identify the subunits of Complex I. Searches for the listed mammalian and yeast proteins and for class III phosphatidylinositol 3-kinase Complex I found no passage in our copy addressing the claimed composition. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [793] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In neurons ATG9 localizes to axons and presynaptic sites, and requires active transport by the kinesin motor KIF1A to direct its localization into distal neurites [30,537].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Not checked — no full text of the sourcecites [30] source
- Partly supportedcites [537] sourceExperimental — accuracy not yet measured
The Discussion reports Atg9A in axons and axon terminals of Purkinje cells and in axon terminals of basket cells, supporting the localization claim. The paper does not establish that KIF1A-dependent active transport is required to direct Atg9A into distal neurites; searches for KIF1A and motor-dependent transport found no supporting passage. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“following ULK1 complex activation, ATG13 relocates to the omegasome, which results in a punctate pattern [748, 749].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [748] sourceExperimental — accuracy not yet measured
The Discussion (Figure 9) reports localization of yeast Atg1 to the PAS and its interaction with Atg13, not relocation of ATG13 to an omegasome. Searches for ULK1, omegasomes, and punctate ATG13 localization found no passage in our copy addressing the claimed sequence of events. (LLM, conf=0.75)
- Could not verifycites [749] sourceExperimental — accuracy not yet measured
The Introduction describes ULK1 activation, and the Discussion describes its complex with ATG13, but neither says ATG13 relocates to an omegasome or forms puncta. Searches for omegasome localization and punctate ATG13 yielded no passage addressing that claim; page numbers were unavailable in our copy. (LLM, conf=0.72)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In Arabidopsis and some mammalian cells it appears that essentially all of the ATG5 and ATG12 proteins exist in the conjugated form, and the expression levels do not change, at least during short-term starvation [291, 808, 809, 811].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Partly supportedcites [291] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) identifies Atg12-Atg5 as a conjugation system, supporting the existence of the conjugated form. It does not say that essentially all ATG5 and ATG12 are conjugated in Arabidopsis or mammalian cells, or that their expression remains unchanged during short-term starvation. (LLM, conf=0.78)
- Could not verifycites [808] sourceExperimental — accuracy not yet measured
The Results section on Atg9 reservoirs describes their movement after 60 minutes of starvation in yeast, not ATG5–ATG12 conjugation or protein expression levels. Searches for Arabidopsis, mammalian cells, ATG5–ATG12 conjugation, and expression during short-term starvation found no passage addressing the attributed claim. (LLM, conf=0.76)
- Could not verifycites [809] sourceExperimental — accuracy not yet measured
The Results passages discuss Atg9 and Atg23 localization and levels in cells with ATG1 deleted, including under starvation conditions. Searches for ATG5–ATG12 conjugation and expression during short-term starvation found no passage addressing those proteins in Arabidopsis or mammalian cells. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [811] source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“It is worth noting, however, that in some cell lines free ATG5 can be detected [812], suggesting that the amount of free ATG5 may be cell line-dependent;”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [812] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) mentions ATG5 as part of the ATG12–ATG5–ATG16L1 complex, and Materials and methods > Transfections lists an ATG5 siRNA. Neither passage addresses detectable free ATG5 or whether its amount varies by cell line; searches for “free ATG5” and unconjugated ATG5 found no such passage. (LLM, conf=0.72)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Yeast Atg9 may cycle between the phagophore assembly site (PAS) and peripheral reservoirs [801]; the latter correspond to tubulovesicular clusters that are precursors to the phagophore [802].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [801] sourceExperimental — accuracy not yet measured
The citation [802] is attached to the claim that yeast Atg9 peripheral reservoirs are tubulovesicular clusters that precede the phagophore. The Introduction and Results passages discuss LC3-associated phagocytosis and autophagy proteins, but do not address those reservoirs. Searches for Atg9, tubulovesicular clusters, and phagophore precursors found no passage supporting or contradicting the claim; page numbers were unavailable in our copy. (LLM, conf=0.78)
- Could not verifycites [802] sourceExperimental — accuracy not yet measured
Citation [801] is attached to the claim that yeast Atg9 may cycle between the PAS and peripheral reservoirs; [802] is attached to the separate claim about tubulovesicular clusters. The Abstract and the section headed “Torin1 Is a Potent and Selective mTOR” discuss yeast autophagy and autophagosome formation, but passages retrieved for Atg9, PAS, and peripheral reservoirs do not address Atg9 cycling. (LLM, conf=0.76)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The co-activation of AMPK and MTORC1 in these cancer cells is associated with increased autophagy flux, with AMPK as the major regulator of autophagy in these conditions [762, 763].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [762] sourceExperimental — accuracy not yet measured
The Discussion identifies AMPK as a regulator of autophagy through Cyclin Y/CDK16. The paper does not report co-activation of AMPK and mTORC1 in acute myeloid leukemia cells, increased autophagic flux under those conditions, or AMPK as the major regulator there. Its Introduction instead describes AMPK inhibiting mTORC1 during nutrient deprivation. (LLM, conf=0.87)
- Not checked — no full text of the sourcecites [763] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“There are two conserved classical adaptor protein sorting signals within the cytosolic N terminus of ATG9, which mediate trafficking of ATG9 from the plasma membrane and trans-Golgi network (TGN) via interaction with AP-1/2 [805, 806].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Not checked — no full text of the sourcecites [805] source
- Partly supportedcites [806] sourceExperimental — accuracy not yet measured
The Introduction reports that ATG9A localizes to the trans-Golgi network and endosomes and that its vesicles move to autophagosome-forming sites under starvation. It does not describe two conserved N-terminal sorting signals, trafficking from the plasma membrane, or interactions with AP-1/2; searches for those terms found no supporting passage in our copy. No page number was supplied for the Introduction passage. (LLM, conf=0.85)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Complex I regulates autophagy, whereas complex II regulates endocytic pathways, LAP, and cytokinesis [794-796].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Could not verifycites [794] sourceExperimental — accuracy not yet measured
The Introduction discusses Vps34p in intracellular protein sorting, and the Additional information section proposes a role for the human complex in trafficking from the Golgi to the lysosome. Neither passage addresses distinct complex I and II functions in autophagy, endocytic pathways, LAP, or cytokinesis. Searches for those terms and for “complex II” found no passage establishing the claimed division of roles. (LLM, conf=0.75)
- Partly supportedcites [795] sourceExperimental — accuracy not yet measured
The Results (page unavailable) show that the Atg14 complex is required for autophagosome formation. The Discussion (page unavailable) suggests that the UVRAG complex may function in endocytic pathways, but says its role remains unknown; our copy does not link it to LAP or cytokinesis. (LLM, conf=0.90)
- Partly supportedcites [796] sourceExperimental — accuracy not yet measured
The Results and Discussion identify complex I with autophagy and complex II with carboxypeptidase Y (CPY) sorting in yeast. The Discussion mentions possible endosomal trafficking involving complex II, but does not establish that it regulates endocytic pathways; it discusses endocytosis as a possible function of additional complexes. The paper does not address LAP or cytokinesis. Page numbers are unavailable in our copy. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the autophosphorylation of Atg1 at Thr226 is required for its kinase activity and for autophagy induction”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Partly supportedcites [742] sourceExperimental — accuracy not yet measured
The section “Atg1 Kinase Activity Is Not Necessary for PAS Recruitment of Atg Proteins but Is Needed for Their Normal Localization” (page unavailable) reports that Atg1 kinase activity has an essential role in autophagy. It studies K54A and K54A,M102A mutants, but our copy does not establish that autophosphorylation at Thr226 is required for either kinase activity or autophagy induction. (LLM, conf=0.87)
- Partly supportedcites [743] sourceExperimental — accuracy not yet measured
The Discussion reports that Atg1 kinase activity is needed for autophagy and discusses Atg1 autophosphorylation. However, the passages do not identify Thr226 or establish that autophosphorylation at that site is required for kinase activity or autophagy induction (searched: Thr226, T226). (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“For example, CSNK2 (casein kinase 2) and ULK1 induce phosphorylation of SQSTM1 at serine 403 and serine 409, respectively, increasing the binding affinity of SQSTM1 for ubiquitin, and enhancing the autophagic degradation of ubiquitinated proteins [429, 711].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked — no full text of the sourcecites [429] source
- Could not verifycites [711] sourceExperimental — accuracy not yet measured
The 'ULK1 induces phosphorylation of Raptor' section identifies Raptor phosphorylation sites, not SQSTM1 sites. Searches for SQSTM1 Ser409 and p62 Ser403 found no passage in our copy addressing CSNK2 or ULK1 phosphorylation of SQSTM1, its ubiquitin-binding affinity, or the claimed effect on degradation. (LLM, conf=0.77)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Although less work has been done on post-transcriptional regulation, several studies implicate microRNAs in controlling the expression of proteins associated with autophagy [334-336, 984-987].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Supportedcites [334] source
The section “miR-101 directly targets STMN1, RAB5A and ATG4D” reports that miR-101 regulates three genes linked to autophagy and reduces Stathmin and RAB5A protein levels. This paper therefore supports its citation as one of several studies implicating microRNAs in the expression of autophagy-associated proteins. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites [335] source
- Could not verifycites [336] sourceExperimental — accuracy not yet measured
The Introduction describes an siRNA screen identifying kinases that regulate autophagy, and the Discussion addresses siRNA-mediated depletion of target proteins. Searches for microRNAs and post-transcriptional regulation found no passage in our copy saying that microRNAs control the expression of autophagy-associated proteins. siRNAs used as experimental tools do not establish the claim about microRNAs. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [984] source
- Could not verifycites [985] sourceExperimental — accuracy not yet measured
The Results section describes ZKSCAN3 regulation of autophagy-related gene expression, and the Introduction and Discussion discuss transcription factors. Searches for microRNAs, miRNAs, and post-transcriptional regulation found no passage in our copy addressing microRNA control of autophagy-associated proteins. The copy therefore does not verify the point attributed to this source. (LLM, conf=0.76)
- Supportedcites [986] source
The Discussion (page unavailable) reports that the microRNA MIR152 inhibits the autophagy-associated protein ATG14 and thereby decreases autophagy. This supports the cited sentence’s general point that microRNAs can regulate proteins associated with autophagy. (LLM, conf=0.87)
- Could not verifycites [987] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) discusses protein interactions and transcription factors that regulate autophagy, but does not address microRNAs. Searches for microRNA, miRNA, and post-transcriptional regulation found no passage in our copy supporting the attributed claim. (LLM, conf=0.74)
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Methotrexate treatment triggers autophagy in time-course experiments, as the mature LC3-II form rapidly increases following MIR27A knockdown, whereas the change is limited in control and MIR27Aoverexpressing HCT116 cells.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [988] sourceExperimental — accuracy not yet measured
The Results section on pharmacological activation reports sulforaphane-induced LAMP2A expression and chaperone-mediated autophagy, not a methotrexate time course. Searches for methotrexate, MIR27A, HCT116 and LC3-II found no passage addressing the claimed comparison. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Finally, CEBPB/C/EBPβ is a transcription factor that regulates autophagy in response to the circadian cycle in mice [983] and zebrafish [926].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [983] sourceExperimental — accuracy not yet measured
The Results (§2.5) discuss PU.1 regulation of autophagy-related genes during AML-cell differentiation, not CEBPB/C/EBPβ regulation in zebrafish. Searches of our copy for CEBPB, zebrafish, and circadian regulation found no passage addressing the claim; the separate mice citation in the citing sentence is not being judged here. (LLM, conf=0.76)
- Could not verifycites [926] sourceExperimental — accuracy not yet measured
Citation [926] is attached to the zebrafish portion of the sentence. The available passages, labeled Abstract with no page number, contain bibliographic information about hypoxia and autophagy in human tumor cells, but no findings about C/EBPβ, zebrafish, or circadian regulation. Searches for those terms and for 'circadian clock' returned no relevant passage from the paper’s text. (LLM, conf=0.73)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“TFEB activity is regulated by starvation and is controlled by both MAPK1/ERK2-, MTOR-, and AKT-mediated phosphorylation at specific serine residues [943, 964-967]; thus, it can serve as a new tool for monitoring transcriptional regulation connected with autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [943] sourceExperimental — accuracy not yet measured
The Results discuss TORC1 activity and EIF4EBP1 phosphorylation in the Bombyx fat body, while the Discussion describes 20E-induced autophagy. Searches for TFEB and its proposed regulation by starvation, MAPK1/ERK2, MTOR, AKT, and serine phosphorylation found no passage addressing that claim. (LLM, conf=0.75)
- Could not verifycites [964] sourceExperimental — accuracy not yet measured
The Results describe starvation-induced VMP1 expression and mTOR inhibition during autophagy, not regulation of TFEB. Searches for TFEB, MAPK1/ERK2, AKT, and serine phosphorylation found no passage in our copy addressing the attributed claim; page numbers were not available. (LLM, conf=0.76)
- Could not verifycites [965] sourceExperimental — accuracy not yet measured
The section “Mammalian VMP1, EI24, and mEPG5 Are Required for Starvation-Induced Autophagy” discusses starvation-induced autophagy, not regulation of TFEB. Searches for TFEB, its phosphorylation, and the named kinases found no passage addressing the attributed claim. Page numbers were not provided for the decisive passages. (LLM, conf=0.75)
- Could not verifycites [966] sourceExperimental — accuracy not yet measured
The Results discuss starvation-induced autophagy after VMP1 depletion, and the Discussion addresses ER contact sites, but neither passage addresses TFEB. Searches of the indexed paper for TFEB and phosphorylation found no passage about starvation regulating TFEB or phosphorylation by MAPK1/ERK2, MTOR, or AKT. (LLM, conf=0.78)
- Could not verifycites [967] sourceExperimental — accuracy not yet measured
The Discussion and the section titled “Molecular Mechanism Underlying Oncogene-associated Autophagy” describe KRAS–PI3K–AKT1 regulation of GLI3 and VMP1, not TFEB. Searches for TFEB, starvation, and MAPK1/ERK2-, MTOR-, or AKT-mediated phosphorylation of TFEB found no passage addressing the claim; page numbers were not available in our copy. (LLM, conf=0.77)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In addition, as BECN1-PIK3C3/VPS34 are the major source of cellular PtdIns3P lipids and can be present in multiple complexes that act during endosome maturation in addition to autophagy [857], caution must be exercised when monitoring localization.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [857] sourceExperimental — accuracy not yet measured
The available passages contain article metadata and keywords, but do not discuss BECN1–PIK3C3/VPS34 complexes, cellular PtdIns3P, or endosome maturation. Searches for those terms and their alternative names returned no relevant passage from our copy. (LLM, conf=0.70)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“The basic helix-loop-helix transcription factor TFEB acts as a master gene of the CLEAR network and positively regulates the expression of both lysosomal and autophagy genes, thus linking the biogenesis of two distinct types of cellular compartments (i.e., autophagosomes and lysosomes) that cooperate in the autophagic pathway.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [943] sourceExperimental — accuracy not yet measured
The Introduction discusses FOXO-mediated upregulation of Atg genes, and the Results and Discussion concern 20-hydroxyecdysone-induced autophagy in the Bombyx fat body. Searches for TFEB, the CLEAR network, and coordinated lysosomal and autophagy gene expression found no passage addressing the claim. Page numbers were not available in our copy. (LLM, conf=0.75)
- Could not verifycites [962] sourceExperimental — accuracy not yet measured
The Introduction describes plant autophagosomes and vacuoles, while the Discussion identifies HsfA1a as a regulator of tomato autophagy genes. Searches for TFEB, the CLEAR network, and lysosome biogenesis found no passage addressing the attributed claim. No page numbers are available in our copy. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [963] source
- Could not verifycites [635] sourceExperimental — accuracy not yet measured
The Introduction describes autophagosomes delivering material to lysosomes, but does not address TFEB or regulation of their biogenesis. Searches for TFEB, the CLEAR network, and transcriptional regulation found no passage supporting the attributed claim; our copy instead focuses on autophagic-lysosomal inhibition and proteasome performance. (LLM, conf=0.73)
- Could not verifycites [636] sourceExperimental — accuracy not yet measured
The passage on embryogenesis discusses autophagy regulators such as Ambra1 and FIP200, not TFEB. Searches for TFEB, the CLEAR network, and coordinated regulation of lysosomal and autophagy genes found no passage in our copy addressing the claim. (LLM, conf=0.75)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Other important autophagy-related proteins such as ATG3, ATG5, ATG7 and ATG18A in plants are also targets for persulfidation, but the role of this modification needs further clarification [1009].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [1009] sourceExperimental — accuracy not yet measured
The section ‘Cysteine as the main sensor of redoxmediated signaling’ mentions S-sulfhydrylation as a possible cysteine modification, while ‘The complex network of autophagy regulation’ discusses ATGs generally. Searches for persulfidation, ATG18A, and plant ATG proteins found no passage identifying ATG3, ATG5, ATG7, or ATG18A as persulfidation targets or discussing the role of that modification in plants. Page numbers were not available in our copy. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Even increases in LC3 mRNA can be quite modest and are cell type-and organism-dependent [989].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Partly supportedcites [989] sourceExperimental — accuracy not yet measured
In “Autophagy undergoes diurnal rhythm during the day” (page unavailable), the paper reports oscillation and starvation-associated elevation of LC3B mRNA, and says rhythmic autophagy-gene expression is less pronounced in skeletal muscle than in heart. It does not describe LC3 mRNA increases as modest or establish that they differ between organisms; its example of modest mRNA oscillation is Becn1, not LC3B. (LLM, conf=0.84)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Interestingly, caspasemediated cleavage of BECN1 inactivates BECN1-induced autophagy and enhances apoptosis in several cell types [854],”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Could not verifycites [854] sourceExperimental — accuracy not yet measured
The paper’s Abstract discusses JNK1-mediated phosphorylation of Bcl-2, release of Beclin 1, and the later onset of apoptosis during starvation. Searches for caspase-mediated cleavage of Beclin 1 and its effects found no passage addressing that mechanism or its occurrence in several cell types. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“This is possibly because excessive mitochondria can be segregated into daughter cells by cell division if growth continues [1041].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [1041] sourceExperimental — accuracy not yet measured
The paper’s main text discusses cell hydration and proteolysis in liver and hepatocytes, not the segregation of mitochondria into daughter cells. Searches for mitochondrial segregation, cell division, nitrogen starvation, and mitophagy found no passage addressing the claim; the indexed passages have no page labels. (LLM, conf=0.76)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“These probes concentrate in mitochondria due to their negative charge and react with the reduced thiols present in mitochondrial matrix proteins [1114][1115][1116].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. Animal mitophagy and pexophagy.
What the sources say
- Not checked — no full text of the sourcecites [1114] source
- Could not verifycites [1115] sourceExperimental — accuracy not yet measured
The C. elegans Strains section mentions mitochondrial staining but does not explain how the dyes or probes work. Searches for negative charge and reduced thiols found no passage addressing mitochondrial accumulation or reactions with matrix proteins; page numbers were not available in our copy. (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [1116] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition to fluorescence methods, aggregates formed by a splice variant of CCND2 (cyclin D2) can also be monitored in electrondense lysosomes and autophagosomes by immunogold labeling and TEM techniques [1089].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Aggrephagy. Aggrephagy is the selective removal of aggregates by autophagy [1084].
What the sources say
- Partly supportedcites [1089] sourceExperimental — accuracy not yet measured
The Electron microscopy section (page unavailable) describes using electron microscopy to examine autophagic intermediates in yeast, including autophagosomes. It does not describe CCND2 splice-variant aggregates, immunogold labeling, or their detection in electron-dense lysosomes. (LLM, conf=0.85)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“The labeling can be done with relative ease both in cultured cells and in live animals [4], and has recently been scaled down to minimize the amount of radioactivity needed in cell culture experiments [26].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [4] source
- Could not verifycites [26] sourceExperimental — accuracy not yet measured
The main text (page unavailable) describes fluorescent labeling of omegasomes and autophagosomes during live imaging of cells, but does not address whether the labeling cited at [4] is easy to perform in both cultured cells and live animals. Searches for labeling in live animals and radioactive labeling found no relevant passage. The scaling-down claim is attached to [26], not this source. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“LGG-1 is essential for allophagosome formation, whereas LGG-2 contributes to their efficient maturation [1106].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > (tm3489) and lgg-2(tm5755).
What the sources say
- Could not verifycites [1106] sourceExperimental — accuracy not yet measured
The Figure 2 passage (page unavailable) discusses TFEB-induced autophagosome formation in dopaminergic neurons, and the MPTP-model section discusses LC3-II and autophagic degradation. Searches for LGG-1, LGG-2, and allophagosome maturation found no passage addressing their respective roles in formation and maturation. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Accumulation of these fragments is time dependent and is blocked by treatment with autophagy inhibitors.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [1024] sourceExperimental — accuracy not yet measured
The Results describe electron-dense fragments of cellular debris inside autophagosomes, but do not report whether those fragments accumulate over time or how autophagy inhibitors affect them. A separate passage describes changes in aggregated huntingtin levels over four days; it does not establish the claim about fragments. Searched for fragments, time-dependent accumulation, and autophagy-inhibitor treatment. (LLM, conf=0.73)
- Not checked — no full text of the sourcecites [1025] source
- Not checked — no full text of the sourcecites [1026] source
- Could not verifycites [1027] sourceExperimental — accuracy not yet measured
The Figure 5 caption (Discussion; page unavailable) describes a residual body containing membrane fragments after 28 hours of starvation, but does not report that fragments accumulate over time. The inhibitor analysis reports that 3-MA inhibits macroautophagic protein degradation, not that it blocks fragment accumulation. Searches for fragments, time-dependent accumulation, and inhibitor effects found no passage establishing the claim. (LLM, conf=0.74)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The relationship between SNCA clearnace and autophagy has also been exploited in yeast studies during chronological aging with SNCA expressed under the control of a constitutive promotor [349,351,368,626].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Aggrephagy. Aggrephagy is the selective removal of aggregates by autophagy [1084].
What the sources say
- Partly supportedcites [349] sourceExperimental — accuracy not yet measured
The Results section reports constitutive α-synuclein expression in yeast and examines its relationship with autophagy during chronological aging. The Discussion says increased autophagic flux likely clears α-synuclein in functionally competent cells, but reports deleterious effects of autophagy in aged cells; it does not establish α-synuclein clearance by autophagy in the aging yeast studied. The copy also does not identify the promoter controlling α-synuclein expression. (LLM, conf=0.84)
- Could not verifycites [351] sourceExperimental — accuracy not yet measured
The Discussion describes a GFP-Atg8 cleavage assay used to monitor autophagic flux in yeast, not SNCA clearance. Searches for SNCA, alpha-synuclein, chronological aging, and a constitutive promoter found no passage addressing the attributed yeast studies. (LLM, conf=0.75)
- Not checked — no full text of the sourcecites [368] source
- Could not verifycites [626] sourceExperimental — accuracy not yet measured
The Results discuss protein changes in lithium-treated rat kidney cells, and the Discussion addresses AQP2 regulation and cell proliferation (page numbers unavailable). Searches for SNCA clearance, autophagy, yeast, and chronological aging found no passage addressing the claimed yeast studies. (LLM, conf=0.77)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“In addition, the polyQ80-luciferase in the aggregated state lacks luciferase activity, whereas soluble polyQ80-luciferase retains activity.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Aggrephagy. Aggrephagy is the selective removal of aggregates by autophagy [1084].
What the sources say
- Could not verifycites [1100] sourceExperimental — accuracy not yet measured
The Results section on Htt103QP aggregation describes GFP-marked aggregates, not polyQ80-luciferase or its activity. Searches for polyQ80-luciferase and for luciferase activity in soluble versus aggregated protein found no passage addressing the claim in our copy; page numbers were not available. (LLM, conf=0.73)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Plate assays for monitoring the activity of peroxisomal oxidases in yeast colonies are also available [690,696].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [690] sourceExperimental — accuracy not yet measured
The paper’s Abstract describes IPMK, autophagy assays in mouse embryonic fibroblasts, and liver regeneration, not plate assays for yeast colonies. Searches for peroxisomal oxidases, yeast colonies, and plate assays found no passage addressing the claimed method. (LLM, conf=0.78)
- Could not verifycites [696] sourceExperimental — accuracy not yet measured
The paper describes a radioactive assay of human ULK1 activity (Abstract; page unavailable) and lists protein purification and crystallography methods (Methods; page unavailable). Searches for peroxisomal oxidases and yeast-colony plate assays found no passage addressing the claimed assays. The bacterial colonies mentioned in the Abstract are part of a protein-expression system, not a yeast plate assay. (LLM, conf=0.76)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“studies suggest that ubiquination of sperm-mitochondria could be required for the initial step of allophagy [1108,1109]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > (tm3489) and lgg-2(tm5755).
What the sources say
- Could not verifycites [1108] sourceExperimental — accuracy not yet measured
The Introduction discusses polyglutamine aggregation and seeding, not sperm mitochondria or allophagy (page unavailable in our copy). Searches for sperm-mitochondrial ubiquitination and paternal mitochondrial autophagy found no passage addressing the proposed initial step of allophagy. (LLM, conf=0.76)
- Partly supportedcites [1109] sourceExperimental — accuracy not yet measured
The section “What is the signal for the degradation of sperm-inherited organelles?” (page unavailable) says that ubiquitination of paternal mitochondria had been proposed as a degradation signal in mouse embryos. But it reports that, in worms, membranous organelles—not mitochondria—were ubiquitinated, and says the signal for mitochondrial degradation remains unknown. It therefore does not establish that mitochondrial ubiquitination is required to initiate allophagy. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This autophagy targeting requires both the ubiquitination of substrates and the loss of sperm mitochondrial membrane potential [1108,1110,1111].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > (tm3489) and lgg-2(tm5755).
What the sources say
- Could not verifycites [1108] sourceExperimental — accuracy not yet measured
The Introduction and Screening of the JHCCL sections concern polyglutamine aggregation and drug screening, not autophagy targeting in sperm. Searches for sperm mitochondrial membrane potential, substrate ubiquitination, and autophagy found no passage establishing either requirement; the autophagy hit was a reference about huntingtin aggregates. (LLM, conf=0.78)
- Partly supportedcites [1110] sourceExperimental — accuracy not yet measured
The discussion of paternal-mitochondria recognition (page not provided) reports that ubiquitinated sperm-derived membranous organelles are engulfed by autophagosomes. But it says there is no direct evidence that ubiquitination is involved in clearing paternal mitochondria in worms, and our copy does not establish a requirement for loss of sperm mitochondrial membrane potential. It therefore does not support the claim that both are required. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [1111] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“These fusion proteins are proteolytically cleaved off from Keima and degraded (whereas Keima is stable).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Could not verifycites [1031] sourceExperimental — accuracy not yet measured
The protein-identification section describes proteolytic fragments of betaine homocysteine methyltransferase, not Keima fusion proteins. Searches for Keima and for stable fluorescent fusion proteins found no passage addressing cleavage of a fusion partner or Keima’s stability; page numbers were unavailable in our copy. (LLM, conf=0.76)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of note, PINK-PRKN-dependent mitophagy is independent of the LC3 subfamily, but strongly requires the GABARAPs [35,36].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. Animal mitophagy and pexophagy.
What the sources say
- Partly supportedcites [35] sourceExperimental — accuracy not yet measured
The Results (Fig. 4B–C) show that GABARAP-deficient cells had markedly impaired parkin-dependent mitochondrial clearance and mitophagic flux. LC3-deficient cells cleared mitochondria at a rate similar to controls, but showed somewhat lower mtKeima flux; the paper therefore does not establish that mitophagy is wholly independent of LC3s. (LLM, conf=0.88)
- Could not verifycites [36] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) describes general autophagy machinery and mentions LC3, but does not address PINK–PRKN-dependent mitophagy or GABARAP requirements. Searches for the claimed LC3 independence and GABARAP dependence found no passage in our copy that speaks to either point. (LLM, conf=0.72)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
None of the sources cited for this claim have been checked yet.
In the paper
“In this case, mitophagy may be induced because the energy demand is lower at post-log phase and the mitochondrial mass exceeds the cell's needs [171, 1064, 1065].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Could not verifycites [171] sourceExperimental — accuracy not yet measured
The supplied passages and searches for post-log-phase mitophagy, mitochondrial mass, and energy demand found no discussion of the proposed explanation. The paper instead discusses autophagy during intracellular Salmonella infection (ABSTRACT; page unavailable). (LLM, conf=0.76)
- Not checked — no full text of the sourcecites [1064] source
- Not checked yetcites [1065] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Could not verify
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These stable cell lines are sensitive to autophagy inducers as measured by the LC3-II:LC3-I ratio by western blot, and also show increased numbers of cytoplasmic GFP-LC3 puncta upon autophagic stimuli (unpublished results R. Muñoz-Moreno, R.I. Galindo, L. Barrado-Gil and C. Alonso).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“A disadvantage of transfecting GFP-LC3 with liposomes is that frequently it leads to an unstable efficiency of transfection, causing a reduction in the number of cells effectively expressing GFP-LC3, and degradation of the plasmid, thus decreasing the numbers of GFP-LC3 puncta.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The Spot function in Imaris automatically locates and enumerates autophagosomes within individual cells based on size and intensity thresholds [404, 405].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Moreover, when autophagosome-lysosome fusion is blocked, larger autophagosomes are detected, possibly due to autophagosome-autophagosome fusion, or to an inability to resolve individual autophagosomes when they are present in large numbers.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“For example, high levels of overexpressed GFP-LC3 can result in its nuclear localization, although the protein can still relocate to the cytosol upon starvation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“This latter point is critical because, even in nutrient-rich conditions, cells display some basal level of GFP-LC3 puncta.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“some cell types (e.g., HeLa cells) may require 1 day for achieving optimal expression to visualize GFP-LC3 puncta, whereas neuronal cell lines such as SH-SY5Y cells typically need at least 48 h of expression prior to performing GFP-LC3 puncta analyses.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“This method can also be used for endogenous LC3, and, therefore, is useful for nontransfected primary cells [417].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
What the sources say
- Not checked — no full text of the sourcecites [417] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Table of Contents
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“One critical point is that autophagy is a highly dynamic, multi-step process.Like other cellular pathways, it can be modulated at several steps, both positively and negatively.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, autophagic responses to drugs may be different in transformed versus nontransformed cells, in confluent versus nonconfluent cells, or in cells grown with or without glucose [5].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Not checked yetcites [5] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
In the paper
“Plant cell-specific structures called provacuoles have a striking similarity to a phagophore, but form in an autophagy-independent manner [62].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Not checked — no full text of the sourcecites [62] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Table of Contents
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“the notoriously slow process of freeze substitution of frozen samples can be accelerated tremendously by sample agitation using either an experimental setup or agitation modules within automated freeze-substitution units [153,154].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [153] Kovács AL, 2004
- Not checked — no full text of the sourcecites [154] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“By responding to perturbations in the extracellular environment, cells tune the autophagic flux to meet intracellular metabolic demands and support repair mechanisms.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“It is the only tool that reveals the morphology of autophagic structures at a resolution in the nm range; shows these structures in their natural environment and position among all other cellular components; allows their exact identification; and, in addition, can support quantitative studies if the rules of proper sampling are followed [13].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Not checked — no full text of the sourcecites [13] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“That is, autophagic activity includes not just the increased synthesis or lipidation of Atg8/LC3/GABARAP (LC3 and GABARAP subfamilies constitute the mammalian homologs of yeast Atg8), or an increase in the formation of autophagosomes, but, most importantly, flux through the entire system, including lysosomes or the vacuole, and the subsequent release of the breakdown products.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“The impact of autophagic flux on cell death and human pathologies, therefore, demands accurate tools to measure not only the current flux of the system, but also its capacity [23], and its response time, when exposed to a defined stress [24].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Not checked yetcites [23] source
- Not matchedcites [24] Seglen PO, 1981, Acta Biol Med Ger
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Also, it is important to realize that while formation of Atg8-PE (or LC3/GABARAP-II) appears to correlate with the induction of autophagy, we do not know, at present, the actual mechanistic relationship between Atg8-PE (or LC3/GABARAP-II) formation and the rest of the autophagic process; indeed, some variants of autophagy proceed in the absence of LC3-II [32][33][34][35][36].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Autophagy can be both selective and nonselective, and TEM can be used to monitor both.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“A potential complication here is that inhibition of protein synthesis, for example, by cycloheximide (CHX), can activate MTORC1 signaling, which in turn impairs autophagy [28].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
What the sources say
- Not checked — no full text of the sourcecites [28] Kovács AL, 2000, Cell Tissue Res source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It should not be assumed that an autophagic system is at steady state in the strict biochemical meaning of this term, as this implies that the level of autophagosomes does not change with time, and the flux through the system is constant.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Degradation of the sequestered material and the corresponding deterioration of ultrastructure commences and runs to completion within the amphisome and the autolysosome after fusion with a late endosome and lysosome (the vacuole in fungi and plants), respectively (Figure 1) [64].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Not checked yetcites [64] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, increases in the level of phosphatidylethanolamine (PE)-modified Atg8-family proteins (Atg8-PE, or LC3/GABARAP-II), or even the appearance of autophagosomes, are not measures of autophagic flux per se, but can reflect the induction of autophagic sequestration and/or inhibition of autophagosome or amphisome clearance.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the use of autophagy markers such as LC3-II must be complemented by assays to estimate overall autophagic flux, or flow, to permit a correct interpretation of the results.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Autophagic bodies can be stabilized, however, by the addition of phenylmethylsulphonylfluoride (PMSF) or genetically by the deletion of the yeast PEP4 gene”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“lipofuscin is fairly easily distinguished from AVs and lysosomes by TEM but can be easily confused with autolysosomes in immunocytochemistry studies at the light microscopy level [77,136]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
What the sources say
- Not checked yetcites [77] source
- Not matchedcites [136] Rez G, 1980, Lab Invest
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“During this period, the membranes of the sequestered organelles (for example the ER or mitochondria) remain intact, and the electron density of ribosomes is conserved at normal levels.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In the case of selective autophagy, the cargo is the specific substrate being targeted for sequestration-bulk cytoplasm is essentially excluded.In contrast, during nonselective autophagy, disposable cytoplasmic constituents are sequestered.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 1. Transmission electron microscopy.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In this respect, 1 h of pre-incubation with 10-20 µM E-64d is sufficient in most cases, because this inhibitor is membrane permeable and rapidly accumulates within lysosomes, but another frequently used inhibitor, leupeptin, requires at least 6 h pre-incubation [79,343].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A significant portion of LAMP1-labeled organelles lack major lysosomal hydrolases, and LAMP1 intensity is not a sensitive readout to assess autophagic deficits in familial amyotrophic lateral sclerosis-linked motor neurons in vivo [190,191].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [190] source
- Not matchedcites [191] Kenny SJ, 2019, bioRxiv
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“and that bafilomycin A1 will ultimately cause a fusion block as well as neutralize the pH [220], but the inhibition of fusion may be due to a block in ATP2A/SERCA activity [305]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Turnover of LC3-II/Atg8-PE: Autophagic flux.
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“However, it is probably prudent to monitor both turnover of LC3-II and an autophagosome substrate in parallel, due to the fact that LC3 might be coupled to endosomal membranes and not just autophagosomes, and the levels of well-characterized autophagosome substrates such as SQSTM1/p62 can also be affected by proteasome inhibitors [342].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [342] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“If there are ribosomes associated with these membranes they can help in distinguishing them from the ribosome-free double-membrane of the phagophore and autophagosome.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Rapid freezing techniques such as high-pressure freezing followed by freeze substitution (i.e., dehydration and chemical fixation at low temperature) have a widely accepted potential for improved sample preparation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
boosted- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Such cryopreparation techniques have already proven especially useful for elucidation of autophagy in yeast [158,159].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [158] Howard V, 1998
- Not checked yetcites [159] Weibel ER., 1979
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Because GABARAP and GABARAPL1 can both be proteolytically processed and lipidated, generating GABARAP-I or GABARAPL1-I and GABARAP-II or GABARAPL1-II, respectively, this may lead to a misassignment of the different bands.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition, ex vivo samples are not typically randomized during processing, further complicating the possibility of valid statistical analyses.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition, interpretation of tomographic images can be problematic.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“There are morphometric procedures to measure or estimate the size range and the number of spherical objects by profiles in sections [162]; however, such methods have been used in autophagy research only a few times [43,151,164,165].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [162] source
- Not checked yetcites [43] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked — no full text of the sourcecites [151] source
- Not checked — no full text of the sourcecites [164] source
- Not checked — no full text of the sourcecites [165] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Finally, many of the chemicals used to inhibit autophagy, such as bafilomycin A1, NH4Cl or CQ (see Autophagy inhibitors and inducers), also directly inhibit the endocytosis/uncoating of viruses (D.R. Smith, personal communication), and other endocytic events requiring low pH, as well as exit from the Golgi (S. Tooze, personal communication).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“At least in neurons, pepstatin A alone is a less effective lysosomal proteolytic block, and combining a lysosomal cysteine protease (i.e., cathepsin) inhibitor with it is most effective [79].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [79] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Consequently, cryopreparation protocols have been established for many molecular biological model organisms and tissue culture [157].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [157] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The most common organelles confused with autophagic vacuoles are mitochondria, ER, endosomes, and also (depending on their structure) plastids in plants.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, it is important to keep in mind that it may not be possible to distinguish between autophagic bodies that are derived from the fusion of autophagosomes with the vacuole, and the single-membrane vesicles that are generated during microautophagy-like processes such as micropexophagy and micromitophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Moreover, pepstatin A is membrane impermeable (ethanol or preferably DMSO must be employed as a vehicle) and requires a prolonged incubation (> 8 h) and a relatively high concentration (>50-100 µM) to fully inhibit lysosomal CTSD (Figure 11).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“LC3, like the other Atg8 homologs, is initially synthesized in an unprocessed form, proLC3, which is converted into a proteolytically processed form lacking amino acids from the C terminus, LC3-I, and is finally modified into the PEconjugated form, LC3-II (Figure 7).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In these cases, however, the possibility that feedback activation of sequestration gets involved in the autophagic process has to be carefully considered.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“For example, starvation-induced autophagosomes should contain cytoplasm (i.e., cytosol and possibly organelles), but autophagosome-related structures involved in specific types of autophagy should show the selective cytoplasmic target, but may be relatively devoid of bulk cytoplasm.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“bafilomycin A1 requires ~30 min to increase lysosomal pH [228,346]; therefore, a preincubation of 30 min is required in case of short autophagy induction times.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The cornerstone of successfully using TEM is the proper identification of autophagic structures, which is also the prerequisite to get reliable quantitative results by EM morphometry.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“For nonspecialists it can be particularly difficult to distinguish among amphisomes, autolysosomes and lysosomes, which are all single-membrane compartments containing material that has been more or less degraded.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence.
None of the sources cited for this claim have been checked yet.
In the paper
“The mammalian Atg8 homologs share from 29% to 94% sequence identity with the yeast protein and have all been demonstrated to be involved in autophagosome biogenesis [200].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Not checked yetcites [200] source
Checked before — its earlier verdict is held back until a new check runs.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Atg8-PE/LC3-II is the only protein marker that is reliably associated with completed autophagosomes, but is also localized to phagophores.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Quantification of autophagy by TEM morphometry can be very useful and accurate, but, unfortunately, unreliable procedures still continue to be used.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Seventh, LC3-I can be fully degraded by the 20S proteasome or, more problematically, processed to a form (LC3-T) appearing equal in size to LC3-II on a western blot; LC3-T was identified in HeLa cells and is devoid of the ubiquitin conjugation domain, thus lacking its adaptor function for autophagy [296].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Not checked yetcites [296] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“Due to the cisternal structure of the ER, double membrane-like structures surrounding mitochondria or other organelles are often observed after sectioning [187], but these can also correspond to cisternae of the ER coming into and out of the section plane [67].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Atg8 is a ubiquitin-like protein that can be conjugated to PE (and possibly to phosphatidylserine [PS] [194]).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Not checked — no full text of the sourcecites [194] source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A point of caution along these lines is that the increase in LC3A-II versus LC3B-II levels may not display equivalent changes in all organisms under autophagyinducing conditions, and it should not be assumed that LC3B is the optimal protein to monitor [283].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
What the sources say
- Not checked — no full text of the sourcecites [283] source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The early heterophagic vacuole formed in this way may appear similar to an autophagosome or, in a later stage, an early autolysosome in that it contains recognizable or identifiable cytoplasmic material.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The duration of the bafilomycin A1 treatment (or any other inhibitor of autophagic flux such as CQ) needs to be relatively short (1)(2)(3)(4) h) [313] to allow comparisons of the amount of LC3 that is lysosomally degraded over a given time frame under one treatment condition to another treatment condition.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Turnover of LC3-II/Atg8-PE: Autophagic flux.
What the sources say
- Not checked — no full text of the sourcecites [313] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Quantification of both isoforms is therefore informative, but requires adequate conditions of electrophoretic separation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Nevertheless, in most published studies, LC3 has been the primary Atg8family homolog examined in mammalian cells and the one that is typically characterized as an autophagosome marker per se.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, because the dynamic range of LC3 immunoblots is generally quite limited, it is imperative that other assays be used in parallel in order to draw valid conclusions about changes in autophagy activity.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 2. Atg8-family protein detection and quantification.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In yeast, it is convenient to identify autophagic bodies that reside within the vacuole lumen, and to quantify them as an alternative to the direct examination of autophagosomes.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“Because the pH in the yeast vacuole is higher than that in mammalian or D. discoideum lysosomes, the levels of free GFP fragments are detectable in yeast even in the absence of lysosomotropic compounds [53].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [53] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hence, a reduction in the intensity of the free GFP band may indicate reduced flux, but it may also be due to efficient turnover.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Monitoring the endogenous Atg8-family proteins obviously depends on the ability to detect these proteins in the system of interest, which is not always possible.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“On the one hand, a putative advantage of mCherry over mRFP is its enhanced photostability and intensity, which are an order of magnitude higher (and comparable to GFP), enabling acquisition of images at similar exposure settings as are used for GFP, thus minimizing potential bias in interpretation [344].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [344] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“For instance, GFP-ATG8 expression in Arabidopsis thaliana is typically highest in the root apical meristem, but the response to the autophagy-inducing conditions in this root zone is much lower compared to the rest of the root.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In the case of a suspected impaired degradation, assessment of lysosomal function (i.e., pH or activity of lysosomal enzymes) is then required to validate the conclusion and to establish the basis.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Quantification of autophagy by measuring GFP-LC3 puncta (or LC3 by immunofluorescence) can, depending on the method used, be more tedious than monitoring LC3-II by western blot; however, the former may be more sensitive and quantitative.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As a note of caution, GFP-LC3 has been demonstrated to be present in protein aggregates in an autophagy-unrelated manner and this association is dependent on its interaction with SQSTMI.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [360] source
Checked before — its earlier verdict is held back until a new check runs.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Accordingly, it is critical that any chimeras should be constructed with the fluorescent tag at the amino terminus of Atg8-family proteins (unless the goal is to monitor Atg4/ATG4 activity).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > As noted above (see Western blotting and ubiquitin-like protein conjugation systems),
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“Dendra2 is an improved version of the green-to-red photoswitchable fluorescent protein Dendra, which is derived from the octocoral Dendronephthya sp [346].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [346] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In particular, if there is any evidence of an increase in LC3-II (or autophagosomes), it is essential to determine whether this represents an induction of autophagy and increased synthesis of LC3, or decreased flux and the subsequent accumulation of LC3 due to a block in fusion or degradation, through the use of inhibitors such as CQ, bafilomycin A1 or lysosomal protease inhibitors.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Also, GFP is relatively resistant to denaturation, and boiling for 5 min may be needed to prevent the folded protein from being trapped in the stacking gel during SDS-PAGE.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The pH optimum of EGFP is important to consider when using GFP-LC3 constructs, as the original GFP-LC3 marker [348] uses the EGFP variant, which may result in a reduced signal upon the formation of amphisomes or autolysosomes.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [348] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Atg4/ATG4 cleaves the residue(s) that follow the C-terminal glycine of Atg8-family proteins that will be conjugated to PE.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > As noted above (see Western blotting and ubiquitin-like protein conjugation systems),
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Using a pool of multiple selected clones may reduce artefacts that can arise from the selection and propagation of individual clones from a single transfected cell (although the use of a pool is also problematic as its composition will change over time).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“procedures that have the advantages of detecting the endogenous protein, obviating the need for transfection and/or the generation of a transgenic organism, as well as avoiding potential artefacts resulting from overexpression.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Leupeptin is an inhibitor of lysosomal cysteine and serine proteases and will therefore inhibit degradation of membrane-conjugated GFP-LC3 that is present within autolysosomes.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A major disadvantage, however, is that flow cytometry only measures changes in total GFP-LC3 levels, which can be subject to modification by changes in transcription or translation, or by pH, and this approach cannot accurately evaluate localization (e.g., to autophagosomes) or lipidation (generation of LC3-II) without further permeabilization of the cell.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Finally, probes measuring the autophagic flux without requiring transfection or permeabilization have also been developed.Such methods are based on dyes that selectively label autophagic vesicles (autophagosomes and autolysosomes) but not lysosomes, and are used for both primary cells [502,503] and cell lines [504,505] from different species (including nonmammals).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [502] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [503] source
- Not checked yetcites [504] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [505] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“LC3-positive autophagosomes can be quantified by confocal microscopy using a software program called Imaris (Oxford Instruments).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nevertheless, manual scoring may be more accurate than relying on a software program”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This approach will only be feasible if the background number of puncta is relatively low.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There are, however, practical issues with counting puncta manually and reliably, especially if there are large numbers per cell.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Another alternative to mRFP or mCherry is to use the Venus variant of YFP, which is brighter than mRFP and less sensitive to pH than GFP [347].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [347] source
Checked before — its earlier verdict is held back until a new check runs.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, there is also a need to be aware that a single cell clone may not be representative of the overall pool.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Another issue to keep in mind is that GFP-Atg8 processing correlates with the surface area of the inner sphere of the autophagosome, and thus provides a smaller signal than assays that measure the volume of the autophagosome.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Both autophagosome-vacuole fusion in yeast and autophagosome-lysosome fusion in mammals has been recently reconstituted, using partially purified fractions of autophagosomes, vacuoles/lysosomes and cytosol [506-508].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [506] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [507] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [508] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Stable cell lines expressing GFP-LC3 can be generated using lentiviral systems and efficiently selected through antibiotic resistance leading to uniform and prolonged expression levels.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“This modified version of the fluorophore has certain properties including a monomeric state, low phototoxic activation and efficient chromophore maturation, which make it suitable for real-time tracking of LC3 and SQSTM1 (Figure 13; [361]).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [361] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“When GFP-Atg8 or GFP-LC3 is delivered to a lysosome/vacuole, the Atg8-family protein part of the chimera is sensitive to degradation, whereas the GFP protein is relatively resistant to hydrolysis (note, however, that GFP fluorescence is quenched by low pH; see GFP-Atg8-family protein fluorescence microscopy and Tandem mRFP/mCherry-GFP fluorescence microscopy).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“An important advantage of transient transfection is that this approach is better for examining the immediate effects of the transfected protein on autophagy; however, the transient transfection approach restricts the length of time that the analysis can be performed, and consideration must be given to the induction of autophagy resulting from exposure to the transfection reagents (see below).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the other hand, a disadvantage of stable transfectants is that the integration sites cannot always be predicted, and expression levels may not be optimal.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition to autophagosome size, the number of puncta visible to the eye will also be influenced by both the level of expression of GFP-LC3 in a given cell (an issue that can be avoided by analyzing endogenous LC3 by immunofluorescence) and by the exposure time of the microscope, if using widefield microscopy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“On the one hand, stable transformants may have reduced background resulting from the lower gene expression, and artefacts resulting from recent exposure to transfection reagents (see below) are eliminated.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“An alternative way to quantify LC3 immunofluorescence staining is to estimate the percentage of LC3 signals originating from puncta over total LC3 signals in the same cell [403].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
What the sources say
- Not checked — no full text of the sourcecites [403] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Upon phagophore closure, LC3-II on the convex side of the membrane is delipidated and recycled back into the cytosol, while that on the concave side is sequestered within the vacuole and delivered into the lysosome for degradation”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > d. HaloTag-LC3 autophagosome completion assay.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, levels as well as chromatin recruitment of USP14 are upregulated in autophagy-deficient cells upon DNA damage, and knockdown of SQSTM1 in autophagy-deficient cells decreases USP14 levels [602, 603].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“puncta may be numerous in neurites, especially within dystrophic swellings and, in many cases, these vacuoles are amphisomes or autolysosomes, reflecting the delayed or inhibited degradation of LC3 despite the presence of abundant hydrolase activity [77,84].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“For example, some commercial antibodies recognize both human and mouse SQSTM1, whereas others detect the human, but not the mouse protein [614].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [614] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“One solution to problems relating to variations in SQSTM1 expression levels is to use a HaloTag ® -p62 (SQSTM1) chimera [585].The chimeric protein can be covalently labeled with HaloTag ® ligands, and the loss of signal can then be monitored without interference by subsequent changes in protein synthesis.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [585] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Finally, in nonmammalian vertebrates, BECN1 is detected during follicular atresia in the ovary of three fish species using paraffin sections; a punctate immunofluorescent staining for BECN1 is scattered throughout the cytoplasm of the follicular cells when they are in intense phagocytic activity for yolk removal [546].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [546] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Deficiency of the LIR domain-containing, SQSTM1interacting SPRED2 results in an accumulation of SQSTM1 in the heart in vivo, accompanied by an altered LC3 turnover and reduced autophagy [560].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [560] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Moreover, SQSTM1 can be regulated by the integrated stress response (ISR), which can promote accumulation of protein in cells that is dependent on the EIF2S1/eIF2α pathway of translational control (R.E.Simmonds, personal communication).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Moreover, in some instances SQSTM1 levels do not change in the soluble fractions despite autophagic degradation, a finding that might be explained by simultaneous transcriptional induction of the gene encoding SQSTM1, because the soluble fraction accounts only for the diffuse or free form of SQSTM1.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Inhibition of autophagy can correlate with increased levels of SQSTM1 in mammals, C. elegans and Drosophila, suggesting that steady state levels of this protein reflect the autophagic status [82,536,[554][555][556][557][558][559].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not matchedcites [82,536,[554][555][556][557][558][559]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“Stabilization of SQST-1::GFP via rpl-43 mutation does not affect the degradation of the autophagy substrates so far tested, and reduced SQST-1::GFP signal is observed in conditions of increased autophagic flux such as starvation [563];”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [563] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In other contexts, a robust loss of SQSTM1 does not correlate with increased autophagic flux as assessed by a luciferase-based measure of flux [338]; a decrease of SQSTM1 can even relate to a blockage of autophagy due to cleavage of the protein, together with other autophagy proteins, by caspases or calpains [562].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Furthermore, the toxicity of tetracycline antibiotics toward mitochondria is well known (these drugs induce a mitochondrial unfolded protein response) [588], such that their use may trigger mitophagy, or other mitochondrial signaling events that interface with the autophagic machinery, thus complicating the interpretation of any results.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [588] source
boostedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Additionally, an alteration in the level of SQSTM1 may not be immediately evident with changes observed in autophagic flux upon certain chemical perturbations (S.Sarkar, personal communication).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“With regard to protein synthesis, it is worth noting that this can be monitored through a nonradioactive method [611].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [611] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“SQSTM1 and SQSTM1-bound polyubiquitinated proteins become incorporated into the completed autophagosome and are degraded in autolysosomes, thus serving as an index of autophagic degradation (Figure 22).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The approach is based on the high affinity of the HiBiT peptide to the inactive luciferase subunit LgBiT, that, upon binding, produces an active NanoBiT luciferase that generates luminescence proportional to the amount of autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“IHC using ABC and 3,3′-diamino-benzidine (DAB) as chromogen has also been used to detect AMBRA1, thus accomplishing a complete map of AMBRA1 protein distribution in mouse brain, and highlighting differential expression in neuronal/glial cell populations.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“A major advantage of this reporter system is that it allows for determination of autophagic flux upon exposure to a large number of conditions at the same time and, therefore, is suitable for large-scale screens using 96-or 386-well plate formats.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, USP14, a major proteasomal deubiquitinase that regulates degradation through the proteasome, interacts with the UBA domain of SQSTM1 as well as LC3.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In fact, SQSTM1 may, itself, be transcriptionally induced by NFE2L2 [594].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [594] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“In neurons in aging or neurodegenerative disease states, LC3 is commonly present in autolysosomes and may be abundant in lipofuscin and other lysosomal residual bodies [77].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [77] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“Synovial fibroblasts obtained from patients with rheumatoid arthritis also exhibit a significant upregulation of SQSTM1 with concomitant increased autophagy flux [575].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [575] source
Checked before — its earlier verdict is held back until a new check runs.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“In the same way, physical exercise, especially when performed during starvation, increases the SQSTM1 mRNA level in skeletal muscle, and can lead to an incorrect interpretation of autophagic flux if only the protein level is measured [579, 580].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“SQSTM1 contains a LIR as well as a ubiquitin binding domain and appears to act by linking ubiquitinated substrates with the autophagic machinery.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Two-h AICAR + MG132 pro-autophagic cotreatment similarly induces the binding of ELAVL1/HuR protein to SQSTM1 mRNA, its loading on polysomes and its translation into de novo protein, an effect that is required to trigger autophagy and is prevented by the protein synthesis inhibitor puromycin [583].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [583] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“SQSTM1 mRNA is also upregulated following prolonged starvation, which can restore the SQSTM1 protein level to that before starvation [577, 578].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Inhibition of autophagy by treatment with 3-MA (5 mM, 4 h) increases accumulation of MAPT/tau oligomers within neurites of primary transgenic (prepared from PS19 mouse embryos, expressing the frototemporal dementia P301S mutant MAPT [600]) cultured neurons, reducing their access to the soma and lysosomes for degradation [601].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“A similar system exists in Drosophila in which a GFP-tagged ref(2)P/SQSTM1 can be expressed using the UAS-GAL4 system [586].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [586] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Differences in AMBRA1 content have been related to specific neuronal features and properties, particularly concerning susceptibility to neurodegeneration, during aging and amyloid pathology [544].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [544] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Inhibition of autophagy leads to accumulation of NeoR-GFP, resulting in enhanced GFP fluorescence [618].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [618] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In developing inner ear and retinal tissue in chicken, BECN1 is detected by immunofluorescence; in chick retina AMBRA1 is also detected [393][394][395].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In fact, the polarization of LC3 within granules is greatly reduced and LC3 IHC even monitored by confocal microscopy demonstrates cytosolic accumulation of the protein, which, despite being increased, loses its polarization within autophagic granules [549].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [549] source
Checked before — its earlier verdict is held back until a new check runs.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, SQSTM1 can also bind RNA substrates, which controls RNA turnover via autolysosomes, a process termed selective RNautophagy [553].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [553] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
In the paper
“Peroxidase depositions in the vacuoles indicate LC3 expression, detected by IHC, and therefore identify those structures as autophagic vacuoles [114].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [114] Réz G, 1996, Eur J Cell Biol
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“NeoR-GFP degradation is completely blocked by autophagic inhibitors such as 3-MA, but does not respond to inhibitors of proteasomal degradation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [618] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“SQSTM1 changes can be treatment specific such that chemotherapyinduced autophagy increases LC3-II without changing SQSTM1, whereas radiation-induced autophagy increases LC3-II and decreases SQSTM1 in ERBB2/HER2-overexpressing mouse mammary carcinoma cells [564].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [564] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“SQSTM1 is also a substrate for CASP6 (caspase 6) and CASP8 (as well as CAPN1 [calpain 1]), which may confound its use in examining cell death and autophagy [608].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [608] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
In the paper
“Inhibition of AMPK activity is mediated primarily by Thr172-dephosphorylating protein phosphatases such as PPP1/PP1 (protein phosphatase 1) and PPP2/PP2A (protein phosphatase 2) [648].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [648] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, AMPK acts as a fine-tuned sensor of the overall cellular energy charge that regulates cellular metabolism to maintain energy homeostasis.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Amino acids acutely activate AMPK, which sustains autophagy under nutrient sufficiency [667].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [667] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Pharmacological or genetic inhibition of the chaperone complex increases proteasome-mediated turnover of ULK1, impairing its kinase activity and ability to promote both starvation-induced autophagy and mitophagy [645].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [645] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Even the autophagy-suppressive effects of AMPK could, conceivably, be mediated through ULK1 phosphorylation, for example, at the inhibitory site Ser638 [686].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [686] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“The enzyme activity of AMPK is dependent on phosphorylation of the PRKAA2/α2-subunit on Thr172 (corresponds to Thr183 in α1) [459,460]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Presumably, AMPK antagonizes the autophagy-inhibitory effect of amino acids (at the level of phagophore assembly) by phosphorylating proteins involved in MTORC1 signaling, such as TSC2 [668] and RPTOR/raptor [668] as well as the MTORC1 target ULK1 (see below) [669-671].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies with mammalian immune cells indicate that TOLLIP is primarily responsible for the final step of autophagy, and facilitates the fusion of lysosomes with autophagosomes, lipid droplets, or peroxisomes [627] [628].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The role of AMPK in autophagy is complex and highly dependent on both cell type and metabolic conditions.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TOLLIP may fulfill its critical function of lysosome fusion through its interaction with phospholipid [629, 630].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“its overexpression induces both autophagy and senescence [635]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [635] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“AMP and ADP promote phosphorylation and AMPK activity, whereas Mg 2+ -ATP has the opposite effect [649].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [649] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
In the paper
“In their absence, cells are more vulnerable to the toxicity resulting from aggregation-prone proteins, showing that CUET proteins, and more generally autophagy, play a critical evolutionarily conserved role in the clearance of cytotoxic protein aggregates [624].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [624] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and, therefore, can be conveniently monitored by western blotting with a phosphospecific antibody against this site.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Compound C thus cannot be used as a stand-alone indicator of AMPK involvement, but can be used along with shRNA-mediated inhibition of AMPK.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ULK3 is a positive regulator of the Hedgehog signaling pathway [634]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [634] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
In the paper
“the ULK1-dependent inhibitory phosphorylation of AMPK subunits appears to generate a negative feedback loop [706].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [706] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Pathologically, TOLLIP-deficient mice tend to develop more severe atherosclerosis as well as neurological defects [628, 631].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The CUET proteins also possess a ubiquitin-binding CUEdomain and an Atg8-family interacting motif (AIM)/LIR sequence that interacts with Atg8-family proteins.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In addition, IPMK (inositol polyphosphate multikinase) can act as a scaffold protein to influence AMPK-dependent ULK phosphorylation [689].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [689] source
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“and there appears to be a completely AMPK-dependent type of autophagy [666].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [666] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The identification of ULK1 as a direct target of MTORC1 and AMPK represents a significant step toward the definition of new tools to monitor the induction of autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“there are two isoforms of the catalytic subunit, PRKAA1/AMPKα1 and PRKAA2/AMPKα2, and these may have distinct effects with regard to autophagy (C.Koumenis, personal communication) [655].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [655] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Finally, a novel protein family of autophagy receptors, named CUET (from Cue5/TOLLIP), was identified, which in contrast to SQSTM1 and NBR1 has members that are present in all eukaryotes [624, 625].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“ULK1 and ATG13 are also phosphorylated by CCNB/cyclin B in mitosis to activate autophagy [690].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [690] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, Thr172 phosphorylation and AMPK activation can be enhanced by PRKDC (protein kinase, DNA-activated, catalytic subunit)mediated phosphorylation of PRKAG1/AMPKγ1, which promotes the lysosomal localization of the AMPK complex [650].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [650] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, ULK3 may play a role that is restricted to senescence and that is independent of the core autophagy machinery.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“There are multiple ULK isoforms in mammalian cells including ULK1, ULK2, ULK3, ULK4 and STK36 [633].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [633] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“Specifically, SHOC2 binds to RPTOR and dislodges it from MTORC1, leading to MTORC1 inactivation and autophagy induction [684, 685].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“ectopic ULK3 displays a punctate pattern upon starvation-induced autophagy induction [635]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [635] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, AMPK is involved in processes that synergize to activate autophagy, by directly activating ULK1, and indirectly impairing MTOR-dependent inhibition of ULK1.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TOLLIP-deficient monocytes are defective in lysosome fusion and are programmed into an inflamed state with elevated CCR5 and enhanced expression of chemokines such as CCL2/MCP1 [629, 631].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“oxidative stress inhibits MTOR, thus allowing autophagy induction, despite the concomitant activation of AKT [209].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [209] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“At present, the use of Atg1/ULK1 kinase activity as a tool to monitor autophagy is limited because only a few physiological substrates have been identified, and the importance of Atg1/ULK1-dependent phosphorylation has not always been determined.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“rapamycin strongly reduces RPS6KB1 phosphorylation, whereas its effect on EIF4EBP1 is more variable.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [734] source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“LAP is a type of phagocytosis in macrophages that involves the conjugation of LC3 to single-membrane pathogen-containing phagosomes, a process that promotes phagosome maturation [249].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [249] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“and ATG9A deficiency in the mouse brain causes axonspecific lesions including neuronal circuit dysgenesis [800].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Not checked yetcites [800] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
In the paper
“Mammalian ATG9A displays partial colocalization with GFP-LC3 [799]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Not checked yetcites [799] source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“PIK3C3/VPS34 is highly conserved though evolution, and belongs to the class III PtdIns3K that phosphorylates the 3'-OH position of phosphatidylinositol (PtdIns) to synthesize PtdIns3P [787, 788].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“suggesting that UNC-51 could have a role in cell death or cell corpse clearance.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“AMPK phosphorylates CCNY, which promotes its interaction with CDK16, a PCTAIRE kinase family member.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“MTOR suppression does not always induce autophagy, such as when BECN1 undergoes inhibitory phosphorylation by the growth factor signaling molecules EGFR and AKT, when microglia are activated by lipopolysaccharide (LPS), a TLR4 ligand [766], or during Salmonella infection [767-769].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [766] source
- Not checked yetcites [767] source
- Not checked yetcites [768] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [769] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“overexpression of CCNY-CDK16 is sufficient to induce autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“There is also evidence that inhibition of MTORC1 is not sufficient to maintain autophagic flux, but requires additional activation of FOXO transcription factors for the upregulation of autophagy gene expression [660].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [660] source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Together, these pathways contribute to the expression of lipoxygenases and downregulation of IFNGinduced autophagy [777].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked yetcites [777] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“UNC-51 (the Atg1/ULK1 homolog in C. elegans) is not required for the clearance of neuroblast corpses in larval worms or released cell fragments in worm embryos [752, 753]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“although directly phosphorylated by MTORC1, the modifications at Thr37 and Thr46 are only partially sensitive to serum and rapamycin [734].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [734] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“phosphorylation of EIF4EBP1 at Thr37 and Thr46 primes the protein for phosphorylation at Ser65”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
What the sources say
- Not checked — no full text of the sourcecites [734] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Conclusion: Assays for Atg1/ULK1 can provide detailed insight into the induction of autophagy, but they are not a direct measurement of the process.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Nonetheless, it must be kept in mind that monitoring changes in the activity of Atg1/ULK1 is not a direct assay for autophagy, although such changes may correlate with autophagy activity.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It is important to be aware, however, that certain forms of autophagy are induced in a BECN1-independent manner and are not blocked by PtdIns3K inhibitors [120, 852, 853]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“It is important to note that an in vitro lipid kinase assay with BECN1 immunoprecipitates represents the total PtdIns3K activity and does not make it possible to distinguish between the production of PtdIns3P by PIK3C3/VPS34 in complex I versus that in complex II.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, monitoring changes in mRNA levels for either ATG genes or autophagy regulators may provide some evidence supporting upregulation of the potential to undergo autophagy, but should be used along with other methods.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These proteins bind PtdIns3P that is present at the phagophore and autophagosome [833,834] and also PtdIns(3,5)P2.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Persulfidation (S-sulfhydration) plays an importal role in mitophagy-related proteins such as PRKN, whose catalytic activity is stimulated by persulfidation, whereas nitrosylation inactivates it [1007].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [1007] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“The mature LC3-II form shows a remarkable dose-dependent increase upon MIR27A knockdown with respect to control and especially MIR27A-overexpressing HCT116 cells [988].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [988] source
Checked before — its earlier verdict is held back until a new check runs.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“A zinc finger family DNA-binding protein, ZKSCAN3, is a master transcriptional repressor of autophagy and lysosome biogenesis; starvation and MTOR inhibition with torin1 induce nucleus-to-cytoplasm translocation of ZKSCAN3 [979].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [979] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
In the paper
“It should be noted that there are two isoforms of WIPI2 (2B and 2D) [838],”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
- Not checked — no full text of the sourcecites [838] source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“TFEB localization may also be studied to monitor MTOR activity, as in most cases TFEB nuclear localization correlates with inhibition of MTOR.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Upon the initiation of the autophagic pathway, WIPI1 and WIPI2 bind PtdIns3P and accumulate at limiting membranes, such as those of the ER, where they participate in the formation of omegasomes and/or autophagosomes.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Autophagy is induced by the release of BECN1 from BCL2 by pro-apoptotic BH3 proteins, phosphorylation of BECN1 by DAPK1 and DAPK2 (at Thr119, located in the BH3 domain) [845, 846], or phosphorylation of BCL2 by MAPK8/JNK1 (at Thr69, Ser70 and Ser87) [847, 848].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Furthermore, fluorescence stopped-flow [835] and chemical cross-linking assays [836] show that Atg18 oligomerizes upon membrane binding, whereas it is mainly monomeric when unbound.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Moreover, NFE2L2/NRF2 is a regulator of Lamp2a transcription, and therefore, it controls CMA [982].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [982] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“Also, EGFR signalling induces multi-site tyrosine phosphorylation of BECN1 to inhibit core autophagy machinery activation [769].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [769] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“however, ATG14 is not localized exclusively to phagophores, as it can also be detected on mature autophagosomes as well as the ER [819, 820].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TFE3 and MITF, two other members of the MiT/TFE family of transcription factors, in some cases can compensate for TFEB and are regulated in a similar manner [967, 971, 972].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [967] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [971] source
Checked before — its earlier verdict is held back until a new check runs.
- Not checked yetcites [972] source
Checked before — its earlier verdict is held back until a new check runs.
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“Indeed, ATG16L1 is located on phagophores, but not on completed autophagosomes [457, 822].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Finally, an AMPK-SKP2-CARM1 signaling cascade has also been reported to play a role in transcriptional regulation of autophagy [974]; CARM1 exerts a transcriptional coactivator function on autophagy and lysosomal genes through TFEB.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [974] source
Checked before — its earlier verdict is held back until a new check runs.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not checked yet
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“GAN mutant neurons exhibit a failure in producing autophagosomes over time upon autophagy induction, hence leading to a defective autophagic flux in subsequent steps.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“As with GFP-LC3, overexpression of WIPI1 or WIPI2 can lead to the formation of aggregates, which are stable in the presence of PtdIns3K inhibitors.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“The EGR1 DNA-binding motif is significantly enriched in the promoters/enhancers of autophagy-associated genes; EGR1 positively regulates the transcription of these genes (including ATG2A, ATG14, ATG3, ATG13, ATG101, LC3B, PIK3C3, PPM1D, ULK1, and ZFYVE1), and thereby increases the autophagic flux [980].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [980] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“ULK1 mRNA undergoes m 6 A modification in the 3' UTR, and the m 6 Amarked ULK1 transcripts can further be targeted for degradation by YTHDF2 (YTH N6methyladenosine RNA binding protein 2).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [1010] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“The expression of the transcription factor EGR1 (early growth response 1) is rapidly increased upon nutrient deprivation and can directly increase transcription of multiple components of the autophagy machinery.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked yetcites [980] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
In the paper
“Mitophagy is also promoted by persulfidation of USP8 (ubiquitin specific peptidase 8), which enhances deubiquitination of PRKN [1008].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked — no full text of the sourcecites [1008] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, changes in autophagy protein levels are not sufficient evidence of autophagy induction and must be accompanied by additional assays as described herein.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Conversely, the modulation of the amount of S-nitrosylated proteins triggered by changes in the activity or expression of the denitrosylase ADH5/GSNOR (alcohol dehydrogenase 5 [class III], chi polypeptide), seems to have no major effects on nonselective autophagy, whereas there is an effect on the recognition of damaged mitochondria to be targeted for selective mitophagy [1005, 1006].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Protein degradation assays represent a well-established methodology for measuring autophagic flux, and they allow good quantification.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TFEB phosphorylation on specific residues also occurs in the nuclear compartment and enables TFEB nuclear export [968-970].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Because ATG16L1 is specifically located on phagophores but not complete autophagosomes, phospho-ATG16L1based autophagy assays are unaffected by a late stage autophagy block, and thus able to circumvent a major caveat of LC3-based assays while serving as an alternative tool with unique advantages to monitor autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 5. Additional autophagy-related protein markers.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“PHO8 encodes a vacuolar phosphatase, which is synthesized as a zymogen before finally being transported to and activated in the vacuole [1032].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked — no full text of the sourcecites [1032] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The contribution of autophagy to SNCA aggregate clearance can be studied by the use of different autophagy mutants or by pharmacological treatment with the proteinase B inhibitor PMSF [1086-1088].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > b. Aggrephagy. Aggrephagy is the selective removal of aggregates by autophagy [1084].
What the sources say
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The autophagy receptor ALLO-1 and its kinase IKKE-1 are required for the recruitment of LGG-1 around sperm-inherited organelles [1108].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > (tm3489) and lgg-2(tm5755).
What the sources say
- Not checked yetcites [1108] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
In the paper
“For example, the neomycin phosphotransferase II-GFP (NeoR-GFP) fusion protein is a target of autophagy [617].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
- Not checked — no full text of the sourcecites [617] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“In WT cells, fluorescence of pHluorin-Atg8 is detectable at neutral pH in the cytosol and at the PAS or on autophagosomes, but not at the lower pH within the vacuole upon starvation.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [1082] source
Checked before — its earlier verdict is held back until a new check runs.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Of note, however, the assay only assesses proteolytic activity, and cannot be used to tell whether the cargo has reached fully active autolysosomes or whether the degraded cargo is recycled to the cytosol.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, particular mutants may display complete maturation of prApe1 under autophagy-inducing conditions, but may still have a defect in other types of selective autophagy, as well as being unable to induce a normal level of nonselective autophagy [150].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [150] source
Checked before — its earlier verdict is held back until a new check runs.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not checked yet
In the paper
“Furthermore, selective degradation of mitochondria can be induced in cells cultured with a fermentable carbon source such as glucose by a shift from nutrient-rich to nitrogen-starvation conditions, which makes it possible to examine mitophagy even in respiratory-deficient cells [1067].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [1067] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“or by mitochondrial oxidative phosphorylation uncouplers such as CCCP [1063].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [1063] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, the sequestration of prApe1 is specific, even under starvation conditions, as it involves the recognition of the propeptide by a receptor, Atg19, which in turn interacts with the scaffold protein Atg11 [1079,1080].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There are many assays that can be used to monitor selective types of autophagy”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > (tm3489) and lgg-2(tm5755).
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim have been checked yet.
In the paper
“Activities of both catalases can be distinguished using an in-gel activity assay after PAGE under nondenaturing conditions by staining with diaminobenzidine [1050, 1051].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: In S. cerevisiae, CTT1 and CTA1 encode catalase activity.
- Rests on an assumption: Only Cta1 is localized in peroxisomes.
None of the sources cited for this claim have been checked yet.
In the paper
“For example, in S. cerevisiae, to induce a substantial level of mitophagy, cells need to be precultured in a nonfermentable carbon source such as lactate or glycerol to stimulate the proliferation of mitochondria (although this is not the case in Komagataella phaffii/Pichia pastoris).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [1041] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: In yeast, nonselective autophagy can be induced by nitrogen-starvation conditions.
- Not checked yet
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This compensation might interfere with control measurements under conditions that attempt to inhibit autophagy; however, as the latter is the major degradative pathway, the contributions of other types of degradation over the course of this type of experiment are most often negligible.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“For example, branched chain amino acids are good indicators of proteolysis in hepatocytes, but not in muscle cells where they are further oxidized (A.J.Meijer, personal communication).”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not matchedcites A.J.Meijer, personal communication
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“In mutants that are either deficient in vacuolar peptidases (atg42∆, pep4∆, prb1∆, prc1∆) or vacuolar acidification (vma4∆) pHluorin-Atg8 is not quenched and pHluorin-Atg8-positive vesicular structures are detected inside their vacuoles, suggesting that autophagic bodies are not efficiently lysed.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [1082] source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Overexpression of prApe1 saturates import by the Cvt pathway, and the precursor form accumulates, but is rapidly matured upon autophagy induction [410].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [410] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These assays may be applied to autophagy-related questions enabling researchers to investigate differential effects in global protein or even organelle degradation studies [1022, 1023].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 8. Transcriptional and translational regulation.
What the sources say
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Finally, it is important to account for biases in sample sectioning to obtain an accurate estimate of autophagic body number or size [149].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked — no full text of the sourcecites [149] source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Mitophagy can also be induced by treatment with ROS to induce mitochondria damage [1062]”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
What the sources say
- Not checked yetcites [1062] source
Checked before — its earlier verdict is held back until a new check runs.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not checked yet
The paper relies on this without support.
There is confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes.
“Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes.”
The authors state this as an assumption.
When autophagic flux is arrested at a given point, the accumulating structure does not feed back on its own rate of formation.
“however, this approach assumes there is no feedback of the accumulating structure on its own rate of formation [27].”
The paper relies on this without support.
The autophagosome:autolysosome ratio varies over time in a cell context-dependent fashion depending on clearance activity.
“as the autophagosome:autolysosome ratio varies in time in a cell context-dependent fashion, depending on their clearance activity.”
The paper relies on this without support.
Residual bodies are especially common in disease states and aged postmitotic cells such as neurons, muscle cells and retinal pigment epithelium.
“An additional category of lysosomal compartments, especially common in disease states and aged postmitotic cells such as neurons, muscle cells and retinal pigment epithelium, is represented by residual bodies.”
The paper relies on this without support.
Lipofuscin has broad spectral emission and is the main cause of autofluorescence in tissues.
“lipofuscin has broad spectral emission, and is the main cause of autofluorescence in tissues.”
The paper relies on this without support.
In quickly frozen and fractured cells the fracture runs preferentially along the hydrophobic plane of the membranes.
“In quickly frozen and fractured cells the fracture runs preferentially along the hydrophobic plane of the membranes, allowing characterization of the limiting membranes of the different types of autophagic vacuoles, and visualization of their limited protein intramembrane particles/integral membrane proteins (IMPs).”
The paper relies on this without support.
The limiting membrane of autophagic bodies in yeast (and presumably plants) is quickly broken down under normal conditions.
“Similarly, the limiting membrane of autophagic bodies in yeast (and presumably plants) is also quickly broken down under normal conditions.”
The paper relies on this without support.
Many subcellular components may be mistaken for autophagic structures.
“The difficulty lies in the fact that many subcellular components may be mistaken for autophagic structures.”
The paper relies on this without support.
Ex vivo samples are not typically randomized during processing.
“In addition, ex vivo samples are not typically randomized during processing, further complicating the possibility of valid statistical analyses.”
The paper relies on this without support.
Interpretation of tomographic images can be problematic.
“In addition, interpretation of tomographic images can be problematic.”
The paper relies on this without support.
Confusion of heterophagic structures with autophagic ones is a major source of misinterpretation.
“The confusion of heterophagic structures with autophagic ones is a major source of misinterpretation.”
The paper relies on this without support.
For nonspecialists it can be particularly difficult to distinguish among amphisomes, autolysosomes and lysosomes.
“For nonspecialists it can be particularly difficult to distinguish among amphisomes, autolysosomes and lysosomes, which are all single-membrane compartments containing material that has been more or less degraded.”
The paper relies on this without support.
Autophagosomes are typically 900 nm to 1.5 µm in diameter.
“Autophagosomes, typically, are 900 nm to 1.5 µm in diameter.”
The paper relies on this without support.
Low magnification images (20X/40X objectives) do not provide enough resolution to obtain quantifiable data.
“Low magnification images (using 20X/40X objectives) do not provide enough resolution to obtain quantifiable data.”
The paper relies on this without support.
The Rosella assay has not been tested in a wide range of mammalian cell types.
“The Rosella assay has not been tested in a wide range of mammalian cell types.”
The paper relies on this without support.
Tandem fluorescent markers show real-time changes in autophagosome fusion with lysosomes due to entry into an acidic environment.
“Tandem fluorescent markers show real-time changes in autophagosome fusion with lysosomes, due to entry into an acidic environment; however, fusion is not definitive evidence of substrate or carrier degradation.”
The paper relies on this without support.
Lysosomes may be able to fuse but be unable to degrade newly delivered cargo, as occurs in some lysosomal storage diseases and aging-related neurodegenerative diseases.
“Lysosomes may be able to fuse, but be unable to degrade newly delivered cargo, as occurs in some lysosomal storage diseases and aging-related neurodegenerative diseases.”
The paper relies on this without support.
Technical limitations have prevented insight into the mechanism of autophagosome-lytic compartment fusion.
“Technical limitations have prevented insight into the mechanism of autophagosome-lytic compartment fusion.”
The paper relies on this without support.
Overexpression of SQSTM1 leads to the formation of protein inclusions.
“Furthermore, it is preferable to examine endogenous SQSTM1 because overexpression of this protein leads to the formation of protein inclusions.”
The paper relies on this without support.
Endogenous SQSTM1 becomes Triton X-100-insoluble in the presence of protein aggregates and when autophagic degradation is inhibited.
“In fact, even endogenous SQSTM1 becomes Triton X-100-insoluble in the presence of protein aggregates and when autophagic degradation is inhibited; thus, results with this protein are often context-dependent.”
The paper relies on this without support.
Western blot analysis of cell lysates prepared using NP40-or Triton X-100-containing lysis buffers in autophagic conditions typically shows a reduction in SQSTM1 levels.
“Western blot analysis of cell lysates prepared using NP40-or Triton X-100-containing lysis buffers in autophagic conditions typically shows a reduction in SQSTM1 levels.”
The paper relies on this without support.
Whereas LC3 changes may be rapid, clearance of autophagy substrates may require a longer time.
“Whereas LC3 changes may be rapid, clearance of autophagy substrates may require a longer time.”
The paper relies on this without support.
Small protoaggregates often stain positively for SQSTM1 and may be similar in size to autophagic puncta.
“Small protoaggregates often stain positively for SQSTM1 and may be similar in size to autophagic puncta.”
The paper relies on this without support.
Some types of aggregates and inclusions will release soluble SQSTM1 or GFP-u/GFP-degron under cell lysis or denaturing conditions, which can skew interpretation of soluble SQSTM1 and/or proteasomal function.
“Finally, some types of aggregates and inclusions will release soluble SQSTM1 or GFP-u/GFP-degron under cell lysis or denaturing conditions, which can skew the interpretation of soluble SQSTM1 and/or proteasomal function, accordingly.”
The paper relies on this without support.
Atg1/ULK1 are central components in autophagy that likely act at more than one stage of the process.
“Atg1/ULK1 are central components in autophagy that likely act at more than one stage of the process.”
The paper relies on this without support.
Depending on the stimulus and cell type, Thr172 is phosphorylated either by CAMKK2/CaMKKβ, STK11/LKB1 or MAP3K7/TAK1.
“Depending on the stimulus and cell type, Thr172 is phosphorylated either by CAMKK2/CaMKKβ, STK11/LKB1 or MAP3K7/TAK1 .”
The paper relies on this without support.
Activation of AMPK is associated with the phosphorylation of downstream enzymes involved in ATP-consuming processes, such as fatty acid (ACAC) and cholesterol (HMGCR) biosynthesis.
“Activation of AMPK is also associated with the phosphorylation of downstream enzymes involved in ATP-consuming processes, such as fatty acid (ACAC [acetyl-CoA carboxylase]) and cholesterol (HMGCR [3hydroxy-3-methylglutaryl-CoA reductase]) biosynthesis.”
The paper relies on this without support.
TORC1 is an autophagy-suppressive regulator that integrates growth factor, nutrient and energy signals.
“TORC1 is an autophagy-suppressive regulator that integrates growth factor, nutrient and energy signals.”
The paper relies on this without support.
In most systems, inhibition of MTOR leads to induction of autophagy, and AMPK activity is generally antagonistic toward MTOR function.
“In most systems, inhibition of MTOR leads to induction of autophagy, and AMPK activity is generally antagonistic toward MTOR function.”
The paper relies on this without support.
MTORC1 mediates the autophagy-inhibitory effect of amino acids, which stimulate the MTOR protein kinase through a RRAG GTPase heterodimer.
“MTORC1 mediates the autophagy-inhibitory effect of amino acids, which stimulate the MTOR protein kinase through a RRAG GTPase heterodimer.”
The paper relies on this without support.
INS (insulin) and growth factors activate MTORC1 through upstream kinases including AKT/protein kinase B and MAPK1/ERK2-MAPK3/ERK1 when the energy supply is sufficient, whereas energy depletion may induce AMPK-mediated MTORC1 inhibition and autophagy stimulation, for example, during glucose starvation.
“INS (insulin) and growth factors activate MTORC1 through upstream kinases including AKT/protein kinase B and MAPK1/ERK2-MAPK3/ERK1 when the energy supply is sufficient, whereas energy depletion may induce AMPK-mediated MTORC1 inhibition and autophagy stimulation, for example, during glucose starvation.”
The paper relies on this without support.
AMPK and MTORC1 regulate autophagy through coordinated phosphorylation of ULK1.
“AMPK and MTORC1 regulate autophagy through coordinated phosphorylation of ULK1.”
The paper relies on this without support.
Under conditions of nutrient sufficiency, high MTORC1 activity prevents ULK1 activation by phosphorylating alternate ULK1 residues and disrupting the interaction between ULK1 and AMPK.
“Under conditions of nutrient sufficiency, high MTORC1 activity prevents ULK1 activation by phosphorylating alternate ULK1 residues and disrupting the interaction between ULK1 and AMPK.”
The paper relies on this without support.
There are commercially available phospho-specific antibodies that recognize different forms of ULK1.
“There are commercially available phospho-specific antibodies that recognize different forms of ULK1.”
The paper relies on this without support.
Phosphorylation at Ser556 in human (Ser555 in mouse), an AMPK site, is indicative of increased autophagy in response to nutrient stress, whereas Ser758 in human (Ser757 in mouse) is targeted by MTOR to inhibit autophagy.
“For example, phosphorylation at Ser556 in human (corresponds to Ser555 in mouse), an AMPK site, is indicative of increased autophagy in response to nutrient stress, whereas Ser758 in human (corresponds to Ser757 in mouse) is targeted by MTOR to inhibit autophagy.”
The paper relies on this without support.
In skeletal muscle, ULK1 is activated by MAPK11/p38β in response to a tumor burden through phosphorylation of Ser555 in mice.
“in skeletal muscle ULK1 is activated by MAPK11/p38β in response to a tumor burden through phosphorylation of Ser555 in mice.”
The paper relies on this without support.
Despite AMPK activation (phosphorylation on Thr172) by factors released from tumor cells, inhibition of AMPK with compound C does not alter ULK1 phosphorylation on Ser555 and activation of autophagy in these conditions.
“Despite AMPK activation (phosphorylation on Thr172) by factors released from tumor cells, inhibition of AMPK with compound C does not alter ULK1 phosphorylation on Ser555 and activation of autophagy in these conditions.”
The paper relies on this without support.
PtdIns3P is essential for the regulation of endocytic pathways and for the generation of various types of autophagosomes and phagosomes.
“PtdIns3P is essential for the regulation of endocytic pathways and for the generation of various types of autophagosomes and phagosomes.”
The paper relies on this without support.
PIK3C3/VPS34 cannot be found alone in the cell but mainly is present in two types of mutually exclusive complexes, complexes I and II.
“However, PIK3C3/VPS34 cannot be found alone in the cell but mainly is present in two types of mutually exclusive complexes, complexes I and II.”
The paper relies on this without support.
Atg9/ATG9A is the only integral membrane Atg protein that is essential for autophagosome formation in all eukaryotes.
“Atg9/ATG9A is the only integral membrane Atg protein that is essential for autophagosome formation in all eukaryotes.”
The paper relies on this without support.
Anterograde movement of Atg9 to the PAS is dependent on Atg11, Atg23, Atg27 and actin.
“Anterograde movement to the PAS is dependent on Atg11, Atg23, Atg27 and actin.”
The paper relies on this without support.
A septin complex regulates Atg9 retrograde transport.
“One such example is a septin complex that regulates Atg9 retrograde transport.”
The paper relies on this without support.
The localization of mammalian ATG9A is regulated by cellular sphingomyelin levels.
“Furthermore, the localization of mammalian ATG9A is regulated by cellular sphingomyelin levels.”
The paper relies on this without support.
The PIK3C3/VPS34 activity is affected by enzyme concentration and substrate (PI) structure.
“The PIK3C3/VPS34 activity is affected by enzyme concentration and substrate (PI) structure.”
The paper relies on this without support.
PI structure and the environment where PI is surrounded, such as the length of acyl chain, and the size and composition of liposomes, largely affect PIK3C3/VPS34 activity.
“Second, the PI structure and the environment where PI is surrounded such as the length of acyl chain, and the size and composition of liposomes largely affect the activity.”
The paper relies on this without support.
PI:PS mixture substrates are good substrates for drug screening but are not physiological.
“Although they are good substrates for drug screening, they are not physiological.”
The paper relies on this without support.
In ADP-Glo assays, if the purified enzyme is contaminated with chaperones, the ATPase activities of the latter dominate the values.
“For ADP-Glo assays, because it measures the ATP-ADP conversion, if the purified enzyme is contaminated with chaperones, the ATPase activities of the latter dominate the values.”
The paper relies on this without support.
Endogenous ULK1 is of low abundance in many systems, making it difficult to detect phospho-ULK1 by western blot analysis.
“One problem in monitoring assembly of the ULK1 complex is the low abundance of endogenous ULK1 in many systems, which makes it difficult to detect phospho-ULK1 by western blot analysis.”
The paper relies on this without support.
Atg1/ULK1 is phosphorylated by multiple kinases, and the amount of phosphorylation at different sites can increase or decrease during autophagy induction.
“In addition, Atg1/ULK1 is phosphorylated by multiple kinases, and the amount of phosphorylation at different sites can increase or decrease during autophagy induction.”
The paper relies on this without support.
The overall phosphorylation states of ULK1 and ATG13 are decreased under conditions that lead to induction of autophagy, despite an increase in phosphorylation at activating sites.
“Thus, although there is an increase in phosphorylation at the activating sites upon induction, the overall phosphorylation states of ULK1 and ATG13 are decreased under conditions that lead to induction of autophagy; therefore, monitoring changes in phosphorylation by following molecular mass shifts upon SDS-PAGE may not be informative.”
The paper relies on this without support.
Phosphorylation/dephosphorylation events occur relatively early (1-2 h) in the signaling cascade of autophagy.
“In addition, such phosphorylation/dephosphorylation events are expected to occur relatively early (1-2 h) in the signaling cascade of autophagy.”
The paper relies on this without support.
Atg1/ULK1 kinase activity appears to increase when autophagy is induced, irrespective of the pathway leading to induction.
“Nonetheless, Atg1/ULK1 kinase activity appears to increase when autophagy is induced, irrespective of the pathway leading to induction.”
The paper relies on this without support.
There is not a complete consensus on the specific residues of ULK1 that are targeted by AMPK or MTOR.
“Finally, there is not a complete consensus on the specific residues of ULK1 that are targeted by AMPK or MTOR.”
The paper relies on this without support.
Apparently contradictory data have been published regarding the association of AMPK and MTOR with the ULK1 kinase complex under different conditions.
“Similarly, apparently contradictory data have been published regarding the association of AMPK and MTOR with the ULK1 kinase complex under different conditions.”
The paper relies on this without support.
Other proteins besides Atg8-family can be used for monitoring autophagy.
“Although Atg8-family proteins have been the most extensively used proteins for monitoring autophagy, other proteins can also be used for this purpose.”
The paper relies on this without support.
ATG9 is conserved in plants including the model plant A. thaliana.
“ATG9 is also conserved in plants including the model plant A. thaliana.”
The paper relies on this without support.
A protease protection assay with microsomes isolated from A. thaliana cells shows that ATG9 has a similar membrane topology, with its N- and C-termini facing the cytosol.
“A protease protection assay with microsomes isolated from A. thaliana cells shows that ATG9 has a similar membrane topology, with its N-and C-termini facing the cytosol”
The paper relies on this without support.
Direct connections between ATG8-positive tubular structures and the ER have been observed using 3-dimensional electron tomography analysis.
“Using 3-dimensional electron tomography analysis, direct connections between these ATG8positive tubular structures and the ER have been observed,”
The paper relies on this without support.
TFEB is phosphorylated by MTORC1 on the lysosomal surface, which prevents its nuclear translocation.
“TFEB is phosphorylated by MTORC1 on the lysosomal surface, preventing its nuclear translocation.”
The paper relies on this without support.
TFEB has low expression levels in most cells and tissues, making the endogenous protein difficult to visualize.
“However, due to the low expression levels of TFEB in most cells and tissues, it may be difficult to visualize the endogenous protein.”
The paper relies on this without support.
Most ATG genes do not show significant changes in mRNA levels when autophagy is induced.
“Most of the ATG genes do not show significant changes in mRNA levels when autophagy is induced.”
The paper relies on this without support.
ATG protein amounts do not always change significantly, and the extent of increase is cell type- and tissue-dependent.
“However, ATG protein amounts do not always change significantly, and the extent of increase is again cell type-and tissue-dependent.”
The paper relies on this without support.
In any cell culture system, mixed populations of cells (for example, those undergoing autophagy or not) exist simultaneously.
“Another general caution pertains to the fact that in any cell culture system mixed populations of cells (for example, those undergoing autophagy or not) exist simultaneously.”
The paper relies on this without support.
Only an average level of protein or mRNA expression can be evaluated with most methods.
“Therefore, only an average level of protein or mRNA expression can be evaluated with most methods.”
The paper relies on this without support.
Mammalian cell lines may have mutations that alter autophagy signaling or execution.
“Finally, researchers need to realize that mammalian cell lines may have mutations that alter autophagy signaling or execution; this problem can be avoided by using primary cells.”
The paper relies on this without support.
Although changes in ATG gene expression coincide with and may be needed for autophagy, in most cases this has not been carefully studied experimentally.
“Although there are changes in ATG gene expression that coincide with, and may be needed for, autophagy, in most cases this has not been carefully studied experimentally.”
The paper relies on this without support.
The use of stable isotopes, such as 13C and 15N, in quantitative MS-based proteomics allows the recording of degradation rates of thousands of proteins simultaneously.
“The use of stable isotopes, such as 13 C and 15 N, in quantitative MS-based proteomics allows the recording of degradation rates of thousands of proteins simultaneously.”
The paper relies on this without support.
Stable isotope labeling with amino acids in cell culture (SILAC) can provide comparative information between different treatment conditions, or between a wild type and mutant.
“Stable isotope labeling with amino acids in cell culture (SILAC) can also provide comparative information between different treatment conditions, or between a wild type and mutant.”
The paper relies on this without support.
During oxidative stress, the expression of the Keima fusion proteins themselves seem to be increased, possibly due to stress-induced activation of the CMV promoter.
“For example, during oxidative stress the expression of the Keima fusion proteins themselves seem to be increased, possibly due to stress-induced activation of the CMV promoter.”
The paper relies on this without support.
A molecular genetic modification that eliminates the first 60 amino acids prevents the mutant (Pho8∆60) from entering the ER, leaving the zymogen in the cytosol.
“A molecular genetic modification that eliminates the first 60 amino acids prevents the mutant (Pho8∆60) from entering the ER, leaving the zymogen in the cytosol.”
The paper relies on this without support.
When autophagy is induced, the mutant zymogen is delivered to the vacuole nonselectively inside autophagosomes along with other cytoplasmic material.
“When autophagy is induced, the mutant zymogen is delivered to the vacuole nonselectively inside autophagosomes along with other cytoplasmic material.”
The paper relies on this without support.
Amino acid release is also regulated by protein synthesis, which in turn is modulated by many different factors.
“however, it is important to keep in mind that amino acid release is also regulated by protein synthesis, which in turn is modulated by many different factors.”
The paper relies on this without support.
The released amino acid may be further metabolized.
“In either case, one potential problem is that the released amino acid may be further metabolized.”
The paper relies on this without support.
The amino acid can be reincorporated into protein.
“In addition, the amino acid can be reincorporated into protein; for this reason, such experiments can be carried out in the presence of CHX, but this raises additional concerns (see Turnover of autophagic compartments).”
The paper relies on this without support.
The perfused organ system allows for testing the reversibility of effects on proteolysis and the use of autophagy-specific inhibitors in the same experimental preparation, which are crucial controls for proper assessment.
“The perfused organ system also allows for testing the reversibility of effects on proteolysis and the use of autophagy-specific inhibitors in the same experimental preparation, which are crucial controls for proper assessment.”
The paper relies on this without support.
If the autophagic protein degradation is low (as it will be in cells in replete medium), it may be difficult to measure it reliably above the relatively high background of nonautophagic degradation.
“If the autophagic protein degradation is low (as it will be in cells in replete medium), it may be difficult to measure it reliably above the relatively high background of nonautophagic degradation.”
The paper relies on this without support.
Most pharmacological protease inhibitors have 'off target' effects that complicate the interpretation of the data.
“Another issue of concern, however, is that most pharmacological protease inhibitors have”
The paper relies on this without support.
Valine may be preferred over leucine due to the strong inhibitory effects of the latter on autophagy.
“although valine may be preferred over leucine due to the strong inhibitory effects of the latter on autophagy”
The paper relies on this without support.
The inclusion of the appropriate unlabeled amino acid (i.e., valine, leucine or methionine) in the starvation medium at a concentration equivalent to that of other amino acids in the chase medium is necessary; otherwise, the released [14C]-amino acid is effectively re-incorporated into cellular proteins, which results in a significant underestimation of protein degradation.
“Note that the inclusion of the appropriate unlabeled amino acid (i.e., valine, leucine or methionine) in the starvation medium at a concentration equivalent to that of other amino acids in the chase medium is necessary; otherwise, the released [ 14 C]-amino acid is effectively re-incorporated into cellular proteins, which results in a significant underestimation of protein degradation.”
The paper relies on this without support.
In this type of assay a considerable fraction of the measured degradation will be nonautophagic.
“In this type of assay a considerable fraction of the measured degradation will be nonautophagic, and thus it is important to also measure, in parallel, cell samples treated with autophagy-suppressive concentrations of 3-MA, SAR-405, bafilomycin A1, CQ, ammonia, or amino acids, or generated under conditions of amino acid depletion, or in samples obtained from mutants missing central ATG components;”
The paper relies on this without support.
Deletion of PHO8 can affect yeast cell physiology, especially depending on the growth conditions.
“Finally, it is also important to realize that the deletion of PHO8 can affect yeast cell physiology, especially depending on the growth conditions, and this may in turn have consequences for the cell wall; cells under starvation stress generate thicker cell walls that can be difficult to degrade enzymatically.”
The paper relies on this without support.
Cells under starvation stress generate thicker cell walls that can be difficult to degrade enzymatically.
“Finally, it is also important to realize that the deletion of PHO8 can affect yeast cell physiology, especially depending on the growth conditions, and this may in turn have consequences for the cell wall; cells under starvation stress generate thicker cell walls that can be difficult to degrade enzymatically.”
The paper relies on this without support.
In S. cerevisiae, CTT1 and CTA1 encode catalase activity.
“In S. cerevisiae there are two genes, CTT1 and CTA1, encoding catalase activity, and only one of these gene products, Cta1, is localized in peroxisomes.”
The paper relies on this without support.
Only Cta1 is localized in peroxisomes.
“In S. cerevisiae there are two genes, CTT1 and CTA1, encoding catalase activity, and only one of these gene products, Cta1, is localized in peroxisomes.”
The paper relies on this without support.
In yeast, nonselective autophagy can be induced by nitrogen-starvation conditions.
“In yeast, nonselective autophagy can be induced by nitrogen-starvation conditions, whereas degradative types of selective autophagy generally require a carbon source change or ER stress for efficient induction.”
The paper relies on this without support.
Degradative types of selective autophagy generally require a carbon source change or ER stress for efficient induction.
“In yeast, nonselective autophagy can be induced by nitrogen-starvation conditions, whereas degradative types of selective autophagy generally require a carbon source change or ER stress for efficient induction.”
The paper relies on this without support.
In Aspergillus oryzae, autophagy mediates degradation of basal hyphal organelles such as peroxisomes, mitochondria and entire nuclei.
“By labeling organelle markers with GFP it is possible to show in Aspergillus oryzae that autophagy mediates degradation of basal hyphal organelles such as peroxisomes, mitochondria and entire nuclei”
The paper relies on this without support.
The Cvt pathway occurs only in yeast.
“The Cvt pathway has been demonstrated to occur only in yeast.”
The paper relies on this without support.
The sequestering vesicles are substantially smaller than typical autophagosomes generated during nonselective autophagy.
“However, under the latter conditions it must be kept in mind that the sequestering vesicles are substantially smaller than typical autophagosomes generated during nonselective autophagy; the Cvt complex (prApe1 bound to Atg19) is smaller than typical peroxisomes or mitochondrial fragments that are subject to autophagic degradation.”
The paper relies on this without support.
The Cvt complex (prApe1 bound to Atg19) is smaller than typical peroxisomes or mitochondrial fragments that are subject to autophagic degradation.
“However, under the latter conditions it must be kept in mind that the sequestering vesicles are substantially smaller than typical autophagosomes generated during nonselective autophagy; the Cvt complex (prApe1 bound to Atg19) is smaller than typical peroxisomes or mitochondrial fragments that are subject to autophagic degradation.”
The paper relies on this without support.
Autophagic bodies may coalesce in the vacuole lumen, making it difficult to obtain an accurate quantification.
“One caveat to the detection of autophagic bodies, however, is that they may coalesce in the vacuole lumen, making it difficult to obtain an accurate quantification.”
The paper relies on this without support.
Plasmid numbers can vary from cell to cell.
“In general, when working with yeast it is preferable to use strains that have the marker proteins integrated into the chromosome rather than relying on plasmid-based expression, because plasmid numbers can vary from cell to cell.”
The paper relies on this without support.
For the GFP-Atg8 processing assay, 2 h of starvation is generally sufficient to detect a significant level of free GFP by western blotting as a measure of nonselective autophagy.
“In addition, for the GFP-Atg8 processing assay, 2 h of starvation is generally sufficient to detect a significant level of free (i.e., vacuolar) GFP by western blotting as a measure of nonselective autophagy.”
The paper relies on this without support.
For selective types of autophagy, the length of induction needed for a clearly detectable free GFP band varies depending on the rate of cargo delivery/degradation.
“For selective types of autophagy, the length of induction needed for a clearly detectable free GFP band will vary depending on the rate of cargo delivery/degradation.”
The paper relies on this without support.
Usually 6 h of mitophagy induction is needed to detect free GFP (e.g., from Om45-GFP) by western blot under starvation conditions.
“Usually 6 h of mitophagy induction is needed to be able to detect free GFP (e.g., from Om45-GFP) by western blot under starvation conditions, whereas stationary phase mitophagy typically requires 2 days before a free GFP band is observed.”
The paper relies on this without support.
Stationary phase mitophagy typically requires 2 days before a free GFP band is observed.
“Usually 6 h of mitophagy induction is needed to be able to detect free GFP (e.g., from Om45-GFP) by western blot under starvation conditions, whereas stationary phase mitophagy typically requires 2 days before a free GFP band is observed.”
The paper relies on this without support.
Aggrephagy can be followed in vitro (in cell culture) and in vivo (in mice) by monitoring the levels of an aggregate-prone protein.
“This process can be followed in vitro (in cell culture) and in vivo (in mice) by monitoring the levels of an aggregate-prone protein such as an expanded polyglutamine (polyQ)-containing protein or mutant MAPT/tau or SNCA/α-synuclein (synuclein alpha).”
The paper relies on this without support.
In yeast, degradation of SNCA aggregates can be followed by promoter shut-off assays.
“In yeast, degradation of SNCA aggregates can be followed by promoter shut-off assays.”
The paper relies on this without support.
Expression of the inducible GAL1 promoter of GFP-tagged SNCA is stopped by glucose repression.
“Expression of the inducible GAL1 promoter of GFP-tagged SNCA is stopped by glucose repression.”
The paper relies on this without support.
In yeast chronological aging model, SNCA toxicity is dependent on Atg11.
“In this model, SNCA toxicity is dependent on Atg11”
The paper relies on this without support.
Fluorescently tagged aggregated proteins such as polyQ80-CFP can be monitored via immunoblot and immunofluorescence.
“Similarly, fluorescently tagged aggregated proteins such as polyQ80-CFP can be monitored via immunoblot and immunofluorescence.”
The paper relies on this without support.
The ratio of luciferase activity from polyQ80-luciferase and a control can be calculated to determine autophagic flux.
“The ratio of luciferase activity from these two constructs can be calculated to determine autophagic flux.”
The paper relies on this without support.
Autophagic clearance of mutated human HTT (huntingtin) protein with a polyQ expansion (HTT103Q) can be observed in budding yeast.
“Autophagic clearance of mutated human HTT (huntingtin) protein with a polyQ expansion (HTT103Q) can also be observed in budding yeast.”
The paper relies on this without support.
After overnight induction from a galactose inducible promotor, HTT103Q proteins form inclusion bodies in yeast cells.
“After overnight induction from a galactose inducible promotor, HTT103Q proteins form inclusion bodies in yeast cells.”
The paper relies on this without support.
The vacuole is easily identified, making the identification of autophagic bodies much simpler.
“First, the vacuole is easily identified, making the identification of autophagic bodies much simpler.”
The paper relies on this without support.
An organelle-targeted Pho8∆60 assay is an alternative method to monitor selective autophagy.
“An alternative method to monitor selective autophagy is to use an organelle-targeted Pho8∆60 assay.”
The paper relies on this without support.
A nonaggregating polyQ19-luciferase or untagged full-length luciferase serve as a control.
“A nonaggregating polyQ19-luciferase or untagged full-length luciferase serve as a control.”
The paper relies on this without support.
Cytosolic lipofuscin appears as an RFP-independent GFP (green) punctum.
“Cytosolic lipofuscin will appear as an RFP-independent GFP (green) punctum.”
The paper relies on this without support.
Soluble polyQ reporters can be degraded by the proteasome.
“soluble polyQ reporters can be degraded by the proteasome”
The paper relies on this without support.
There is no consensus at the present time with regard to the best method for monitoring mitophagy in animal cells.
“There is no consensus at the present time with regard to the best method for monitoring mitophagy in animal cells.”
The paper relies on this without support.
Changes in mRNA levels of mitophagy-associated factors (e.g., PINK1, PRKN) do not necessarily reflect mitophagic activity.
“changes in mRNA levels of these factors do not necessarily reflect mitophagic activity”
The paper relies on this without support.
Induction of mitophagy promotes the formation of ring-shaped/spheroid mitochondria interacting with structures positive for LC3 and lysosomal proteins.
“induction of mitophagy also promotes the formation of ring-shaped/spheroid mitochondria interacting with structures positive for LC3 and lysosomal proteins (based on immuno-EM).”
The paper relies on this without support.
MitoTracker® Green FM is not retained well after aldehyde fixation, whereas MitoTracker® Red CMXRos works under these conditions.
“MitoTracker® Green FM is not retained well after aldehyde fixation, whereas MitoTracker® Red CMXRos works under these conditions.”
The paper relies on this without support.
The various mitochondrial dyes are not identical in terms of their properties, and not all are suitable for use following fixation.
“the various mitochondrial dyes are not identical in terms of their properties, and not all are suitable for use following fixation.”
The paper relies on this without support.
MitoTracker® probes are lipophilic cations that include a chloromethyl group and a fluorescent moiety.
“Among the MitoTracker® probes are lipophilic cations that include a chloromethyl group and a fluorescent moiety.”
The paper relies on this without support.
For certain cell lines (e.g., SH-SY5Y), at least 48 h of transient expression is required for sufficient targeting/import of mitochondrial GFP/RFP prior to analyzing mitophagy.
“When using matrix-targeted fluorophores for certain cell lines (e.g., SH-SY5Y), it is important to allow at least 48 h of transient expression for sufficient targeting/import of mitochondrial GFP/RFP prior to analyzing mitophagy.”
The paper relies on this without support.
Many protein aggregates fail to enter the resolving gel and are retained in the stacking gel.
“many protein aggregates fail to enter the resolving gel and are retained in the stacking gel.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The presence of yellow puncta suggests autophagic flux is being blocked by inhibition of lysosome fusion with the autophagosome74–77, and can be induced by the addition of autophagy blocker, Bafilomycin A1 (BAFA1) (Supplementary Fig. 8k).”
From GRAMD1B is a regulator of lipid homeostasis, autophagic flux and phosphorylated tau (2025) · cites this paper as [75]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Currently, autophagic flux assays are the gold standard method for assessing autophagy in a given cell or tissue [91].”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [91]
The cited source says what the claim attributes to it.
In the citing paper
“LAMP2 (along with LAMP1) is widely accepted as a structural lysosomal membrane protein marker used to identify lysosomes and late endo/lysosomal compartments”
From TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models (2026) · cites this paper as Klionsky et al. 2021
In the citing paper
“double- membraned autophagosomes were identified according to well established criteria”
From Nilotinib restores memory function by preventing dopaminergic neuron degeneration in a mouse model of Alzheimer’s Disease (2021) · cites this paper as Klionsky et al., 2021
In the citing paper
“In the cytoplasm of both WT and Tg2576 neurons we detected double-membraned autophagosomes (Fig. 4A) characterized by electron dense material at different stages of degradation (Klionsky et al., 2021).”
From Nilotinib restores memory function by preventing dopaminergic neuron degeneration in a mouse model of Alzheimer’s Disease (2021) · cites this paper as Klionsky et al., 2021
In the citing paper
“In addition, the static evaluation of autophagy-related proteins, and particularly LC3-II, is not always a reliable method to determine autophagy alterations [63].”
From Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology (2023) · cites this paper as [63]
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Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
“upon binding, produces an active NanoBiT luciferase that generates luminescence proportional to the amount of autophagy.”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > Cautionary notes:
“Induction of autophagy, such as through starvation, or MTORC1 inhibition via PP242 treatment or siRNA knockdown of RPTOR, decrease luminescence readings.Conversely, blockade of autophagy flux, for example by treatment with CQ, increases the luminiscence readings (Figure 20A).”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
“Even the autophagy-suppressive effects of AMPK could, conceivably, be mediated through ULK1 phosphorylation, for example, at the inhibitory site Ser638 [686].”
§ Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4th edition) 1 > 3. SQSTM1 and related LC3-binding protein turnover assays.
“In mammalian cells, the phosphorylation status of ULK1 at the activating sites (Ser317, 777 [position in the murine sequence, not conserved in human], 467, 556, 638, or Thr575 in the human sequence) or dephosphorylation at inactivating sites (Ser638, 758 in the human sequence) can be determined by western blot using phosphospecific antibodies [670-672, 686, 746, 747].”
Cited works that were retracted
Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
“Gu J, Wang Y, Wang X, et al. Effect of the LncRNA GAS5-MiR-23a-ATG3 Axis in Regulating Autophagy in Patients with Breast Cancer. Cell Physiol Biochem. 2018;48(1):194-207. doi: 10.1159/000491718. PubMed PMID: 30007957. 3111. Zhang N, Yang GQ, Shao XM, et al. GAS5 modulated autophagy is a mechanism modulating cisplatin sensitivity in NSCLC cells. Eur Rev Med Pharmacol Sci. 2016 Jun;20(11):2271-7. PubMed PMID: 27338051. 3112. Li L, Huang C, He Y, et al. Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability. Cell Physiol Biochem. 2018;48(4):1723-1734. doi: 10.1159/000492300. PubMed PMID: 30078013. 3113. Mata IF, Samii A, Schneer SH, et al. Glucocerebrosidase gene mutations: a risk factor for Lewy body disorders. Archives of neurology. 2008 Mar;65(3):379-82. doi: 10.1001/archneurol.2007.68. PubMed PMID: 18332251; PubMed Central PMCID: PMC2826203. 3114.”
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A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
“10.1242/jcs.144816”
Cited work 10.1242/jcs.144816 · retracted 2022-07-25 · notice 10.1242/jcs.259757 · this paper published 2021-01-02
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
“10.7554/eLife.34532”
Cited work 10.7554/elife.34532 · retracted 2022-09-02 · notice 10.7554/elife.82988 · this paper published 2021-01-02
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In the paper
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Cited work 10.1111/jpi.12247 · retracted 2024-06-17 · notice 10.1111/jpi.12978 · this paper published 2021-01-02
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
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Cited work 10.1038/sj.bjc.6603654 · retracted 2025-04-30 · notice 10.1038/s41416-025-03036-y · this paper published 2021-01-02
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
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Cited work 10.1038/ncb3192 · retracted 2024-03-04 · notice 10.1038/s41556-024-01383-1 · this paper published 2021-01-02
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In the paper
“10.1073/pnas.1113421108”
Cited work 10.1073/pnas.1113421108 · retracted 2025-08-04 · notice 10.1073/pnas.2518460122 · this paper published 2021-01-02
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
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Citations
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Duan, T., Yang, X., Kuang, J., Sun, W., Li, J., Ge, J., Zhang, M., Cai, X., Yu, P., Yang, J. J., et al. (2023) · Journal of Hepatocellular Carcinoma · doi:10.2147/jhc.s399855 · Cited by 8
Self-citationSESN2 Could Be a Potential Marker for Diagnosis and Prognosis in Glioma
Xu, L., Liu, Z., Wang, H. H., Lu, J., Xu, J., Meng, Y., Huang, K., & Liu, B. (2023) · Genes · doi:10.3390/genes14030701 · Cited by 7
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Self-citationEffect of Lacking ZKSCAN3 on Autophagy, Lysosomal Biogenesis and Senescence
Li, X., Wen, J.-H., Feng, Z.-S., Wu, Y.-S., Li, D.-Y., Liang, S., Wu, D., Wu, H.-L., Li, S., Ye, Z.-N., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24097786 · Cited by 7
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Self-citationAutophagy induced by human adenovirus B7 structural protein VI inhibits viral replication
Zhang, L., Duan, Y., Wang, W., Li, Q., Tian, J., Zhu, Y., Wang, R., & Xie, Z. (2023) · Virologica Sinica · doi:10.1016/j.virs.2023.08.002 · Cited by 7
Self-citationNrf2 depletion in the context of loss-of-function Keap1 leads to mitolysosome accumulation
Naidu, S. D., Angelova, P. R., Knatko, E. V., Leonardi, C., Novak, M. J., de la Vega, L., Ganley, I. G., Abramov, A. Y., & Dinkova‐Kostova, A. T. (2023) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2023.09.009 · Cited by 7
Self-citationProtein modification regulated autophagy in Bombyx mori and Drosophila melanogaster
Wu, W., Lin, L., Zhao, Y., Li, H., & Zhang, R. (2023) · Frontiers in Physiology · doi:10.3389/fphys.2023.1281555 · Cited by 7
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Self-citationProtective effects and mechanisms of dapagliflozin on renal ischemia/reperfusion injury
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Self-citationEvidence for cytoprotective autophagy in response to HER2-targeted monoclonal antibodies
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Role of autophagy-related genes in liver cancer prognosis
Zhou, Y., Shan, R., Xie, W., Zhou, Q., Yin, Q., Su, Y., Xiao, J., Luo, P., Yao, X., Fang, J., et al. (2024) · Genomics · doi:10.1016/j.ygeno.2024.110852 · Cited by 7
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Self-citationResearch progress of T cell autophagy in autoimmune diseases
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Self-citationArmengol, E. G., Merckx, C., Sutter, H. D., Bleecker, J. D., & Paepe, B. D. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26020439 · Cited by 7
Monterrubio-Ledezma, F., Salcido-Gómez, A., Zavaleta-Vásquez, T. I., Navarro‐García, F., Cisneros, B., & Massieu, L. (2025) · GeroScience · doi:10.1007/s11357-024-01501-9 · Cited by 7
Self-citationThe effect of an exercise- and passive-induced heat stress on autophagy in young and older males
McCormick, J. J., King, K. E., Goulet, N., Carrillo, A. E., Fujii, N., Amano, T., Boulay, P., & Kenny, G. P. (2025) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00232.2024 · Cited by 7
da Cruz, L. L., Sinzato, Y. K., Paula, V. G., Fioretto, M. N., Gallego, F. Q., Barco, V. S., Camargo, A. C. L., Corrente, J. E., Justulin, L. A., Rodrigues, T., et al. (2025) · Journal of Developmental Origins of Health and Disease · doi:10.1017/s204017442400045x · Cited by 7
Self-citationShi, H., Yang, Y., Gao, J., Kumar, S., Xie, H. Y., Chen, Z., Lyu, J., Sihto, H. J., Koljonen, V., Vega-Rubín-de-Celis, S., et al. (2025) · Autophagy · doi:10.1080/15548627.2025.2477385 · Cited by 7
Self-citationCeramide and the membrane-fusion activity of LC3/GABARAP autophagy proteins
Varela, Y. R., Aguirre, C. C., Iriondo, M. N., Ballesteros, U., Collado, M. I., Etxaniz, A., Montes, L. R., Goñi, F. M., & Alonso, A. (2025) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-025-05811-9 · Cited by 7
Self-citationCai, S., Chen, Y., Chen, C., & Liu, M. (2025) · Cell Biology and Toxicology · doi:10.1007/s10565-025-10070-2 · Cited by 7
Self-citationShah, B., Khan, R., Shah, W., Aftab, A., Khan, M., Dil, S., & Shi, Q. (2021) · Mammalian Genome · doi:10.1007/s00335-021-09879-z · Cited by 7
Autophagy-Associated IL-15 Production Is Involved in the Pathogenesis of Leprosy Type 1 Reaction
Silva, B. J. D. A., Bittencourt, T. L., Leal-Calvo, T., Mendes, M. A., Prata, R. B. D. S., Barbosa, M. G. D. M., Andrade, P. R., Côrte‐Real, S., da Silva, G. M. S., Moraes, M. O., et al. (2021) · Cells · doi:10.3390/cells10092215 · Cited by 7
Self-citationAn indole-based fluorescent chemosensor targeting the autophagosome
Park, S. Y., Kim, K., Cho, D., Jo, E.-Y., Kang, C., & Lee, M. H. (2022) · Chemical Communications · doi:10.1039/d1cc06681a · Cited by 7
Self-citationKoskela, A. K. J., Manai, F., Basagni, F., Liukkonen, M., Rosini, M., Govoni, S. M., Monte, M. D., Smędowski, A., Kaarniranta, K., & Amadio, M. (2022) · Antioxidants · doi:10.3390/antiox11071385 · Cited by 7
Self-citationMachihara, K., Kageyama, S., Oki, S., Makino, H., Sasaki, M., Iwahashi, H., & Namba, T. (2022) · Aging · doi:10.18632/aging.204303 · Cited by 7
Park, S., Jeong, S., Nam, Y. H., Yum, Y., & Jung, S. (2022) · Tissue Engineering and Regenerative Medicine · doi:10.1007/s13770-022-00489-7 · Cited by 7
Self-citationUrolithin B: Two-way attack on IAPP proteotoxicity with implications for diabetes
Raimundo, A., Ferreira, S., Pobre, V., Lopes‐da‐Silva, M., Brito, J. A., dos Santos, D. J. V. A., Saraiva, N., dos Santos, C. N., & Menezes, R. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1008418 · Cited by 7
Kim, J., Kim, Y., Kim, J. Y., Lee, S., Kim, M., & Jekarl, D. W. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24032872 · Cited by 7
Self-citationPicca, A., Wohlgemuth, S. E., McDermott, M. M., Saini, S. K., Dayanidhi, S., Zhang, D., Xu, S., Kosmac, K., Tian, L., Ferrucci, L., et al. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.122.027088 · Cited by 7
Self-citationDoes Exercise Regulate Autophagy in Humans? A Systematic Review and Meta-Analysis
Chen, X., Zheng, C., Siu, P. M., Sun, F., Wong, S. H., & Chun‐Hang, A. (2023) · Autophagy Reports · doi:10.1080/27694127.2023.2190202 · Cited by 7
Self-citationSARS-CoV-2 Infection, Inflammation, Immunonutrition, and Pathogenesis of COVID-19
Yu, L., Ghani, M. K. A., Aghemo, A., Barh, D., Bassetti, M., Catena, F., Gallo, G., Gholamrezanezhad, A., Kamal, M. A., Lal, A., et al. (2023) · Current Medicinal Chemistry · doi:10.2174/0929867330666230330092725 · Cited by 8
Self-citationKomlós, M., Szinyákovics, J., Falcsik, G., Sigmond, T., Jezsó, B., Vellai, T., & Kovács, T. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24098100 · Cited by 7
Self-citationXiong, Q., Feng, R., Fischer, S., Karow, M. A., Stumpf, M., Meßling, S., Nitz, L., Müller, S., Clemen, C. S., Song, N., et al. (2023) · Cells · doi:10.3390/cells12111514 · Cited by 7
Self-citationInducin Triggers LC3‐Lipidation and ESCRT‐Mediated Lysosomal Membrane Repair
Corkery, D., Ursu, A., Lucas, B., Grigalunas, M., Kriegler, S., Oliva, R., Dec, R., Koska, S., Pahl, A., Sievers, S., et al. (2023) · ChemBioChem · doi:10.1002/cbic.202300579 · Cited by 7
Self-citationGhosh, S., Chakraborti, S., Devi, D., Sahu, R., Mandal, S., & Mandal, L. (2023) · Nucleic Acids Research · doi:10.1093/nar/gkad1047 · Cited by 8
Zanon, A. B., Silva, A. O., Franco, N., Picon, R. V., Lenz, G., Lopez, P. L. D. C., & Filippi‐Chiela, E. C. (2024) · Journal of Cellular Biochemistry · doi:10.1002/jcb.30517 · Cited by 7
Self-citationFote, G., Eapen, V. V., Lim, R. G., Yu, C., Salazar, L., McClure, N. R., McKnight, J. I., Nguyen, T. B., Heath, M. C., Lau, A., et al. (2024) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2319091121 · Cited by 9
Self-citationLung transplantation: candidate selection and timing of transplant
Shah, P., & Neujahr, D. C. (2021) · Current Opinion in Organ Transplantation · doi:10.1097/mot.0000000000000879 · Cited by 7
The interplay between pathogens and Atg8 family proteins: thousand‐faced interactions
Toth, D. M., Horváth, G. V., & Juhász, G. (2021) · FEBS Open Bio · doi:10.1002/2211-5463.13318 · Cited by 8
Self-citationHolling, T., Bhavani, G. S., von Elsner, L., Shah, H. H., Kausthubham, N., Bhattacharyya, S. S., Shukla, A., Mortier, G. R., Schinke, T., Danyukova, T., et al. (2022) · Human Mutation · doi:10.1002/humu.24368 · Cited by 7
Self-citationZhelavskyi, M. M., Kernychnyi, S., Dmytriv, O. Y., & Betlinska, T. V. (2022) · Ukrainian Journal of Veterinary and Agricultural Sciences · doi:10.32718/ujvas5-1.02 · Cited by 7
Clavière, M., Lavedrine, A., Lamiral, G., Bonnet, M., Verlhac, P., Petkova, D. S., Espert, L., Duclaux‐Loras, R., Lucifora, J., Rivoire, M. L., et al. (2022) · Autophagy · doi:10.1080/15548627.2022.2107309 · Cited by 7
Self-citationAberrant regulation of autophagy disturbs fibrotic liver regeneration after partial hepatectomy
Lian, Y., Bai, Y., Lai, J., & Huang, A.-M. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.1030338 · Cited by 7
Self-citationVerdev, P. T., Potokar, M., Korva, M., Rus, K. R., Kolenc, M., Avšič‐Županc, T., Zorec, R., & Jorgačevski, J. (2022) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-022-04578-7 · Cited by 7
Lee, H. J., Kim, S. H., Kim, Y. H., Ys, K., Oh, G. S., Bae, J.-E., Kim, J. B., Park, N. Y., Park, K. H., Yeom, E., et al. (2022) · Cells · doi:10.3390/cells12010146 · Cited by 7
Self-citationAutophagy increase in Merosin-Deficient Congenital Muscular Dystrophy type 1A
Mastrapasqua, M., Rossi, R., Cosmo, L. D., Resta, A., Errede, M., Bizzoca, A., Zampatti, S., Resta, N., Giardina, E., Ruggieri, M., et al. (2023) · European Journal of Translational Myology · doi:10.4081/ejtm.2023.11501 · Cited by 7
Autophagy in Atherosclerosis: Not All Foam Cells Are Created Equal
Francis, G. A., & Razani, B. (2022) · Circulation Research · doi:10.1161/circresaha.122.320857 · Cited by 7
Self-citationXie, L., Hao, X., Xie, J., Mo, J., Yuan, C., & Chen, W. (2024) · Food & Function · doi:10.1039/d4fo00185k · Cited by 7
Self-citationNon-autophagic Golgi-LC3 lipidation facilitates TFE3 stress response against Golgi dysfunction
Kang, J., Li, C. M., Kim, N., Baek, J., & Jung, Y. (2024) · The EMBO Journal · doi:10.1038/s44318-024-00233-y · Cited by 6
Self-citationImpairment of proteasome-associated deubiquitinating enzyme Uchl5/UBH-4 affects autophagy
Jha, S., Pispa, J., & Holmberg, C. I. (2025) · Biology Open · doi:10.1242/bio.061644 · Cited by 6
Self-citationZhu, G., Zuo, Q., Liu, S., Zheng, P., Zhang, Y., Zhang, X., Rollins, J. A., Liu, J., & Pan, H. (2025) · New Phytologist · doi:10.1111/nph.70151 · Cited by 6
Self-citationLuis-Ravelo, D., Fumagallo-Reading, F., Febles-Casquero, A., López-Fernández, J., Marcellino, D. J., & González‐Hernández, T. (2025) · Cells · doi:10.3390/cells14090652 · Cited by 6
Self-citationda Costa, R. M., Bruder‐Nascimento, A., Alves, J. V., Awata, W. M. C., Singh, S., Rodrigues, D., Bruder-Nascimento, T. B., & Tostes, R. C. (2025) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00829.2024 · Cited by 6
Self-citationTRIM16 mediates secretory autophagy in head and neck cancer-associated fibroblasts
Ly, T., Pickard, B., Pandey, A., Yap, M., Opara, J. K., Arnold, L., Martínez-Rivera, N., Rosa‐Molinar, E., New, J., Werner, L. R., et al. (2025) · Autophagy · doi:10.1080/15548627.2025.2508064 · Cited by 6
Self-citationRest, Repair, Repeat: The Complex Relationship of Autophagy and Sleep
Ullern, H., Schnur, P., Boccara, C. N., & Knævelsrud, H. (2025) · Journal of Molecular Biology · doi:10.1016/j.jmb.2025.169227 · Cited by 8
Self-citationCottignies-Calamarte, A., Marteau, F., He, F., Belouzard, S., Dubuisson, J., Tudor, D., Viollet, B., & Bomsel, M. (2025) · Journal of Virology · doi:10.1128/jvi.00394-25 · Cited by 6
ATF7 – PINK1 Axis Governs Mitophagy and Intestinal Inflammation in Ulcerative Colitis
Chen, Y., Zhang, X., Li, J., Liu, F., Yu, Q., Li, J., & Zhu, L. (2025) · The FASEB Journal · doi:10.1096/fj.202500813r · Cited by 6
Self-citationTargeting Dio3 to enhance mitophagy and ameliorate skeletal muscle wasting in sepsis
Wang, G., Chen, M., Zhang, Y., Wang, D., Gao, T., Duan, J., Lu, H., Cheng, M., Xu, Y., Li, X., et al. (2025) · Redox Biology · doi:10.1016/j.redox.2025.103751 · Cited by 6
Self-citationTorrecilla-Parra, M., Pardo, V., Fuentes-Fayos, A. C., G-García, M. E., Frutos, M. F.-D., López-Aceituno, J. L., Puigdueta, C., Zamora, C., Pérez-García, A., Aranda, J. F., et al. (2025) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-025-03504-6 · Cited by 7
Seghieri, G., Campesi, I., Tonolo, G., Bennardini, F., Stendardi, I., Matucci, R., & Franconi, F. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26168097 · Cited by 6
Self-citationThe space-time continuum in neurological disorders of the autophagosome-lysosome fusion machinery
Dafsari, H. S., Schuler, J., Schober, E., Möller, B., Antebi, A., Fanto, M., & Jungbluth, H. (2025) · Autophagy Reports · doi:10.1080/27694127.2025.2560903 · Cited by 6
Self-citationNetting, D. J., López‐Haber, C., Hutchins, Z., Martina, J. A., Puertollano, R., & Mantegazza, A. R. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2511539122 · Cited by 6
Self-citationTelusma, B., Farré, J., Cui, D. S., Subramani, S. E., & Davis, J. H. (2025) · Cell Reports · doi:10.1016/j.celrep.2025.116585 · Cited by 6
The impact of exercise on brain mitochondrial health and its relevance to Alzheimer's disease
Csikós, V., Thyfault, J. P., & Wilkins, H. (2025) · Brain and Environment · doi:10.1016/j.braen.2025.100012 · Cited by 6
Malcangi, G., Inchingolo, A. M., Casamassima, L., Trilli, I., Ferrante, L., Longo, M., Inchingolo, F., Marinelli, G., Palermo, A., Dipalma, G., et al. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27020700 · Cited by 6
ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications
Yang, W.-J., & Sheng, R. N. (2026) · Acta Pharmacologica Sinica · doi:10.1038/s41401-025-01724-2 · Cited by 6
Self-citationSREBP-1 increases glucose uptake to promote tumor resistance to lysosome inhibition
Zhong, Y., Geng, F., Su, H., Mazik, L., Yin, X., Pan, M., Li, N., Chiang, C. W., Tonniges, J. R., Mo, X. M., et al. (2026) · Science Translational Medicine · doi:10.1126/scitranslmed.adx6873 · Cited by 7
Self-citationAutophagy in Obesity and Type 2 Diabetes: Beyond the Protective Paradigm
Angarita-Planchez, M. E., Sánchez-Rodríguez, P., Múnera‐Rodríguez, A. M., Leiva‐Castro, C., Benítez-Márquez, J. M., Reina-Pérez, I., Palomares, F., & López-Enríquez, S. (2026) · Current Obesity Reports · doi:10.1007/s13679-026-00716-5 · Cited by 6
Okugbeni, N., du Toit, A., Cole-Holman, V., Johnson, G., Loos, B., & Kinnear, C. J. (2022) · Pathogens · doi:10.3390/pathogens12010024 · Cited by 6
Self-citationVision Beyond Vision: Lessons Learned from Amblyopia
WONG, A. M. F. (2023) · Journal of Binocular Vision and Ocular Motility · doi:10.1080/2576117x.2023.2188836 · Cited by 6
Cheramangalam, R. N., Anand, T., Pandey, P., Balasubramanian, D., Varghese, R., Singhal, N., Nagarkar-Jaiswal, S., & Jaiswal, M. (2023) · PLoS Genetics · doi:10.1371/journal.pgen.1010493 · Cited by 6
Scharte, F., Franzkoch, R., & Hensel, M. (2023) · Molecular Microbiology · doi:10.1111/mmi.15104 · Cited by 7
Alterations of Autophagy Modify Lipids in Epidermal Keratinocytes
Geng, Q., Wei, G., Hu, Y., Xu, J., & Song, X. (2023) · Clinical Cosmetic and Investigational Dermatology · doi:10.2147/ccid.s410252 · Cited by 6
Self-citationChen, W., Chi, X., Song, H., Wang, H., Wang, Y., Liu, Z., & Xu, B. (2023) · Insect Molecular Biology · doi:10.1111/imb.12869 · Cited by 6
Self-citationda Cunha, F. F. M., Tonon, Â. P., Machado, F. C., Travassos, L. R., Grazzia, N., Possatto, J. F., de Sant’ana, A. K. C., Lopes, R. D. M., Rodrigues, T., Miguel, D. C., et al. (2023) · Journal of Chemotherapy · doi:10.1080/1120009x.2023.2264585 · Cited by 6
Self-citationDu, Y., Huang, F., Guan, L., & Zeng, M. (2023) · PubMed Central · doi:10.11817/j.issn.1672-7347.2023.220581 · Cited by 6
Liu, T., Yue, X., Chen, X., Yan, R., Wu, C., Li, Y., Bu, X., Han, H., & Liu, R. (2024) · Cellular Oncology · doi:10.1007/s13402-024-00927-9 · Cited by 6
Self-citationWang, H., Wang, W., Xue, Z., & Gong, H. (2024) · Shock · doi:10.1097/shk.0000000000002366 · Cited by 6
Self-citationSilva, A. D., Dalmasso, G., Larabi, A. B., Hoang, M. H. T., Billard, E., Barnich, N., & Nguyen, H. T. T. (2024) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2024.1268243 · Cited by 7
Self-citationRobeyns, R., Sisto, A., Iturrospe, E., da Silva, K. M., van de Lavoir, M., Timmerman, V., Covaci, A., Stroobants, S. G., & van Nuijs, A. L. N. (2024) · Metabolites · doi:10.3390/metabo14050248 · Cited by 6
Self-citationSyed, R. U., Alshammari, M. D., Banu, H., Khojali, W. M. A., Jafar, M., Nagaraju, P., & Alshammari, A. D. (2024) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-024-03153-0 · Cited by 6
Masson, J.-D., Badran, G., Gherardi, R. K., Authier, F., & Crépeaux, G. (2024) · Toxics · doi:10.3390/toxics12070491 · Cited by 6
Dihydroorotase MoPyr4 is required for development, pathogenicity, and autophagy in rice blast fungus
Wang, J.-Y., Cai, Y., Li, L., Zhu, X., Shen, Z.-F., Wang, Z., Liao, J., Lu, J., Liu, X., & Lin, F. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01741-4 · Cited by 6
Self-citationJing, D., Liu, J., Qin, D., Lin, J., Li, T., Li, Y., & Duan, M. (2024) · Renal Failure · doi:10.1080/0886022x.2024.2368090 · Cited by 6
Self-citationSu, X., Wang, S., Tian, Y., Teng, M., Wang, J., Zhang, Y., Ji, W., & Zhang, Y. (2024) · Molecular Neurobiology · doi:10.1007/s12035-024-04431-x · Cited by 6
Self-citationHSV-2 Manipulates Autophagy through Interferon Pathway: A Strategy for Viral Survival
Dass, D., Banerjee, A., Dhotre, K., Sonawane, V., More, A. N., & Mukherjee, A. (2024) · Viruses · doi:10.3390/v16091383 · Cited by 6
Self-citationFlorencio‐Silva, R., Sasso, G. R. D. S., Sasso‐Cerri, E., Cerri, P. S., Gil, C. D., & Simões, M. D. J. (2024) · Annals of Anatomy - Anatomischer Anzeiger · doi:10.1016/j.aanat.2024.152318 · Cited by 6
Effect of CFTR Modulators on Oxidative Stress and Autophagy in Non-CFTR-Expressing Cells
Scialò, F., Cernera, G., Polise, L., Castaldo, G., Amato, F., & Villella, V. R. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms251910360 · Cited by 6
Gezer, A., Üstündağ, H., SARI, E. K., Bedir, G., Gür, C., Mendĭl, A. S., & Duysak, L. (2024) · Food and Chemical Toxicology · doi:10.1016/j.fct.2024.115040 · Cited by 6
Metadata
- Authors
- Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., Adamopoulos, I. E., Adeli, K., Adolph, T. E., Adornetto, A., Aflaki, E., Agam, G., Agarwal, A., Aggarwal, B. B., Agnello, M., Agostinis, P., Agrewala, J. N., Agrotis, A., Aguilar, P. V., Ahmad, S. T., Ahmed, Z. M., Ahumada-Castro, U., Aits, S., Aizawa, S., Akkoc, Y., Akoumianaki, T., Akpinar, H. A., Al-Abd, A. M., Al-Akra, L., Al-Gharaibeh, A., Alaoui-Jamali, M. A., Alberti, S., Alcocer-Gómez, E., Alessandri, C., Ali, M., Alim Al-Bari, M. A., Aliwaini, S., Alizadeh, J., Almacellas, E., Almasan, A., Alonso, A., Alonso, G. D., Altan-Bonnet, N., Altieri, D. C., Álvarez, É. M. C., Alves, S., Alves da Costa, C., Alzaharna, M. M., Amadio, M., Amantini, C., Amaral, C., Ambrosio, S., Amer, A. O., Ammanathan, V., An, Z., Andersen, S. U., Andrabi, S. A., Andrade-Silva, M., Andres, A. M., Angelini, S., Ann, D., Anozie, U. C., Ansari, M. Y., Antas, P., Antebi, A., Antón, Z., Anwar, T., Apetoh, L., Apostolova, N., Araki, T., Araki, Y., Arasaki, K., Araújo, W. L., Araya, J., Arden, C., Arévalo, M.-A., Arguelles, S., Arias, E., Arikkath, J., Arimoto, H., Ariosa, A. R., Armstrong-James, D., Arnauné-Pelloquin, L., Aroca, A., Arroyo, D. S., Arsov, I., Artero, R., Asaro, D. M. L., Aschner, M., Ashrafizadeh, M., Ashur-Fabian, O., Atanasov, A. G., Au, A. K., Auberger, P., Auner, H. W., Aurelian, L., Autelli, R., Avagliano, L., Ávalos, Y., Aveic, S., Aveleira, C. A., Avin-Wittenberg, T., Aydin, Y., Ayton, S., Ayyadevara, S., Azzopardi, M., Baba, M., Backer, J. M., Backues, S. K., Bae, D.-H., Bae, O.-N., Bae, S. H., Baehrecke, E. H., Baek, A., Baek, S.-H., Baek, S. H., Bagetta, G., Bagniewska-Zadworna, A., Bai, H., Bai, J., Bai, X., Bai, Y., Bairagi, N., Baksi, S., Balbi, T., Baldari, C. T., Balduini, W., Ballabio, A., Ballester, M., Balazadeh, S., Balzan, R., Bandopadhyay, R., Banerjee, S., Banerjee, S., Bánréti, Á., Bao, Y., Baptista, M. S., Baracca, A., Barbati, C., Bargiela, A., Barilà, D., Barlow, P. G., Barmada, S. J., Barreiro, E., Barreto, G. E., Bartek, J., Bartel, B., Bartolome, A., Barve, G. R., Basagoudanavar, S. H., Bassham, D. C., Bast, R. C., Basu, A., Batoko, H., Batten, I., Baulieu, E. E., Baumgarner, B. L., Bayry, J., Beale, R., Beau, I., Beaumatin, F., Bechara, L. R. G., Beck, G. R., Beers, M. F., Begun, J., Behrends, C., Behrens, G. M. N., Bei, R., Bejarano, E., Bel, S., Behl, C., Belaid, A., Belgareh-Touzé, N., Bellarosa, C., Belleudi, F., Belló Pérez, M., Bello-Morales, R., Beltran, J. S. D. O., Beltran, S., Benbrook, D. M., Bendorius, M., Benitez, B. A., Benito-Cuesta, I., Bensalem, J., Berchtold, M. W., Berezowska, S., Bergamaschi, D., Bergami, M., Bergmann, A., Berliocchi, L., Berlioz-Torrent, C., Bernard, A., Berthoux, L., Besirli, C. 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- Affiliations
- University of Michigan (US)
- Department of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt; Department of Experimental Oncology, IEO, European Institute of Oncology IRCCS, Milan, Italy
- Johannes Gutenberg University Mainz (DE)
- Medical University of Graz (AT)
- Pasteur Institute of Iran (IR)
- Leibniz Institute of Plant Biochemistry (DE)
- Hebrew University of Jerusalem (IL)
- University of Copenhagen (DK)
- UiT The Arctic University of Norway (NO)
- Hospital Universitario de Canarias, Research Unit; CIBERNED and Universidad de La Laguna, ITB, Santa Cruz de Tenerife, Spain
- University of California, Davis (US)
- University of Toronto (CA)
- Innsbruck Medical University (AT)
- University of Calabria (IT)
- National Institutes of Health (US)
- Ben-Gurion University of the Negev (IL)
- University of Alabama at Birmingham (US)
- Inflammation Research Center, San Diego, CA, USA
- University of Palermo (IT)
- VIB-KU Leuven Center for Cancer Biology (BE)
- Indian Institute of Technology Ropar (IN)
- University of Dundee (GB)
- The University of Texas Medical Branch at Galveston (US)
- Colby College (US)
- University of Maryland, Baltimore (US)
- Universidad Mayor (CL)
- Lund University (SE)
- Nihon University (JP)
- Koç University School of Medicine, Department of Molecular Biology and Genetics and KUTTAM Research Center for Translational Medicine, Istanbul, Turkey
- University of Crete (GR)
- Institute of Cancer Research (GB)
- Gulf Medical University (AE)
- The University of Sydney (AU)
- Insight Institute of Neurosurgery & Neuroscience, Department of Research, Flint, MI, USA
- McGill University, Departments of Medicine and Oncology and Segal Cancer Centre, Montreal, Quebec, Canada
- Biotechnologisches Zentrum (DE)
- Universidad de Sevilla, Departamento de Psicología Experimental, Facultad de Psicología, Sevilla, Spain
- Sapienza University of Rome (IT)
- Johns Hopkins University (US)
- University of Rajshahi, Department of Pharmacy, Rajshahi, Bangladesh
- Islamic University of Gaza (PS)
- University of Manitoba (CA)
- The Francis Crick Institute (GB)
- Cleveland Clinic (US)
- University of the Basque Country (ES)
- Universidad de Buenos Aires (AR)
- Laboratory of Host-Pathogen Dynamics, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA
- The Wistar Institute (US)
- Universidade do Porto (PT)
- Université Côte d'Azur, INSERM, CNRS, IPMC, team labeled Laboratory of Excellence (LABEX) Distalz, Valbonne, France
- University of Pavia (IT)
- Università di Camerino (IT)
- Telethon Institute Of Genetics And Medicine (IT)
- The Ohio State University (US)
- Save as Ravi Manjithaya
- University of California, San Francisco (US)
- Aarhus University (DK)
- Universidade Nove de Julho (BR)
- Cedars-Sinai Medical Center (US)
- University of Bologna (IT)
- City Of Hope National Medical Center (US)
- University of Tennessee at Knoxville (US)
- Northeast Ohio Medical University (US)
- Universidade Nova de Lisboa (PT)
- University of Cologne (DE)
- University of Bristol (GB)
- University of Helsinki (FI)
- INSERM, U1231, Dijon, France
- Universitat de València (ES)
- National Center of Neurology and Psychiatry (JP)
- The University of Osaka (JP)
- Tokyo University of Pharmacy and Life Sciences (JP)
- Universidade Federal de Viçosa (BR)
- Jikei University School of Medicine (JP)
- Newcastle University (GB)
- Instituto Cajal, Consejo Superior de Investigaciones Científicas (CSIC) and CIBERFES, Madrid, Spain
- University of Seville, Faculty of Pharmacy, Department of Physiology, Seville, Spain
- Albert Einstein College of Medicine (US)
- Howard University (US)
- Tohoku University (JP)
- Imperial College London (GB)
- Toulouse University, CNRS, UPS, Center for Integrative Biology (CBI), Research Center on Animal Cognition (CRCA), Toulouse, France
- Iowa State University, Department of Genetics, Development and Cell Biology, Roy J. Carver Co-Laboratory, Ames, IA, USA
- Consejo Nacional de Investigaciones Científicas y Técnicas (AR)
- York College, City University of New York (US)
- Translational Genomics Group, Incliva Health Research Institute, Burjasot, Valencia, Spain; Interdisciplinary Research Structure for Biotechnology and Biomedicine (ERI BIOTECMED), University of Valencia, Burjasot, Valencia, Spain
- Sabancı Üniversitesi (TR)
- Meir Medical Center, Translational Hemato-Oncology Laboratory, Kfar-Saba, Israel; Tel Aviv University, Department of Human Molecular Genetics and Biochemistry, Sackler School of Medicine, Tel Aviv, Israel
- Bulgarian Academy of Sciences (BG)
- Children's Hospital of Pittsburgh (US)
- Inserm (FR)
- Stanford Medicine (US)
- University of Turin (IT)
- University of Milan (IT)
- Universidad de Santiago de Chile (CL)
- Città della Speranza Foundation (IT)
- Centro de Neurociências e Biologia Celular (PT)
- The Hebrew University of Jerusalem, Alexander Silberman Institute of Life Sciences, Department of Plant and Environmental Sciences, Edmond Safra Campus, Jerusalem, Israel
- Tulane Health Sciences Center, Department of Pathology and Laboratory Sciences, New Orleans, LA, USA
- The University of Melbourne (AU)
- University of Arkansas for Medical Sciences (US)
- University of Malta (MT)
- Kogakuin University (JP)
- Eastern Michigan University (US)
- Hanyang University (KR)
- Yonsei University (KR)
- University of Massachusetts Chan Medical School (US)
- Konkuk University (KR)
- Seoul National University (KR)
- Adam Mickiewicz University/Faculty of Biology, Institute of Experimental Biology, Department of General Botany, Poznan, Poland
- Iowa State University (US)
- Kunming University of Science and Technology (CN)
- National Jewish Health (US)
- The University of Texas at San Antonio Health Science Center (US)
- Jadavpur University (IN)
- Karolinska Institutet (SE)
- University of Genoa (IT)
- University of Siena (IT)
- University of Urbino (IT)
- Baylor College of Medicine (US)
- Institute for Research and Technology in Food and Agriculture (IRTA), Animal Breeding and Genetics Programme, Caldes de Montbui, Spain
- Max Planck Institute of Molecular Plant Physiology (DE)
- UCL Queen Square Institute of Neurology (GB)
- University of Miami (US)
- Centre National de la Recherche Scientifique (FR)
- Shanghai Jiao Tong University (CN)
- Universidade de São Paulo. Department of Biochemistry, Institute of Chemistry, Sao Paulo, Brazil
- University of Rome Tor Vergata (IT)
- Edinburgh Napier University (GB)
- Universitat Pompeu Fabra (ES)
- University of Limerick (IE)
- Danish Cancer Society Research Center, Copenhagen, Denmark
- Rice University (US)
- Columbia University, Department of Medicine, New York, NY, USA
- Jawaharlal Nehru Centre for Advanced Scientific Research (IN)
- Indian Council of Agricultural Research (IN)
- The University of Texas MD Anderson Cancer Center (US)
- University of North Texas Health Science Center (US)
- UCLouvain (BE)
- Trinity College Dublin (IE)
- University of South Carolina Upstate (US)
- Université de Pau et des Pays de l'Adour (FR)
- Universidade de São Paulo (BR)
- Emory University (US)
- University of Pennsylvania (US)
- The University of Queensland (AU)
- Munich Cluster for Systems Neurology (DE)
- Medizinische Hochschule Hannover (DE)
- Tufts University (US)
- Bar-Ilan University (IL)
- Boston University, Metcalf Science Center, Boston, MA, USA
- Sorbonne Université, CNRS UMR8226, Institut de Biologie Physico-Chimique, Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes, Paris, France
- Fondazione Italiana Fegato (IT)
- Istituto Pasteur (IT)
- Centro Nacional de Biotecnología-CNB-CSIC, Madrid, Spain
- Universidad Autónoma de Madrid, Departamento de Biología Molecular, Madrid, Spain
- Universidad Mayor, Center for Integrative Biology, Santiago, Chile
- OU Health Stephenson Cancer Center (US)
- Washington University in Saint Louis, School of Medicine, Department of Psychiatry, Saint Louis MO, USA
- Universidad Francisco de Vitoria, Madrid, Spain
- South Australian Health and Medical Research Institute (AU)
- Centre Hospitalier Universitaire Vaudois (CH)
- Queen Mary University of London (GB)
- Magna Graecia University (IT)
- Université Paris Descartes, Institut Cochin, INSERM U1016, CNRS UMR8104, Paris, France
- Université du Québec à Trois-Rivières (CA)
- University of Montpellier, CNRS/UMR5235 LPHI, Montpellier, France
- Ghent University (BE)
- University of Oxford (GB)
- University of New Mexico (US)
- Comenius University, Department of Biochemistry, Bratislava, Slovakia
- University of Oklahoma Health Sciences Center (US)
- Vanderbilt University Medical Center (US)
- Post Graduate Institute of Medical Education and Research (IN)
- Louisiana State University Health Sciences Center Shreveport (US)
- National Institute of Technology Rourkela (IN)
- Michigan Technological University (US)
- Dalian Medical University (CN)
- Garvan Institute of Medical Research (AU)
- McGill University (CA)
- Eötvös Loránd University (HU)
- Federal University of São Paulo, Department of Pharmacology, Paulista School of Medicine, São Paulo, Brazil
- University Hospital of North Norway, The Heart and Lung Clinic; University of Tromso-The Artic University of Norway, Department of Clinical Medicine, Tromso, Norway
- Norwegian University of Science and Technology, Department of Biomedical Laboratory Science, Trondheim, Norway
- University of York (GB)
- University of Valencia, Faculty of Medicine, Department of Physiology, Valencia, Spain; CIBERehd, Valencia, Spain
- University of Lodz, Faculty of Biology and Environmental Protection, Lodz, Poland
- Linköping University (SE)
- Karolinska University Hospital (SE)
- Indiana University School of Medicine (US)
- St. Jude Children's Research Hospital (US)
- University of Zagreb (HR)
- University of Pennsylvania, Department of Basic and Translational Sciences, Philadelphia, PA, USA
- Burnet Institute (AU)
- University College Cork (IE)
- University of Padua (IT)
- West Virginia University (US)
- The Open University (GB)
- University of Freiburg (DE)
- University Children's Hospital Zurich (CH)
- Case Western Reserve University (US)
- Washington State University (US)
- Universidade de Santiago de Compostela (ES)
- Centro de Investigaciones Biológicas Margarita Salas (ES)
- Swedish University of Agricultural Sciences (SE)
- Connecticut Agricultural Experiment Station (US)
- Goethe University Frankfurt (DE)
- Danube Private University (AT)
- University of Göttingen (DE)
- Universidad de Chile, Instituto de Nutrición y Tecnología de los Alimentos (INTA), Santiago, Chile
- Université de Paris, Sorbonne Université, Centre de Recherche des Cordeliers, INSERM U1138, Paris, France
- National Autonomous University of Mexico, Faculty of Chemistry, Department of Biology, Mexico city, Mexico
- San Francisco General Hospital (US)
- University of Pittsburgh (US)
- Washington University in St. Louis (US)
- Genentech (US)
- University of California, Los Angeles (US)
- University of Colorado Anschutz (US)
- University of Minnesota (US)
- University of Sao Paulo, School of Physical Education and Sport, Cellular and Molecular Exercise Physiology Laboratory, Sao Paulo, SP, Brazil
- Hospital for Sick Children (CA)
- Telethon Institute of Genetics and Medicine (TIGEM), Pozzuoli, Naples, Italy
- University of Insubria (IT)
- Monash University, School of Biological Sciences, Melbourne, Victoria, Australia
- University of Salento (IT)
- University Duisburg-Essen, Essen University Hospital, Department of Gastroenterology and Hepatology, Essen, Germany; Department of Gastroenterology, Hepatology & Endocrinology, Hannover Medical School, Hannover, Germany
- Thomas Jefferson University (US)
- University of Nebraska Medical Center (US)
- University of Arizona (US)
- University of Iowa (US)
- Montana BioAg. Inc. Missoula, MT, USA
- University of Chile (CL)
- KU Leuven (BE)
- University of Medicine and Pharmacy of Craiova (RO)
- St Thomas' Hospital (GB)
- University of Córdoba (ES)
- Rockefeller University (US)
- Stockholm University (SE)
- University of Verona (IT)
- Instituto Murciano de Investigación Biosanitaria (ES)
- Universidad Nacional Autónoma de México, Faculty of Sciences, Department of Cell Biology, Fibrosis Lab, Mexico City, Mexico
- New York University (US)
- Wenzhou Medical University (CN)
- University of Louisville (US)
- Rutgers, The State University of New Jersey (US)
- Universitat de Barcelona (ES)
- University of Las Palmas de Gran Canaria, Department of Physical Education and Research Institute of Biomedical and Health Sciences (IUIBS), Las Palmas de Gran Canaria, Spain; Norwegian School of Sport Sciences, Department of Physical Performance, Oslo, Norway
- University of Alabama (US)
- University of Georgia (US)
- Agostino Gemelli University Polyclinic (IT)
- Universidad de Zaragoza (ES)
- University of Cordoba, Department of Cell Biology, Physiology and Immunology, Córdoba, Spain
- University of São Paulo, Department of Immunology, Laboratory of Transplantation Immunobiology, São Paulo, SP, Brazil
- University of London (GB)
- Loyola University Chicago (US)
- University of Ottawa, Department of Chemistry and Biomolecular Sciences and Department of Biochemistry, Microbiology and Immunology, Host-Microbe Interactions Laboratory, Ottawa, ON, Canada
- University of Sassari (IT)
- Université Côte d'Azur (FR)
- Universidad San Sebastián (CL)
- Federal University of São Paulo, Department of Medicine, Nephrology Division, Laboratory of Clinical and Experimental Immunology, São Paulo, SP, Brazil
- IRBLleida-University of Lleida,Department of Experimental Medicine, Lleida, Spain
- Xiamen University (CN)
- University of Campania "Luigi Vanvitelli" (IT)
- Universidade da Coruña (ES)
- University of Wisconsin–Madison (US)
- University of Geneva, Department of Biochemistry, Faculty of Science, Switzerland
- Universidad Mayor, Center for Integrative Biology, and Geroscience Center for Brain Health and Metabolism, Santiago, Chile
- Universidad Nacional Autónoma de México, Institute of Biotechnology, Plant Molecular Biology Department, Cuernavaca, Morelos, México
- University of Arizona Cancer Center (US)
- BC Cancer – Victoria (CA)
- University of Graz, Institute of Molecular Biosciences, NAWI Graz, Graz, Austria
- Federal University of Rio de Janeiro, Institute of Microbiology, Department of Immunology, Rio de Janeiro, Brazil
- Marche Polytechnic University (IT)
- University of Modena and Reggio Emilia (IT)
- University Medical Center Hamburg-Eppendorf (DE)
- University of Lisbon (PT)
- Universitat Autònoma de Barcelona (ES)
- Consejo Superior de Investigaciones Científicas (ES)
- University of Valparaíso (CL)
- Complutense University, Instituto de Investigaciones Sanitarias San Carlos (IdISSC), Department of Biochemistry and Molecular Biology, School of Biology, Madrid, Spain
- Casa Sollievo della Sofferenza (IT)
- University of Concepción (CL)
- Universidade de Lisboa, Faculty of Pharmacy, Research Institute for Medicines (iMed.ULisboa), Lisboa, Portugal
- Universidad de La Laguna, Departamento de Ciencias Médicas Básicas, Tenerife, Spain
- Universidad Nacional Autónoma de México (UNAM), Instituto de Fisiologia Celular, Ciudad Universitaria, Ciudad de México, México
- Scripps Research Institute (US)
- University of Coimbra, Portugal, CNC – Center for Neuroscience and Cell Biology & Faculty of Pharmacy, Coimbra, Portugal
- University of Pisa (IT)
- Universität Innsbruck (AT)
- Biomedical Research Institute of Murcia, IMIB-Arrixaca, Telomerase, Cancer and Aging Group, Surgical Department, Murcia, Spain
- Research Center Borstel, Leibniz Lung Center, Priority Area Infections, Division Cellular Microbiology, Borstel, Germany
- Medical University of Bialystok, Department of Pharmaceutical Biochemistry, Bialystok, Poland
- Vita-Salute San Raffaele University (IT)
- Hospital Universitari de Tarragona Joan XXIII, Institut d'Investigació Sanitària Pere Virgili, Madrid, Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain
- University of Minho (PT)
- Universidade Federal de São Paulo (BR)
- Università degli Studi della Tuscia (IT)
- Ege University, Faculty of Medicine, Department of Medical Biology, Izmir, Turkey
- Jeonbuk National University (KR)
- Kaohsiung Medical University (TW)
- University of Calcutta (IN)
- Saha Institute of Nuclear Physics (IN)
- Justus-Liebig-Universität Gießen (DE)
- University of Hong Kong (HK)
- Queen's University (CA)
- Chinese University of Hong Kong (HK)
- Tulane University (US)
- QB3 (US)
- National University of Singapore (SG)
- Southeast University (CN)
- University of East Anglia (GB)
- Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U964, CNRS UMR7104, University of Strasbourg, Illkirch, France
- Translational Health Science and Technology Institute (IN)
- Banaras Hindu University (IN)
- University of Washington (US)
- Institute of Life Sciences (IN)
- University College London (GB)
- National Cheng Kung University (TW)
- Institute of Biological Chemistry, Academia Sinica (TW)
- University of Southern California (US)
- Qingdao University (CN)
- Army Medical University (CN)
- Wuhan Sports University (CN)
- Nankai University (CN)
- Wuhan University (CN)
- Duke University (US)
- Chinese Academy of Sciences, Institute of Modern Physics, Lanzhou, China
- University of Sydney, Sydney Medical School, Renal Medicine, St Leonards, NSW, Australia
- Temple University, Lewis Katz School of Medicine, Cardiovascular Research Center and Department of Physiology, Philadelphia, PA, USA
- Sun Yat-sen University (CN)
- Sun Yat-sen University, School of Life Science, Guangzhou, China
- 2nd Affiliated Hospital of Zhejiang University School of Medicine, Department of Respiratory and Critical Care Medicine, Hangzhou, China
- Capital Medical University (CN)
- Northwestern University (US)
- East China Normal University (CN)
- University of Florida (US)
- National Cancer Center Korea, Goyang, Gyeonggi, Korea
- Lomonosov Moscow State University (RU)
- INSERM U1242, University of Rennes, Rennes, France; Centre de Lutte Contre le Cancer Eugène Marquis, Rennes, France
- University of North Carolina at Charlotte (US)
- The University of Hong Kong, Queen Mary Hospital, Department of Paediatrics and Adolescent Medicine, Pokfulam, Hong Kong, China
- University of Milano-Bicocca (IT)
- Istituto di Fisiologia Clinica (IT)
- University of Oslo (NO)
- IFOM (IT)
- Advanced Center for Chronic Diseases (CL)
- Taipei Veterans General Hospital (TW)
- Istituto di Farmacologia Traslazionale (IT)
- Kyungpook National University (KR)
- Wonkwang University (KR)
- Weill Cornell Medicine (US)
- Indian Institute of Chemical Biology (IN)
- BC Cancer Agency (CA)
- Agency for Science, Technology and Research (SG)
- Asan Medical Center (KR)
- Bambino Gesù Children's Hospital (IT)
- Instytut Biologii Doświadczalnej im. Marcelego Nenckiego (PL)
- University of Cologne, Faculty of Medicine and University Hospital Cologne, Department of Pediatrics, Cologne, Germany; University of Cologne, Faculty of Medicine and University Hospital Cologne, Center for Molecular Medicine (CMMC), Cologne, Germany
- University of Liverpool (GB)
- Istituto Superiore di Sanità (IT)
- Roma Tre University (IT)
- Biomedical Research Networking Center on Neurodegenerative Diseases (ES)
- University of Belgrade (RS)
- Centre for Research in Agricultural Genomics (CRAG), CSIC-IRTA-UAB-UB, Campus UAB, Bellaterra, Barcelona, Spain
- University of Sheffield (GB)
- Instituto de Histología y Embriología (IHEM)-Universidad Nacional de Cuyo-CONICET, Facultad de Ciencias Médicas, Mendoza, Argentina
- Yale University School of Medicine, Department of Neuroscience and Department of Cell Biology, New Haven, CT, USA
- Unité de Nutrition Humaine (FR)
- Universidade Federal de São Carlos (BR)
- Bellvitge University Hospital (ES)
- Umeå Centre for Microbial Research (SE)
- German Cancer Research Center (DE)
- University of Zurich (CH)
- University of Oviedo, Department of Morphology and Cell Biology, Oviedo, Spain
- CSIC-Universidad de Sevilla, Instituto de Bioquímica Vegetal y Fotosíntesis, Sevilla, Spain
- Department of Anatomy, Cell and Developmental Biology, Eötvös Loránd University, Budapest, Hungary
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- National University of Mar del Plata (AR)
- McGill University Health Centre (CA)
- Medical University of Lublin, Department of Pathophysiology, Lublin, Poland
- Istituto Ortopedico Rizzoli (IT)
- Università Campus Bio-Medico (IT)
- Istituto Dermopatico dell'Immacolata (IT)
- University of Florida Health (US)
- University of Chieti-Pescara (IT)
- Universidade Federal de Sergipe (BR)
- University of Nevada, Reno (US)
- Vienna Biocenter (AT)
- University of Naples Federico II (IT)
- Xi'an Jiaotong University (CN)
- First Hospital of Jilin University (CN)
- University of Salerno, Department of Medicine, Surgery and Dentistry “Scuola Medica Salernitana”, Baronissi, SA, Italy
- University of Padova, Department of Biology, Padova, Italy
- Research Center Borstel - Leibniz Lung Center (DE)
- Christian-Albrechts-University Kiel, Biochemical Institute, Kiel, Germany
- Russian Academy of Sciences (RU)
- Texas Tech University Health Sciences Center (US)
- Max Delbrück Center (DE)
- Swansea University (GB)
- Stellenbosch University (ZA)
- University of Dundee School of Medicine, Division of Cellular Medicine, Dundee, Scotland, UK
- University of Calabria, Department of Farmacy Health and Nutritional Sciences, Rende, Italy
- Ghent University, Translational Nuclear Receptor Research, VIB Center for Medical Biotechnology, Department of Biomolecular Medicine, Ghent, Belgium
- “Sapienza” University of Rome, Department of Radiotherapy, Policlinico Umberto I, Rome, Italy
- University of Verona, Azienda Ospedaliera Universitaria Integrata-Verona, Department of Medicine, Verona; Italy
- Oswaldo Cruz Foundation, Oswaldo Cruz Institute, Leprosy Laboratory, Rio de Janeiro, Brazil
- University of Antwerp, Laboratory of Physiopharmacology, Antwerp, Belgium
- Department of Oncology-Pathology, Cancer Center Karolinska, Karolinska Institute, Stockholm, Sweden.
- Sapienza University of Rome, Ospedale Sant'Andrea, Rome, Italy
- Università degli Studi di Milano, Department of Medical Biotechnology and Translational Medicine, Milano, Italy
- University of Urbino Carlo Bo, Department of Biomolecular Sciences, Unit of Pharmacology and Public Health, Urbino, Italy
- University of Fribourg, Department of Biology, Fribourg, Switzerland
- Danish Cancer Society Research Center, Cell Stress and Survival Unit, Center for Autophagy, Recycling and Disease (CARD), Copenhagen, Denmark
- Boston University (US)
- Universidad Nacional Autónoma de México (MX)
- Medical University of South Carolina (US)
- University of Michigan, Life Sciences Institute, Ann Arbor, MI, USA
- AREA Science Park (IT)
- Virginia Commonwealth University (US)
- University of South Australia (AU)
- University of North Carolina at Chapel Hill (US)
- Institut National de la Recherche Scientifique (CA)
- Institut d'Investigació Biomédica de Bellvitge (ES)
- University of California San Diego (US)
- University of Perugia, Department of Chemistry, Biology and Biotechnology, Perugia, Italy
- Sapienza University of Rome, Department of Biochemical Sciences A. Rossi Fanelli, Rome, Italy
- Philipps University of Marburg, Department of Visceral, Thoracic and Vascular Surgery, Marburg, Germany
- IRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, Dino Ferrari Center, Neuroscience Section, University of Milan, Department of Pathophysiology and Transplantation, Milan, Italy
- University of Teramo, Faculty of Veterinary Medicine, Teramo, Italy
- Western University, Department of Physiology and Pharmacology, London, ON, Canada
- Harvard Medical School, Boston Children’s Hospital, F.M. Kirby Neurobiology Center, Translational Neuroscience Center, Department of Neurology, Boston, MA, USA
- National Institute for Infectious Diseases “L. Spallanzani” IRCCS, Rome, Italy
- University of Rome “Tor Vergata”, Department of Biology, Rome, Italy
- National and Kapodistrian University of Athens (GR)
- University of Cincinnati (US)
- University of Alcalá, Deparment of Systems Biology, Biochemistry and Molecular Biology, Alcalá de Henares, Madrid, Spain
- Arizona State University (US)
- Université de Montréal (CA)
- Goethe University, Institute of Biochemistry II, Faculty of Medicine, Frankfurt am Main, Germany
- Zhejiang University (CN)
- University of Kansas Medical Center (US)
- University of Belgrade, Institute of Molecular Genetics and Genetic Engineering, Belgrade, Serbia
- Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
- Centre de Recherche des Cordeliers, INSERM UMRS 1138, Sorbonne Université, Université de Paris, Equipe 11 labellisée par la Ligue contre le Cancer, 75006 Paris, France; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, 94805 Villejuif, France
- University of Calgary (CA)
- Universidad de Colima (MX)
- University of Canterbury (NZ)
- Hacettepe University, Faculty of Medicine, Department of Medical Biology, Ankara, Turkey
- University of Kentucky (US)
- Shanghai Sixth People's Hospital (CN)
- Goethe University, Institute of Biophysical Chemistry, Frankfurt, Germany
- Nanjing University (CN)
- Umeå University (SE)
- University of Arkansas at Fayetteville (US)
- Tel Aviv University (IL)
- University of British Columbia (CA)
- The University of Texas Health Science Center at Houston (US)
- National Institute of Biological Sciences, Beijing (CN)
- Central South University (CN)
- Cardiff University (GB)
- Shanghai Proton and Heavy Ion Center, Department of Research & Development, Pudong, Shanghai, China
- Department of Neurology, Boston Children’s Hospital, Boston, MA, USA
- Medical University of Vienna (AT)
- United Arab Emirates University (AE)
- University of Graz (AT)
- University of California, Irvine (US)
- Ain Shams University (EG)
- Institut de Recerca Biomèdica Catalunya Sud (ES)
- University of Illinois at Chicago, Department of Pathology, College of Medicine, Chicago, IL, USA
- Florida International University, Department of Immunology and Nano-Medicine, Miami, FL, USA
- Children’s Cancer Hospital Egypt 57357, Tumor Biology Research Program, Cairo, Egypt
- Damietta University, Faculty of Science, Biochemistry Department, Damietta, Egypt
- University Hospital Carl Gustav Carus (DE)
- Philipps University of Marburg, Department of Cytobiology and Cytopathology, Marburg, Germany
- Damietta University (EG)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Boğaziçi University (TR)
- Pfizer (United States) (US)
- Oslo University Hospital (NO)
- University of Bergen (NO)
- Instituto de Investigaciones Biomédicas Sols-Morreale (ES)
- Universität zu Köln, CECAD Forschungszentrum, Institut für Genetik, Köln, Germany
- University of Turku (FI)
- Medical University of Lodz (PL)
- Institute for Advanced Chemistry of Catalonia (IQAC-CSIC), Department of Biological Chemistry; Networking Biomedical Research Centre on Hepatic and Digestive Diseases (CIBER-EHD), Barcelona, Spain
- Max Planck Institute for Biophysical Chemistry (DE)
- La Trobe University (AU)
- Universitat de Miguel Hernández d'Elx (ES)
- Dresden University Medical Center, Department of Neurology, Dresden, Germany
- University of South Carolina (US)
- First Affiliated Hospital of Guangzhou University of Chinese Medicine (CN)
- King's College London (GB)
- National Institutes of Health, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA
- Lyon 1 Université (FR)
- University of Würzburg (DE)
- Temple University (US)
- State Key Laboratory of Respiratory Disease (CN)
- Sir Run Run Shaw Hospital (CN)
- Chinese Academy of Sciences (CN)
- University of São Paulo (USP), Ribeirão Preto Medical School, Department of Genetics, Ribeirão Preto, SP, Brazil.
- Howard Hughes Medical Institute (US)
- Institute of Biomedical Research of Barcelona (IIBB)-CSIC, Barcelona, Spain; Liver Unit, Hospital Clinic i Provincial de Barcelona, IDIBAPS and CIBEREHD, Barcelona, Spain; Research Center for ALPD, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA
- Columbia University (US)
- Università degli Studi del Piemonte Orientale “Amedeo Avogadro” (IT)
- University of California, San Diego, Department of Cellular and Molecular Medicine, La Jolla, CA, USA
- Universidade Federal do Rio Grande do Sul (UFRGS), Morphological Sciences Department, Porto Alegre, RS, Brazil; Clinicas Hospital of Porto Alegre, Porto Alegre, RS, Brazil
- Danish Cancer Society (DK)
- Gladstone Institutes (US)
- University at Buffalo, State University of New York (US)
- Norwegian University of Science and Technology (NO)
- Central University of Tamil Nadu (IN)
- Babraham Institute (GB)
- Ospedale Policlinico San Martino (IT)
- Montreal Neurological Institute and Hospital (CA)
- University of Nebraska–Lincoln (US)
- Istituto Nazionale Biostrutture e Biosistemi (IT)
- Icahn School of Medicine at Mount Sinai (US)
- Institute of Science and Technology Austria (AT)
- Clinica Universidad de Navarra (ES)
- University of Extremadura, Centro de Investigación Biomedica en Red de Enfermedades Neurodegenerativas (CIBERNED), Instituto de Investigación Biosanitaria de Extremadura (INUBE), Department of Biochemistry, Molecular Biology and Genetics, Faculty of Nursing and Occupational Therapy, Cáceres, Spain
- Kyushu University (JP)
- Tokyo Institute of Technology (JP)
- Juntendo University (JP)
- University of Chicago (US)
- University of Gdańsk (PL)
- New York University Abu Dhabi (AE)
- Universidad Castilla La Mancha, Facultad de Farmacia, Área Tecnología Farmacéutica, Albacete, Spain
- Beckman Research Institute at City of Hope, Department of Systems Biology, Monrovia, CA, USA
- Université Paris Cité (FR)
- Edinburgh Cancer Research (GB)
- Air Force Medical University (CN)
- Harbin Institute of Technology (CN)
- South China University of Technology (CN)
- Universitat de Lleida, Department of Experimental Medicine, IRBLleida, Lleida, Spain
- Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Microbiología, Inmunología y Biotecnología, Cátedra de Inmunología, Buenos Aires, Argentina; Universidad de Buenos Aires, CONICET, Instituto de Estudios de la Inmunidad Humoral (IDEHU), Buenos Aires, Argentina
- Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales (IQUIBICEN), Buenos Aires, Argentina
- National Center for Biotechnology (CNB)-CSIC, Laboratory of Intracellular Bacterial Pathogens, Madrid, Spain
- Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Anatomía, Histología y Neurociencia, Madrid, Spain
- Universidad Autonoma de Nuevo Leon, School of Medicine, Department of Histology, Monterrey, Nuevo Leon, Mexico
- Universidad de Salamanca, Institute of Functional Biology and Genomics (IBFG), Instituto de Investigación Biomédica de Salamanca (IBSAL), Salamanca, Spain
- Department of Cell Biology and Histology, Faculty of Biology, University of Murcia, IMIB-Arrixaca, Murcia, Spain
- Department of Cell Death and Proliferation, Institute of Biomedical Research of Barcelona (IIBB- CSIC); Liver Unit, Hospital Clinic i Provincial de Barcelona, IDIBAPS, CIBEREHD, Barcelona, Spain
- Cajal Institute/CSIC and CIBERNED, ISCIII, Madrid, Spain
- University of Bonn (DE)
- Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA
- Tsinghua University (CN)
- Women's Hospital, School of Medicine, Zhejiang University (CN)
- Albert Ludwigs University of Freiburg, Faculty of Medicine, Institute of Molecular Medicine and Cell Research, Freiburg, Germany
- Mortimer B. Zuckerman Mind Brain Behavior Institute (US)
- Heinrich Heine University Düsseldorf (DE)
- Kerman University of Medical Sciences, Institute of Neuropharmacology, Neuroscience Research Center, Kerman, Iran
- Shiraz University (IR)
- University of Sussex (GB)
- Democritus University of Thrace (GR)
- Cornell University (US)
- University of Ferrara (IT)
- University of Coimbra, Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, Coimbra, Portugal; University of Coimbra, Center for Innovative Biomedicine and Biotechnology, Coimbra, Portugal
- Universidad de Sevilla (ES)
- Ludwig Cancer Research (BE)
- Medical University of Warsaw, Department of Immunology, Warsaw, Poland
- University of Auckland (NZ)
- Luxembourg Institute of Health (LU)
- Instituto Butantan (BR)
- University of Groningen, University Medical Center of Groningen, Department of Biomedical Sciences of Cells and Systems, Groningen, The Netherlands
- Leiden University Medical Center, Department of Cell and Chemical Biology and Oncode Institute, Leiden, The Netherlands
- Albert Einstein College of Medicine, Department of Developmental and Molecular Biology, Bronx, NY, USA
- University of the Basque Country, Instituto Biofisika (UPV/EHU, CSIC), and Department of Biochemistry and Molecular Biology, Leioa, Spain
- University of León, Institute of Biomedicine (IBIOMED) and Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), León, Spain
- University of La Laguna, Institute of Biomedical Technologies, Department of Basic Medical Sciences, La Laguna, Tenerife, Spain
- University of Alberta (CA)
- Henry M. Jackson Foundation (US)
- TUM Klinikum (DE)
- Canada's Michael Smith Genome Sciences Centre (CA)
- Harvard University (US)
- Jena University Hospital (DE)
- University of the West of England (GB)
- Flinders University (AU)
- Université de Strasbourg/CNRS UPR 3572 Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France
- Max Planck Institute for Biology of Ageing (DE)
- Medical University of Vienna, Department of Dermatology, Division for Biology and Pathobiology of the Skin, Vienna, Austria
- German Institute of Human Nutrition (DE)
- Lanzhou University (CN)
- Case Comprehensive Cancer Center (US)
- Centro de Investigacion Principe Felipe (ES)
- Universidad Complutense de Madrid (ES)
- Dalhousie University (CA)
- Maine Medical Center Research Institute (US)
- Tongji University (CN)
- University of Virginia (US)
- Institute of Microbial Technology (IN)
- Deakin University (AU)
- University of California, San Diego, Skaggs School of Pharmacy and Pharmaceutical Sciences, La Jolla, CA, USA
- Medical College of Wisconsin (US)
- ICAR-Indian Veterinary Research Institute, FMD VP Laboratory, Bengaluru, India
- University of Eastern Finland (FI)
- Brandeis University (US)
- Tokai University (JP)
- Hasselt University (BE)
- University of Surrey (GB)
- Johns Hopkins University Bloomberg School of Public Health, W. Harry Feinstone Department of Molecular Microbiology and Immunology, Baltimore, MD, USA
- Goethe University, Institute for Molecular Biosciences, Frankfurt/Main, Germany
- University of Occupational and Environmental Health Japan (JP)
- Monash Health (AU)
- University of Malaya, Institute of Biological Sciences (Genetics), Kuala Lumpur, Malaysia
- Leibniz-Forschungsinstitut für Molekulare Pharmakologie (DE)
- California Institute of Technology (US)
- Sichuan University (CN)
- Jinan University (CN)
- D'Youville University (US)
- University Medical Center Groningen (NL)
- University of Glasgow (GB)
- Navarre Institute of Health Research (ES)
- Université de Bordeaux, Institut des Maladies Neurodégénératives (IMN), CNRS UMR 5293, Bordeaux, France
- University of Barcelona, Barcelona Hepatic Hemodynamic Unit, Liver Unit, Hospital Clinic, Hospital Clínic-Institut d’Investigacions Biomèdiques (IDIBAPS), Centro de Investigación Biomédica Red de enfermedades Hepáticas y Digestivas (CIBERehd), Barcelona, Spain
- Hunan Normal University (CN)
- Universitat de Lleida (ES)
- Buck Institute for Research on Aging (US)
- University of Bern (CH)
- The University of Texas Southwestern Medical Center (US)
- Los Alamos National Laboratory (US)
- University of Waterloo (CA)
- Yale University (US)
- University of Birmingham, College of Medical and Dental Sciences, Institute of Inflammation and Ageing, Birmingham, UK
- Kyungpook National University, School of Medicine, Department of Physiology, Daegu, Korea
- European Molecular Biology Laboratory (DE)
- Chung Shan Medical University (TW)
- National Yang Ming Chiao Tung University (TW)
- University of Plymouth (GB)
- Anhui University of Science and Technology (CN)
- Soochow University (CN)
- Southern Medical University Shenzhen Hospital (CN)
- National Tsing Hua University (TW)
- Chinese Academy of Medical Sciences & Peking Union Medical College, Institute of Materia Medica, State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Molecular Immunology and Cancer Pharmacology Group, Beijing, China
- Northwest A&F University (CN)
- SUNY Downstate Health Sciences University (US)
- Huazhong University of Science and Technology (CN)
- Chongqing University (CN)
- Second Affiliated Hospital of Xi'an Jiaotong University (CN)
- First Affiliated Hospital Zhejiang University (CN)
- University Hospital Jena, Institute of Human Genetics, Jena, Thuringia, Germany
- University of Otago (NZ)
- Max Planck Institute of Biophysics (DE)
- University of California, Berkeley (US)
- Durham University (GB)
- University of Indonesia (ID)
- University of Messina (IT)
- Medical Institute of Bioregulation, Kyushu University (JP)
- Osaka International Cancer Institute (JP)
- Istituto Nazionale per le Malattie Infettive Lazzaro Spallanzani (IT)
- Akita University (JP)
- Augusta University (US)
- University of Illinois Chicago (US)
- University of Copenhagen, Copenhagen Biocentre, Faculty of Health and Medical Sciences, Biotech Research & Innovation Centre (BRIC), Neuroinflammation Unit, Copenhagen N, Denmark
- Chiba University (JP)
- Keio University (JP)
- Instituto de Salud Carlos III (ES)
- Hampton University (US)
- RIKEN Center for Sustainable Resource Science (JP)
- University of Technology - Iraq (IQ)
- Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán (MX)
- University of Warwick (GB)
- Université Paris-Saclay, INSERM ,UMR-S 1193, Châtenay-Malabry, France
- Delft University of Technology (NL)
- University of Innsbruck, Institute for Biomedical Aging Research, Department of Molecular Biology, Innsbruck, Austria
- University Hospital Regensburg (DE)
- Mossakowski Medical Research Institute, Polish Academy of Sciences (PL)
- Taipei Medical University (TW)
- Université de Sherbrooke (CA)
- UMR7242, CNRS, Université de Strasbourg, Strasbourg, France
- Institute of Experimental Medicine CAS, Department of Neuroregeneration, Prague, Czech Republic
- Aarhus University Hospital (DK)
- Jiangsu Province Hospital (CN)
- Shanghai University of Traditional Chinese Medicine (CN)
- Purdue University West Lafayette (US)
- Nanjing First Hospital (CN)
- King's College London, Institute of Psychiatry, Psychology & Neuroscience, Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London, UK
- First Affiliated Hospital of Xi'an Jiaotong University (CN)
- Chungnam National University (KR)
- University of Rochester Medicine (US)
- Indian Institute of Science Bangalore (IN)
- Radboud University Medical Center (NL)
- Universidad Castilla La Mancha, Departmento Ciencias Medicas, Albacete, Spain
- Shanghai Medical College of Fudan University (CN)
- University of Suwon (KR)
- Instituto Nacional de Enfermedades Respiratorias (MX)
- Gwangju Institute of Science and Technology (KR)
- Korea Food Research Institute (KR)
- Ewha Womans University (KR)
- Memorial Sloan Kettering Cancer Center (US)
- Universität Ulm (DE)
- University of Tartu (EE)
- Universitätsmedizin Göttingen (DE)
- University of California, San Francisco UCSF Diabetes Center, Department of Cell and Tissue Biology, San Francisco, CA, USA
- Regional Centre for Biotechnology (IN)
- National Research Council (IT)
- European Bioinformatics Institute (GB)
- Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland
- Gifu University (JP)
- Shimane University (JP)
- Chungbuk National University (KR)
- Center of Advanced European Studies and Research (DE)
- Niigata University (JP)
- Florida Atlantic University (US)
- Semmelweis University (HU)
- Hokkaido University (JP)
- Max Planck Institute for Infection Biology (DE)
- Doshisha Women's College of Liberal Arts (JP)
- Commonwealth Scientific and Industrial Research Organisation (AU)
- Chang Gung University (TW)
- Philipps University of Marburg (DE)
- Oregon Health & Science University (US)
- University of Münster (DE)
- University of Illinois Urbana-Champaign (US)
- Queen Mary University of London, Barts Cancer Institute, London, UK
- MRC Laboratory for Molecular Cell Biology (GB)
- Maastricht University Medical Centre (NL)
- University of Sadat City (EG)
- Indiana University – Purdue University Indianapolis (US)
- Barkatullah University (IN)
- Charité – Universitätsmedizin Berlin (DE)
- Daegu Gyeongbuk Institute of Science and Technology (KR)
- Dankook University Dental Hospital (KR)
- Sookmyung Women's University (KR)
- Hospital for Sick Children, Program in Cell Biology Department, Toronto, Canada; University of Toronto, Department of Biochemistry, Toronto, Canada
- Korea Research Institute of Chemical Technology (KR)
- Pennsylvania State University (US)
- Weizmann Institute of Science (IL)
- NYU Langone’s Laura and Isaac Perlmutter Cancer Center (US)
- National Institute of Biomedical Innovation, Health and Nutrition (JP)
- AstraZeneca (United Kingdom) (GB)
- University of Utah (US)
- St. Boniface Hospital (CA)
- Vavilov Institute of General Genetics RAS, Department of Epigenetics, Moscow, Russia
- S&J Kishi Research Corporation, Jupiter, FL, USA
- Nihon Pharmaceutical University (JP)
- St. Marianna University School of Medicine (JP)
- Nagasaki University (JP)
- University of Copenhagen, Department of Neuroscience, Copenhagen, Denmark
- Ludwig-Maximilians-Universität München (DE)
- Universitätsklinikum Erlangen (DE)
- Hong Kong Polytechnic University (HK)
- New York Institute of Technology (US)
- University Hospital Münster (DE)
- University Hospital Frankfurt (DE)
- Division of Brain Disease Research, Korea National Institute of Health, Cheongju-si, Republic of Korea
- Sapporo Higashi Tokushukai Hospital (JP)
- Nationwide Children's Hospital (US)
- Earlham Institute, Norwich, UK
- Koç University (TR)
- Hiroshima University (JP)
- Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Química Biológica Ciencias Exactas y Naturales (IQUIBICEN), Facultad de Ciencias Exactas y Naturales, Departamento de Química Biológica, Laboratorio de Disfunción Celular en Enfermedades Neurodegenerativas y Nanomedicina, Buenos Aires, Argentina
- China National Rice Research Institute (CN)
- Kanazawa Medical University (JP)
- Queen's University Belfast (GB)
- Université Lyon, Université Claude Bernard Lyon 1, CNRS UMR 5310, INSERM U1217, Institut NeuroMyoGène, Lyon, France
- Tokyo University of Science (JP)
- Indian Institute of Integrative Medicine (IN)
- North Carolina Central University (US)
- Shiga University of Medical Science (JP)
- Indian Institute of Technology Guwahati (IN)
- Sabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla, Istanbul, Turkey
- University of California, Irvine School of Medicine, Irvine, CA, USA
- Université de Bourgogne (FR)
- University of Ottawa (CA)
- Huazhong Agricultural University (CN)
- National Yang Ming University (TW)
- Johannes Kepler University of Linz (AT)
- Mayo Clinic (US)
- Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Instituto de Investigación Sanitaria La Paz (IdiPaz), Instituto de Investigaciones Biomédicas Alberto Sols UAM-CSIC, Madrid, Spain; Universidad Autónoma de Madrid, School of Medicine, Department of Biochemistry, Madrid, Spain
- Macau University of Science and Technology (MO)
- Macau University of Science and Technology, State Key Laboratory of Quality Research in Chinese Medicine, Taipa, Macau, China
- The Hong Kong Polytechnic University, Faculty of Health and Social Sciences, Department of Health Technology and Informatics, Hunghom, Hong Kong
- University of Nottingham, School of Life Sciences, Nottingham, UK
- Université Paris Saclay, Institut des Neurosciences Paris-Saclay (Neuro-PSI)-CNRS UMR 9197, Orsay France
- Research Institute of the McGill University Health Centre, Meakins-Christie Laboratories and Translational Research in Respiratory Diseases Program, Montréal, Québec, Canada; McGill University, Department of Critical Care and Division of Experimental Medicine, Montréal, Québec, Canada; UQAM, Faculté des Sciences, Département des Sciences de l'activité physique, Montréal, Canada
- National Taipei University of Nursing and Health Science (TW)
- Korea Advanced Institute of Science and Technology (KR)
- Hannam University (KR)
- Guangzhou Medical University Cancer Hospital (CN)
- Universidade Federal do Rio Grande do Sul (BR)
- University of Luxembourg (LU)
- Royal Veterinary College (GB)
- La Jolla Institute for Immunology (US)
- Sun Yat-sen University, Sun Yat-sen Memorial Hospital, Department of Pathology, Guangzhou, Guangdong Province, China
- Children's Hospital of Suzhou University (CN)
- South China Normal University (CN)
- Boston Children's Hospital (US)
- Institute of Plant Protection (CN)
- Nanjing Agricultural University (CN)
- Institute of Cellular and Organismic Biology, Academia Sinica (TW)
- Nathan Kline Institute for Psychiatric Research (US)
- IRCCS San Raffaele Roma (IT)
- E-Da Hospital (TW)
- Mackay Memorial Hospital (TW)
- National Health Research Institutes (TW)
- Chang Gung University of Science and Technology (TW)
- The Ohio State University Wexner Medical Center (US)
- Jiangsu University (CN)
- Brigham and Women's Hospital (US)
- Universidade Federal do Rio de Janeiro (BR)
- Indiana University Indianapolis (US)
- Poznan University of Medical Sciences (PL)
- Institute of Neuroscience of Soochow University, Suzhou, China
- Guangdong Medical College (CN)
- Columbia University Irving Medical Center (US)
- Henan Academy of Agricultural Sciences (CN)
- Shenyang Pharmaceutical University (CN)
- University of Bourgogne Franche-Comté, Team ’Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism (EA7270)/Inserm, Faculty of Sciences Gabriel, Dijon, France
- Universitat Autonoma de Barcelona, Departament of Biochemistry and Institut Neurosciences, Faculty of Medicine, Bellaterra, Barcelona, Spain
- Medical University of Graz, Division of Cardiology, Graz, Austria
- Bellvitge Biomedical Research Institute-IDIBELL, Oncobell Program. L'Hospitalet de Llobregat, Barcelona, Spain
- London School of Hygiene & Tropical Medicine, Department of Infection Biology, London, UK
- University College London, Department of Neuroscience, Physiology and Pharmacology, London, UK
- Universidad Autónoma de Madrid, Departamento de Biología Molecular, Madrid, Spain and Centro de Biología Molecular Severo Ochoa (CSIC-UAM), Madrid, Spain
- University of Macau (MO)
- University of Macau, Institute of Chinese Medical Sciences, State Key Laboratory of Quality Research in Chinese Medicine, Taipa, Macao, China
- University of St Andrews (GB)
- Universidad de La Laguna (ES)
- Kunming Institute of Zoology (CN)
- RWTH Aachen University (DE)
- University Hospital Brno (CZ)
- Shandong Normal University (CN)
- Soochow University, Institute of Neuroscience, Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Suzhou, Jiangsu, China
- Xijing Hospital (CN)
- Albert Einstein College of Medicine, Department of Pathology. Bronx, NY, USA
- Albert Einstein College of Medicine, Institute for Aging Studies, Department of Developmental and Molecular Biology, Bronx, NY, USA
- Tokyo Medical and Dental University (JP)
- Universidad Autónoma de Madrid, Department of Biology, Madrid, Spain
- Central Michigan University (US)
- Università Cattolica del Sacro Cuore (IT)
- Massachusetts General Hospital (US)
- Sapienza University of Rome, Department of Experimental Medicine, Rome, Italy
- University of Vienna (AT)
- KU Leuven, Department of cellular and Molecular Medicine, Laboratory of cellular transport systems, Leuven, Belgium
- Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria (INIA), Department of Biotechnology, Madrid, Spain
- Laboratorio de Genética Bioquímica (LAGENBIO), Centro de Encefalopatías y Enfermedades Transmisibles Emergentes, Instituto Agroalimentario de Aragón-IA2, Instituto de Investigación Sanitaria Aragón-IISA, Universidad de Zaragoza, Zaragoza, Spain; Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Instituto Carlos III, Zaragoza, Spain
- University of Las Palmas de Gran Canaria, Department of Physical Education and Research Institute of Biomedical and Health Sciences (IUIBS), Las Palmas de Gran Canaria, Spain
- Instituto de Investigaciones Biomédicas “Alberto Sols”, CSIC-UAM, Madrid, Spain
- University of Antwerp (BE)
- University of Cambridge (GB)
- Centro de Investigaciones Biológicas Margarita Salas, CSIC, Madrid, Spain
- National Institute of Environmental Health Sciences (US)
- Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco, AC, Unidad de Biotecnología Médica y Farmacéutica, Guadalajara, Jalisco, México
- Vall d'Hebron research Institute-UAB/Neurodegenerative Diseases Group, Barcelona, Spain
- Centro de Inovação em Biomedicina e Biotecnologia (PT)
- Institut Jean-Pierre Bourgin, INRAE, AgroParisTech, Université Paris-Saclay, 78000 Versailles, France
- MRC Laboratory of Molecular Biology (GB)
- Ikerbasque (ES)
- Mexican Social Security Institute (MX)
- PSL Research University, Equipe labelisée par la Ligue Contre le Cancer, Institut Curie, Inserm, U830, Stress and Cancer laboratory, Paris, France
- University of Szeged, Department of Medical Microbiology and Immunobiology, Szeged, Hungary
- Central Arkansas Veterans Healthcare System (US)
- Queens College, CUNY (US)
- Northwestern University Feinberg School of Medicine, Department of Neurology, Chicago, IL, USA
- University of Science and Technology of China (CN)
- Laboratory of Cell Biology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil
- Heidelberg University (DE)
- Tianjin Medical University (CN)
- INSERM Institute of Metabolic and Cardiovascular Diseases (I2MC), Université de Toulouse, Toulouse, France
- Shandong University, School of Life Science, Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, Qingdao, China
- Hirosaki University (JP)
- European Neuroscience Institute (ENI) - A Joint Initiative of the University Medical Center Göttingen and the Max Planck Society, Göttingen, Germany
- Kashan University of Medical Sciences (IR)
- Indian Institute of Technology Jodhpur (IN)
- Department of Neurophysiology, Institute for Biological Research “Siniša Stanković” – National Institute of Republic of Serbia, University of Belgrade, Belgrade, Serbia
- Central Drug Research Institute (IN)
- Université Toulouse III - Paul Sabatier (FR)
- Université Toulouse III, Toulouse, France
- Sapporo Medical University (JP)
- Health Sciences University of Hokkaido (JP)
- Tokyo Medical University (JP)
- Ehime University (JP)
- University of Kaiserslautern (DE)
- Centro di Riferimento Oncologico (IT)
- University of Exeter (GB)
- Universidad de Las Palmas de Gran Canaria (ES)
- Ifremer (FR)
- Ifremer, SG2M-LGPMM, Laboratoire de Génétique et Pathologie des Mollusques Marins, La Tremblade, France
- Pharmaceutical Research and Technology Institute, Kindai University (JP)
- Pontificia Universidad Católica de Chile (CL)
- London School of Hygiene & Tropical Medicine (GB)
- Universidade Federal do Ceará (BR)
- Federal University of Ceara, Drug Research and Development Center, Fortaleza, CE, Brazil
- Texas Tech University, Department of Nutritional Sciences & Obesity Research Institute, Lubbock, TX, USA
- Indian Council of Medical Research (IN)
- Morgan Adams Foundation (US)
- University of Colorado Denver, Children's Hospital Colorado, Morgan Adams Foundation Pediatric Brain Tumor Research Program, Aurora, CO
- Departmento de Biología Celular e Histología, Facultad de Biología, Universidad de Murcia, Instituto Murciano de Investigación Biosanitaria (IMIB)-Arrixaca, Murcia, Spain
- Institució Catalana de Recerca i Estudis Avançats (ES)
- ICREA, Pompeu Fabra University (UPF), Department of Experimental and Health Sciences, Ciberned, Barcelona, Spain; Spanish National Cardiovascular Research Center (CNIC), Madrid, Spain
- National Hospital for Paraplagics (Sescam) Research Unit, Molecular Neuroprotection Group, Toledo, Spain
- Royal College of Surgeons in Ireland (IE)
- Baqiyatallah University of Medical Sciences (IR)
- Kyoto University (JP)
- University of South Florida (US)
- Brain Research Institute, Niigata University (JP)
- Nelson Mandela University, Department of Biochemistry and Microbiology, Port Elizabeth, South Africa
- Georgia State University (US)
- Trinity College Dublin, Department of Clinical Medicine, Trinity Centre for Health Sciences, Dublin, Ireland
- National Hospital for Paraplegics (SESCAM), Research Unit, Molecular Neuroprotection Group, Toledo, Spain
- East Tennessee State University (US)
- University of Kansas (US)
- Faculdade de Medicina e Ciências Biomédicas, Universidade do Algarve, Faro, Portugal; ABC-RI, Algarve Biomedical Center Research Institute, Faro, Portugal; Centre for Biomedical Research, Faro, Portugal
- Universidad Miguel Hernández (UMH), Instituto de Investigación, Desarrollo e Innovación en Biotecnología Sanitaria de Elche (IDiBE), Elche, Spain
- Doshisha University (JP)
- Université de Paris, Centre de recherche sur l'inflammation, Team Gut Inflammation, Inserm, U1149, CNRS, ERL8252, Paris, France
- University of Iceland (IS)
- Hollings Cancer Center, Department of Biochemistry and Molecular Biology, Charleston, SC, USA
- Chosun University (KR)
- Yamaguchi University (JP)
- Hyogo Medical University (JP)
- University of Perugia (IT)
- Amgen (United States) (US)
- Hacettepe University (TR)
- The Norwegian Radium Hospital, Institute for Cancer Research, Department of Molecular Cell Biology, Montebello, Oslo, Norway; University of Oslo, Faculty of Mathematics and Natural Sciences, The Department of Biosciences, Oslo, Norway
- Children's Hospital of Philadelphia (US)
- Suez Canal University (EG)
- Oslo University Hospital and University of Oslo, Department of Pathology, Tumor Immunology Lab, Oslo, Norway
- Istanbul University-Cerrahpasa, Cerrahpasa Faculty of Medicine, Medical Biology Department, Istanbul, Turkey
- Texas Biomedical Research Institute (US)
- Beth Israel Deaconess Medical Center (US)
- Chonnam National University (KR)
- Sanofi (France) (FR)
- University of Potsdam (DE)
- Universidad Nacional Autónoma de México, Instituto de Biotecnología, Departamento de Medicina Molecular y Bioprocesos, Laboratorio de Neuroinmunobiología, Cuernavaca, Morelos, México
- Friedrich-Loeffler-Institut (DE)
- Weizmann Institute of Science, Department of Plant and Environmental Sciences, Rehovot, Israel
- Istituto Nazionale Tumori IRCCS "Fondazione G. Pascale" (IT)
- Universidade Estadual Paulista (Unesp) (BR)
- São Paulo State University, College of Agronomy Sciences, Department of Bioprocesses and Biotechnology, Center for Evaluation of Environmental Impact on Human Health (TOXICAM), Botucatu, SP, Brazil
- Universidad de Granada (ES)
- SUNY Upstate Medical University (US)
- State University of New York, Upstate Medical University, Departments of Medicine, Microbiology and Immunology, Biochemistry and Molecular Biology, Syracuse, NY, USA
- Xavier University (US)
- Université Côte d'Azur, Université Nice Sophia Antipolis, CEA/DRF/Institut Frédéric Joliot, Faculté de Médecine, UMR E-4320 TIRO-MATOs, Nice, France
- Medical University of Lodz, Department of Laboratory Diagnostics, Lodz, Poland
- Consejo Superior de Investigaciones Científicas (CSIC), Instituto de Biología Molecular y Celular del Cáncer (IBMCC), Centro de Investigación del Cáncer (CSIC-Universidad de Salamanca), Universidad de Salamanca, Campus Unamuno, Salamanca. Spain
- Tel Aviv University, School of Neurobiology, Biochemistry and Biophysics, Tel Aviv, Israel
- Achucarro Basque Center for Neuroscience, Department of Pharmacology, University of the Basque Country EHU/UPV, Leioa, Bizkaia, Spain
- UCL Queen Square Institute of Neurology, London, UK
- Monash University (AU)
- Mahidol University (TH)
- Georg-August-Universität Göttingen, Institute for Microbiology and Genetics, Department of Molecular Microbiology and Genetics, Göttingen, Germany
- Erasmus University Medical Center, Department of Epidemiology; Division of Pharmacology, Department of Internal Medicine, Rotterdam, The Netherlands
- Jagiellonian University (PL)
- Eberhard Karls University Tübingen, Interfaculty Institute of Cell Biology, Tübingen, Germany
- University of Cyprus (CY)
- China Pharmaceutical University (CN)
- Dartmouth College (US)
- Tehran University of Medical Sciences (IR)
- State University of New York, University at Buffalo, Jacobs School of Medicine and Biomedical Sciences, Departments of Ophthalmology/Biochemistry and Neuroscience Program, Buffalo, NY, USA
- Southern University of Science and Technology (CN)
- Department of Biotechnology (IN)
- Johannes Gutenberg University-Mainz, Institute of Developmental Biology and Neurobiology, Mainz, Germany
- Hospital Nacional de Parapléjicos (ES)
- Wright State University (US)
- University of Wyoming (US)
- Qingdao Agricultural University (CN)
- Botucatu Medical School, São Paulo State University, Botucatu, SP, Brazil
- Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France
- INSERM U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Nice, France; Université de Nice Sophia Antipolis, UFR de Médecine, Nice, France
- Universidade Estadual de Campinas (UNICAMP) (BR)
- University of Campinas (UNICAMP), School of Applied Science, Department of Sport Sciences, Limeira, Brazil
- Clínica Universidad de Navarra, Metabolic Research Laboratory, CIBEROBN, IdiSNA, Pamplona, Spain
- University of Barcelona, School of Medicine, Unit of Anatomy, Department of Pathology and Experimental Therapeutics, Barcelona, Spain; L'Hospitalet de Llobregat, Institut d'Investigació Biomèdica de Bellvitge -IDIBELL, Molecular Mechanisms and Experimental Therapy in Oncology Program (oncobell), Barcelona, Spain
- Kansas City University (US)
- Consejo Superior de Investigaciones Científicas, Instituto de Bioquímica Vegetal y Fotosíntesis (CSIC-IBVF), Sevilla, Spain
- Georgetown University (US)
- Vita-Salute San Raffaele University & IRCCS San Raffaele Scientific Institute, Division of Immunology, Transplantation and Infectious Diseases, Milano, Italy
- Centre International de Recherche en Infectiologie (CIRI), University Lyon, Inserm, U1111, Université Claude Bernard Lyon 1, CNRS, UMR5308, ENS Lyon, Lyon, France
- Technische Hochschule Mannheim (DE)
- Australian Regenerative Medicine Institute (AU)
- Stazione Zoologica Anton Dohrn (IT)
- Institute of Food Science (IT)
- Russian Cancer Research Center NN Blokhin (RU)
- University of Seoul (KR)
- University of Pittsburgh Medical Center (US)
- Forschungszentrum Jülich (DE)
- Rutgers New Jersey Medical School (US)
- Oregon State University (US)
- Boston Children's Hospital and Harvard Medical School, Boston, MA, USA
- Institute for Research in Biomedicine (ES)
- Florida State University (US)
- Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), Research Group in Critical Disorders (GREPAC), Barcelona, Spain
- University of Minho, School of Medicine, Life and Health Sciences Research Institute (ICVS), Braga, Portugal; ICVS/3B's - PT Government Associate Laboratory, Braga/Guimarães, Portugal
- CABD/CSIC/Universidad Pablo de Olavide, Departamento de Fisiología, Anatomía y Biología Celular, Sevilla, Spain
- University of Malaga, Department of Molecular Biology and Biochemistry, Malaga, Spain
- Imperial College London, Section of Paediatric Infectious Disease & Virology, London, UK
- Jawaharlal Nehru University (IN)
- Institute for Stem Cell Biology and Regenerative Medicine (IN)
- University of Delhi (IN)
- University of Notre Dame (US)
- University of Calgary, Department of Comparative Biology & Experimental Medicine, Calgary, AB, Canada
- Amsterdam University Medical Centers (NL)
- Centro di Riferimento Oncologico, CRO-IRCCS, Molecular Oncology Unit, Aviano, Italy
- University of Campania L. Vanvitelli, Dipartimento di Scienze Mediche Traslazionali, Naples, Italy
- Helmholtz Centre for Infection Research (DE)
- Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology, Barcelona, Spain; Departament de Bioquímica i Biomedicina Molecular, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain
- Dokuz Eylül University (TR)
- Dokuz Eylul University, Izmir International Biomedicine and Genome Institute, Izmir, Turkey
- Shenzhen University Health Science Center (CN)
- Defence Research and Development Organisation (IN)
- Van Andel Institute (US)
- Fudan University (CN)
- Juntendo University Graduate School of Medicine, Department of Treatment and Research in Multiple Sclerosis and Neuro-intractable Disease, Bunkyo-ku, Tokyo, Japan
- Agharkar Research Institute (IN)
- National Sun Yat-sen University (TW)
- Achucarro Basque Center for Neuroscience, Department of Neurosciences, University of the Basque Country EHU/UPV, Leioa, Bizkaia, Spain
- Cancer Research Center of Toulouse, UMR 1037 Inserm-university of Toulouse, Toulouse, France
- Sanjay Gandhi Post Graduate Institute of Medical Sciences (IN)
- Institute of Biochemistry and Biophysics, Polish Academy of Sciences (PL)
- Masaryk University (CZ)
- Washington State University, Institute of Biological Chemistry, Pullman, WA, USA
- Dong-A University (KR)
- University of Malaya (MY)
- University of Geneva (CH)
- Shandong University (CN)
- Guangzhou University of Chinese Medicine (CN)
- Department of Clinical Psychopharmacology and Neurotoxicology, National Institute of Mental Health and Neurosciences, Bengaluru-560029, Karnataka, India
- University of Kentucky, Department of Toxicology and Cancer Biology, Lexington, KY, USA
- Institute of Molecular Biology and Pathology (IT)
- Western University (CA)
- Jožef Stefan Institute (SI)
- Fondazione Santa Lucia (IT)
- Instituto Oswaldo Cruz (BR)
- Hangzhou Normal University (CN)
- Second Affiliated Hospital of Zhejiang University (CN)
- University of Tennessee Health Science Center (US)
- University of Pennsylvania, Perelman School of Medicine, Department of Medicine, Philadelphia, PA, USA
- University of Missouri, Division of Animal Science and Department of Obstetrics, Gynecology & Women's Health, Columbia, MO, USA
- York University (CA)
- Hong Kong Baptist University (HK)
- Ohio University (US)
- University of Rzeszow, Institute of Biology and Biotechnology, Department of Biotechnology, Rzeszow, Poland
- Chengdu Medical College (CN)
- Oslo University Hospital, Institute for Cancer Research, Department of Molecular Cell Biology, Oslo, Norway
- RIKEN Center for Brain Science (JP)
- Hubei University of Technology (CN)
- Association of Rheumatologists of Russia (RU)
- University of Porto, Faculty of Pharmacy, UCIBIO, REQUIMTE, Porto, Portugal
- Chulalongkorn University (TH)
- Carl von Ossietzky Universität Oldenburg (DE)
- Institute of Genomics and Integrative Biology (IN)
- South China Agricultural University (CN)
- University of Defense, Faculty of Military Health Sciences, Department of Radiobiology, Hradec Kralove, Czech Republic
- Wayne State University (US)
- Universidad de Oviedo (ES)
- University of Oviedo, Department of Functional Biology, Physiology, Oviedo, Asturias, Spain
- University of Belgrade, Faculty of Medicine, Institute of Microbiology and Immunology, Belgrade, Serbia
- University of Southampton (GB)
- Imperial College London, Department of Life Sciences, London, UK
- Université de Moncton (CA)
- Jožef Stefan Institute, Department of Biochemistry and Molecular and Structural Biology, Ljubljana, Slovenia
- Komarov Botanical Institute of the Russian Academy of Sciences (RU)
- Nottingham Trent University, School of Science and Technology, Nottingham, UK
- John Radcliffe Hospital (GB)
- Sechenov University (RU)
- Mie University (JP)
- Osnabrück University (DE)
- University of Liverpool, Institute of Translational Research, Cellular and Molecular Physiology, Liverpool, UK
- University of Tübingen, Center for Plant Molecular Biology (ZMBP), Tübingen, Germany
- University of Buenos Aires, Institute of Biochemistry and Molecular Medicine, Pathophysiology Department, School of Pharmacy and Biochemistry, CONICET, Buenos Aires, Argentina
- Columbia University, Vagelos College of Physicians and Surgeons, Department of Pathology and Cell Biology, New York, NY, USA
- Instituto de Investigaciones Biomedicas Alberto Sols (CSIC-UAM), Madrid, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERdem), Instituto de Salud Carlos III, Madrid, Spain
- KU Leuven, Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, Leuven, Belgium
- Vanderbilt University (US)
- Vanderbilt University School of Medicine, Department of Pathology, Microbiology and Immunology, Nashville, TN, USA
- Instituto de Investigaciones Biomedicas “Alberto Sols” (CSIC-UAM) and CIBERER (CIBER, ISCiii), Madrid, Spain
- Universitätsklinikum Essen, Institute for Cell Biology (Cancer Research), Essen, Germany
- Academy of Athens (GR)
- VIB-KU Leuven Center for Brain & Disease Research (BE)
- Service of Endocrinology, University Hospital Doctor Peset, Foundation for the Promotion of Health and Biomedical Research in the Valencian Region (FISABIO)-Department of Physiology, University of Valencia, Valencia, Spain
- Universidade NOVA de Lisboa, CEDOC, NOVA Medical School, Faculdade de Ciências Médicas, Lisboa, Portugal
- European Institute of Oncology (IEO) IRCCS, Department of Experimental Oncology, Milan, Italy; University of Milano, Department of Oncology and Hemato-Oncology, Milan, Italy
- Hospital Universitario La Paz (ES)
- University of Toulouse, Institute of Metabolic and cardiovascular Diseases, INSERM UMR 1048, Toulouse, France
- Università Cattolica del Sacro Cuore, Department of Life Science and Public Health Section of Histology and Embryology, Rome, Italy
- University of Zagreb School of Medicine, Department of Physiology and Croatian Institute for Brain Research, Zagreb, Croatia
- Simon Fraser University (CA)
- Eurac Research (IT)
- University of Oxford, Oxford Parkinson's Disease Centre, Department of Physiology, Anatomy and Genetics, Oxford, UK
- Fukushima Medical University (JP)
- Shanxi Agricultural University (CN)
- Shanxi Agricultural University, Shanxi Key Laboratory of Ecological Animal Science and Environmental Veterinary Medicine, Taigu, Shanxi, China
- Feinstein Institute for Medical Research (US)
- Zhujiang Hospital of Southern Medical University, Department of Neurology, Guangzhou, Guangdong Province, China
- Cleveland Clinic, Department of Cardiovascular Medicine/Heart and Vascular Institute, Cleveland, OH, USA
- University of South Dakota (US)
- Fujian Medical University (CN)
- Cincinnati Children's Hospital Medical Center (US)
- University of Gdansk, Department of Molecular Biology, Gdansk, Poland
- University of Denver (US)
- Amsterdam UMC Location University of Amsterdam (NL)
- Norwich Research Park (GB)
- Queensland University of Technology (AU)
- Institut Pasteur (FR)
- Kanazawa University (JP)
- Southwest Medical University, Luzhou Key Laboratory of Activity Screening and Druggability Evaluation for Chinese Materia Medica, Jiangyang District, Luzhou, China
- University of Maryland School of Medicine, Center for Shock, Trauma and Anesthesiology Research (STAR), Departments of Anesthesiology, Anatomy & Neurobiology, Baltimore, MD, USA
- University of North Dakota (US)
- Wenzhou Medical University, State Key Laboratory of Ophthalmology, Optometry and Visual Science, School of Optometry and Ophthalmology and the Eye Hospital, Wenzhou, China
- Soochow University, Department of Pathogenic Biology, Suzhou, Jiangsu Province, China
- The Chinese University of Hong Kong, Department of Anaesthesia and Intensive Care, Hong Kong, China
- Broad Institute (US)
- Shenzhen University (CN)
- University of Electronic Science and Technology of China (CN)
- University of Electronic Science and Technology of China, School of Medicine, Chengdu, China; Sichuan Academy of Medical Sciences & Sichuan Provincial People’s Hospital, Department of Pharmacy, Chengdu, Sichuan, China
- Southwest Hospital, Third Military Medical University (Army Medical University), Key Laboratory of Hepatobiliary and Pancreatic Surgery, Institute of Hepatobiliary Surgery, Chongqing, China
- Shanghai Jiao Tong University, School of Life Sciences and Biotechnology, Shanghai, China
- Shanghai Sixth People's Hospital, Department of Cardiovascular Medicine, and Shanghai Jiaotong University School of Medicine, Shanghai Institute of Immunology, Shanghai, China
- Purdue University, Department of Botany and Plant Pathology, West Lafayette, IN, USA
- Kyoto Institute of Technology (JP)
- Asahikawa Medical University (JP)
- University of Kentucky, Department of Cancer Biology & Toxicology, Lexington, KY, USA
- The Fourth Military Medical University, Xijing Hospital, Department of Orthopaedics, Xi'an, China
- Shandong Tumor Hospital (CN)
- Tang Du Hospital (CN)
- Duke-NUS Medical School (SG)
- Queen Mary Hospital (CN)
- ETH Zurich (CH)
- Tabriz University of Medical Sciences (IR)
- Tianjin University of Traditional Chinese Medicine (CN)
- Tsinghua University, School of Life Sciences, Tsinghua University-Peking University Joint Center for Life Sciences, State Key Laboratory of Membrane Biology, Beijing, China
- Centre for Addiction and Mental Health (CA)
- City University of Hong Kong (HK)
- University of Brescia (IT)
- Cancer Research UK Scotland Institute (GB)
- University of Monastir (TN)
- Soochow University, Department of Pharmacology and Laboratory of Cerebrovascular Pharmacology, College of Pharmaceutical Science, Suzhou, Jiangsu, China
- Chinese Academy of Medical Sciences & Peking Union Medical College, Institute of Medicinal Biotechnology, Beijing, China
- University of Maryland, Molecular Virology Laboratory, VA-MD College of Veterinary Medicine, College Park, MD, USA
- Nanjing Medical University, Nanjing First Hospital, Department of Neurology, Nanjing, China
- Sichuan University, West China School of Basic Medical Sciences & Forensic Medicine, Chengdu, China
- Central China Normal University (CN)
- Beijing Academy of Agriculture and Forestry Sciences (CN)
- Nanjing University of Chinese Medicine (CN)
- Guangxi Medical University (CN)
- Peking University First Hospital, Renal Division, Xi Cheng District, Beijing, China
- Zhengzhou University (CN)
- University California, San Diego, Division of Biological Sciences, Section of Molecular Biology, CA, USA
- Institute for Research in Biomedicine (IRB Barcelona), Barcelona, Spain; Universitat de Barcelona, Departament de Bioquímica I Biomedicina Molecular, Barcelona, Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain
- Chongqing Medical University (CN)
- Inserm U1138, Centre de Recherche des Cordeliers, Sorbonne Université, Université de Paris, Paris, France
- Lovelace Respiratory Research Institute (US)
- ORCID
- Klionsky, Daniel J.
- Abdelfatah, Sara
- Abdellatif, Mahmoud
- Abdoli, Asghar
- Abel, Steffen
- Abeliovich, Hagai
- Abildgaard, Marie H.
- Abudu, Yakubu Princely
- Adamopoulos, Iannis E.
- Adeli, Khosrow
- Adolph, Timon E.
- Adornetto, Annagrazia
- Agam, Galila
- Agarwal, Anupam
- Aggarwal, Bharat B.
- Agostinis, Patrizia
- Agrewala, Javed N.
- Agrotis, Alexander
- Ahmed, Zubair M.
- Ahumada-Castro, Ulises
- Aits, Sonja
- Akpinar, Hafize Aysin
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- Imagawa, Yusuke
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- Iovanna, Juan
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- Jin, Hongchuan
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- Jun, Youngsoo
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- Jung, Sung-Chul
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- Jungverdorben, Johannes
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- Kaasik, Allen
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- Karmakar, Parimal
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- Stathopulos, Peter B.
- Stefan, Sven Marcel
- Stefanis, Leonidas
- Steffan, Joan S.
- Steinkasserer, Alexander
- Stenmark, Harald
- Sterneckert, Jared
- Stoka, Veronika
- Storch, Stephan
- Stork, Björn
- Strappazzon, Flavie
- Strohecker, Anne Marie
- Su, Huanxing
- Su, Ling-Yan
- Su, Longxiang
- Suarez-Fontes, Ana M.
- Subauste, Carlos S.
- Subbian, Selvakumar
- Sue, Carolyn M.
- Sui, Xinbing
- Sun, Guangchao
- Sun, Jun
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- Sunahara, Karen K.S.
- Sundberg, Eva
- Suzuki, Hidekazu
- Sweeney, Gary
- Symons, J. David
- Sze, Stephen Cho Wing
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- Taylor, Gregory A.
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- Tegeder, Irmgard
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- Thirumalaikumar, V.P.
- Thomas, Sufi Mary
- Thomes, Paul G.
- Thorburn, Andrew
- Thukral, Lipi
- Thum, Thomas
- Thumm, Michael
- Till, Andreas
- Timmerman, Vincent
- Titorenko, Vladimir I.
- Todi, Sokol V.
- Todorova, Krassimira
- Toivonen, Janne M.
- Tomaipitinca, Luana
- Tomar, Dhanendra
- Tomić, Sergej
- Tong, Benjamin Chun-Kit
- Tong, Xin
- Tooze, Sharon A.
- Torgersen, Maria L.
- Torii, Satoru
- Torres-López, Liliana
- Torriglia, Alicia
- Towers, Christina G.
- Toyokuni, Shinya
- Tramontano, Donatella
- Tran, Quynh-Giao
- Travassos, Leonardo H.
- Trelford, Charles B.
- Tremel, Shirley
- Triola, Gemma
- Tsao, Betty P.
- Tschan, Mario P.
- Tse, Hung-Fat
- Tsugawa, Hitoshi
- Tsvetkov, Andrey S.
- Tumbarello, David A.
- Tuñón, María J.
- Turcotte, Sandra
- Turk, Boris
- Turner, Bradley J.
- Tuxworth, Richard I.
- Tyutereva, Elena V.
- Uchiyama, Yasuo
- Uhlig, Holm H.
- Ulasov, Ilya V.
- Ungermann, Christian
- Unno, Rei
- Uribe-Carretero, Elisabet
- Uversky, Vladimir N
- Vaccari, Thomas
- Vahsen, Björn F.
- Vakifahmetoglu-Norberg, Helin
- Valdor, Rut
- Valente, Maria J.
- Valko, Ayelén
- van der Veen, Stijn
- van Loosdregt, Jorg
- van Wijk, Sjoerd J.L.
- Vandenberghe, Wim
- Vanhorebeek, Ilse
- Vannier-Santos, Marcos A.
- Vannini, Nicola
- Vanrell, M. Cristina
- Vantaggiato, Chiara
- Varano, Gabriele
- Varga, Máté
- Vasconcelos, M. Helena
- Vats, Somya
- Vavvas, Demetrios G.
- Velasco, Guillermo
- Vellai, Tibor
- Vellenga, Edo
- Velotti, Francesca
- Verdier, Mireille
- Verginis, Panayotis
- Vergne, Isabelle
- Verkade, Paul
- Verma, Manish
- Verstreken, Patrik
- Vervliet, Tim
- Vervoorts, Jörg
- Vessoni, Alexandre T.
- Vidal, Michel
- Vidoni, Chiara
- Vierstra, Richard D.
- Vihinen, Helena
- Vila, Miquel
- Vilar, Marçal
- Villalobo, Antonio
- Villarroya, Francesc
- Villarroya, Joan
- Vincent, Olivier
- Viret, Christophe
- Vitale, Ilio
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- Volonté, Cinzia
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- Vomero, Marta
- Vooijs, Marc A.
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- Waguri, Satoshi
- Wakatsuki, Shuji
- Walker, David W.
- Walker, Mark J.
- Walker, Simon A.
- Walter, Jochen
- Wandosell, Francisco G.
- Wang, Bo
- Wang, Chen
- Wang, Chenwei
- Wang, Fangyang
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- Wang, Hao
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- Wang, Hong-Gang
- Wang, Jigang
- Wang, Jiou
- Wang, Kui
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- Wang, Liming
- Wang, Maggie Haitian
- Wang, Meiqing
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- Wang, Peipei
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- Wang, Qiong A.
- Wang, Wuyang
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- Warnes, Gary
- Warnsmann, Verena
- Watada, Hirotaka
- Watchon, Maxinne
- Wawrzyńska, Anna
- Wehman, Ann M.
- Wei, Huafeng
- Wei, Lei
- Wei, Taotao
- Weiergräber, Oliver H.
- Weindl, Günther
- Weiskirchen, Ralf
- Wells, Alan
- Wen, Runxia H.
- Wen, Xin
- Weykopf, Beatrice
- Wheatley, Sally P.
- Whitton, J. Lindsay
- Whitworth, Alexander J.
- Wiktorska, Katarzyna
- Wildenberg, Manon E.
- Wilkinson, Simon
- Willbold, Dieter
- Williams, Brett
- Williams, Robin S.B.
- Williamson, Peter R.
- Wilson, Richard A.
- Winner, Beate
- Winsor, Nathaniel J.
- Witkin, Steven S.
- Wodrich, Harald
- Woehlbier, Ute
- Wollert, Thomas
- Wong, Esther
- Wong, Vincent Kam Wai
- Wu, Chengbiao
- Wu, Jian
- Wu, Min
- Wu, Shan-Ying
- Wu, Xiaohong
- Wu, Xiaoqing
- Wu, Yao-Wen
- Wu, Yihua
- Xavier, Ramnik J.
- Xia, Hongguang
- Xia, Lixin
- Xia, Zhengyuan
- Xiao, Guozhi
- Xiao, Hengyi
- Xiao, Lan
- Xiao, Shi
- Xiao, Yin
- Xie, Min
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- Xu, Wen Wen
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- Yakhine-Diop, Sokhna M.S.
- Yamaguchi, Masamitsu
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- Yang, Ying
- Yao, Honghong
- Yao, Shenggen
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- Yao, Yong-Gang
- Yasui, Takahiro
- Yen, Paul M.
- Yi, Cong
- Yin, Xiao-Ming
- Yin, Yanhai
- Yin, Zhangyuan
- Yin, Ziyi
- Yip, Calvin K.
- Yiu, Stephanie Pei Tung
- Yoshida, Kiyotsugu
- Yoshii, Saori R.
- Yousefi, Bahman
- Yu, Boxuan
- Yu, Haiyang
- Yu, Ming-Lung
- Yu, Victor C.
- Yu, W. Haung
- Yu, Zhou
- Yuan, Junying
- Yuan, Ling-Qing
- Yuan, Shilin
- Yuan, Shyng-Shiou F.
- Yuan, Yanggang
- Yuan, Zengqiang
- Yue, Jianbo
- Yue, Zhenyu
- Yun, Jeanho
- Yung, Raymond L.
- Zaffagnini, Gabriele
- Zambelli, Vanessa O.
- Zanella, Isabella
- Zang, Qun S.
- Zanivan, Sara
- Zappavigna, Silvia
- Zaragoza, Pilar
- Zarbalis, Konstantinos S.
- Zarebkohan, Amir
- Zarrouk, Amira
- Zeng, Jialiu
- Žerovnik, Eva
- Zhan, Lixuan
- Zhang, Bin
- Zhang, Donna D.
- Zhang, Hanlin
- Zhang, Honghe
- Zhang, Huafeng
- Zhang, Hui
- Zhang, Jianbin
- Zhang, Jianhua
- Zhang, Kalin Y.B.
- Zhang, Leshuai W.
- Zhang, Lin
- Zhang, Lu
- Zhang, Luoying
- Zhang, Peng
- Zhang, Sheng
- Zhang, Wei
- Zhang, Xiaolei
- Zhang, Xiaoyan
- Zhang, Xin
- Zhang, Xinxin
- Zhang, Xu Dong
- Zhang, Yi
- Zhang, Yingmei
- Zhang, Yuchen
- Zhang, Zhe
- Zhang, Zhengguang
- Zhang, Zhibing
- Zhang, Zhihai
- Zhang, Zhiyong
- Zhang, Zili
- Zhao, Lei
- Zhao, Shuang
- Zhao, Tongbiao
- Zhao, Yongchao
- Zhao, Yongliang
- Zhao, Yuting
- Zheng, Guoping
- Zheng, Ling
- Zheng, Shizhong
- Zheng, Xi-Long
- Zheng, Yi
- Zheng, Zu-Guo
- Zhivotovsky, Boris
- Zhong, Qing
- Zhou, Ben
- Zhou, Cefan
- Zhou, Gang
- Zhou, Hao
- Zhou, Hong
- Zhou, Hongbo
- Zhou, Jie
- Zhou, Jiyong
- Zhou, Kailiang
- Zhou, Rongjia
- Zhou, Yinghong
- Zhou, Yubin
- Zhou, Zhou
- Zhu, Binglin
- Zhu, Changlian
- Zhu, Guo-Qing
- Zhu, Haining
- Zhu, Hua
- Zhu, Wei-Guo
- Zhu, Yanping
- Zhu, Yushan
- Zhuang, Haixia
- Zhuang, Xiaohong
- Ziviani, Elena
- Zorov, Dmitry B.
- Zou, Zhen
- Zuryn, Steven
- Zwerschke, Werner
- Dong, X. Charlie
- Lin, Yong
- Oshima, Shigeru
- Rong, Yueguang
- Sluimer, Judith C.
- Stallings, Christina L.
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2021-01-02
- Volume
- 17
- Issue
- 1
- Pages
- 1-382
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- PMC
- PMC7996087
- OpenAlex
- W3108936441
- Cited by
- 2,897
- References
- 4,083
- Citations by year
- 2026: 528 · 2025: 458 · 2024: 518 · 2023: 485 · 2022: 567 · 2021: 338
- FWCI
- 179.11
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed Central (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, other-oa)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- Research Publications (Maastricht University) (publishedVersion, cc-by-nc-sa)
- Discovery Research Portal (University of Dundee) (publishedVersion)
- idUS (Universidad de Sevilla) (publishedVersion, cc-by-nc-nd)
- Pure Amsterdam UMC (publishedVersion, cc-by)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion, other-oa)
- IRTA (Institut de Recerca i Tecnologia Agroalimentaries) (publishedVersion, cc-by)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion)
- Middlesex University Research Repository (Middlesex University Of London) (acceptedVersion)
- White Rose Research Online (University of Leeds, The University of Sheffield, University of York) (acceptedVersion)
- Nottingham Trent University's Institutional Repository (Nottingham Trent Repository) (acceptedVersion)
- Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
- Warwick Research Archive Portal (University of Warwick) (acceptedVersion)
- Zurich Open Repository and Archive (University of Zurich) (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (acceptedVersion)
- Research Information System of Ardabil University of Medical Sciences (Ardabil University of Medical Sciences) (acceptedVersion)
- Open Research Online - ORO (The Open University) (acceptedVersion)
- Repositori ObertUDL (University of Lleida) (acceptedVersion)
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- OpenAgrar (submittedVersion)
- Apollo (University of Cambridge) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, cc-by-nc-sa)
- Padua Research Archive (University of Padova) (submittedVersion)
- Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Utrecht University Repository (Utrecht University) (submittedVersion)
- Digital Repository at the University of Maryland (University of Maryland College Park) (public-domain)
- Apollo
- Open Access CRIS of the University of Bern
- Zurich Open Repository and Archive (University of Zurich)
- Funders
- National Institute of General Medical Sciences (GM131919)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- assay interpretation, autophagy monitoring
- MeSH terms
- Autophagosomes, Autophagy-Related Proteins, Animals, Autophagy, Biological Assay, Humans, Lysosomes, Biomarkers
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-11-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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