The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index; 6 of the 37 sources its claims cite were checked for support.
Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis
Open accessAbstract
Clathrin-mediated endocytosis of surface receptors and their bound ligands (i.e., cargo) is highly regulated, including by the cargo itself. One of the possible sources of the observed heterogeneous dynamics of clathrin-coated pits (CCPs) might be the different cargo content. Consistent with this, we show that CCP size and dynamic behavior varies with low density lipoprotein receptor (LDLR) expression levels in a manner dependent on the LDLR-specific adaptors, Dab2 and ARH. In Dab2-mCherry–expressing cells, varying LDLR expression leads to a progressive increase in CCP size and to the appearance of nonterminal endocytic events. In LDLR and ARH-mCherry–expressing cells in addition to an increase in CCP size, turnover of abortive CCPs increases, and the rate of CCP maturation decreases. Altogether, our results underscore the highly dynamic and cargo-responsive nature of CCP assembly and suggest that the observed heterogeneity is, in part, related to compositional differences (e.g., cargo and adaptors) between CCPs.
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TL;DR
In BSC1 cells, LDLR cargo and its adaptors Dab2 and ARH regulate clathrin-coated pit (CCP) size and dynamics in cargo- and adaptor-specific ways. Dab2 can drive formation of large, endocytically inactive clathrin lattices, whereas ARH is AP2-dependent, partially rescues saturated CD8/LDLR uptake, and increases cargo packaging without speeding productive CCP maturation.
Key findings
- CCP size varied with CD8/LDLR and adaptor expression: negative-stain EM ventral CCP area was 0.013 ± 0.03 µm² with no CD8/LDLR, 0.45 ± 0.38 µm² at low CD8/LDLR, 3.31 ± 2.49 µm² at high CD8/LDLR with Dab2, and 0.89 ± 0.54 µm² at high CD8/LDLR with ARH (Table I). TfnR overexpression on the dorsal surface gave smaller CCPs than control (0.008 ± 0.003 vs. 0.011 ± 0.004 µm²).
- Dab2 and ARH were differentially recruited: ARH was predominantly nuclear under control conditions, exited the nucleus upon CD8/LDLR expression, and required AP2 binding for CCP recruitment; ARH-F259A failed to bind AP2 and was not recruited to CCPs, while ARH-S117Y;F165A failed to exit the nucleus.
- ARH partially rescued saturated CD8/LDLR endocytosis in an AP2-dependent manner: ARH-252A255 only slightly increased uptake efficiency, ARH-F259A had no effect, and µ2 siRNA knockdown ablated the rescue. TfnR uptake was not rescued by ARH.
- CD8/LDLR overexpression reduced the productive CCP contribution from 50.7 ± 2.0% to 41.3 ± 2.1% and increased productive CCP lifetime from 62.8 ± 3.1 s to 75.5 ± 5.0 s; added ARH did not alter productive lifetime (76.3 ± 5.2 s). Abortive CCP initiation increased from 0.29 ± 0.071 to 0.41 ± 0.093 pits/min/µm² with CD8/LDLR, while productive CCP initiation remained ~0.088–0.089 pits/min/µm².
Methods
- BSC1 cells stably expressing LCa-EGFP or σ2-EGFP were infected with tet-repressible CD8/LDLR adenovirus and transfected or selected for wild-type or mutant Dab2/ARH constructs; assays included TIR-FM, spinning-disk confocal FRAP, negative-stain EM of unroofed ventral membranes, cell fractionation/Western blotting, and anti-CD8 internalization ELISA.
- CCP dynamics were analyzed by automated particle detection and lifetime tracking, with CCP subpopulations classified as early abortive, late abortive, productive, and persistent; intensity profiles were averaged for CCP cohorts by lifetime.
- Statistical comparisons used jackknifed cell-to-cell errors, Kolmogorov-Smirnov tests, and reported P values; CCP trajectory numbers included 100,823 control, 70,955 CD8/LDLR, and 23,394 CD8/LDLR + ARH trajectories.
Limitations
- The paper states that CD8/LDLR clustering could not be followed directly because overexpression strongly decreased the plasma-membrane signal-to-noise ratio, impeding automated tracking of cargo-laden CCPs.
- The paper states that ARH nuclear shuttling and possible nuclear function are beyond the scope of the study, and that additional studies are required to determine mechanisms controlling clathrin polymerization.
- Evident from the text: most experiments use BSC1 cells with exogenous CD8/LDLR chimeras and overexpressed or mutant adaptors, so findings may not directly reflect native LDLR trafficking or other cell types; the checkpoint hypothesis is proposed but not fully tested.
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Claims the paper makes
6 of 37 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured
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
“Together, these data strongly suggest that the observed heterogeneity in the dynamic behavior of CCPs (Merrifield et al., 2005; Rappoport et al., 2005; Yarar et al., 2005) could reflect differences in their content of cargo and adaptor molecules.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion
What the sources say
- Not checked — no full text of the sourcecites Merrifield et al., 2005 source
- Supportedcites Rappoport et al., 2005 source
The citation is attached to the observed heterogeneity in CCP dynamics, rather than to the citing authors’ subsequent explanation for it. The Abstract describes static, appearing, laterally moving, and disappearing clathrin spots; the Results and Discussion also distinguish static from disappearing spots by AP-2 content. No page number is available in our copy. (LLM, conf=0.92)
- Supportedcites Yarar et al., 2005 source
In “F-actin Is Associated with Several Diverse Behaviors of CCSs,” the paper reports heterogeneous behaviors, including splitting, coalescence, and movement at different speeds. “CCS Lateral Motility and Actin Dynamics” further suggests that laterally mobile structures may differ from those undergoing internalization in molecular composition, particularly cargo-adaptor content. These passages support the cited possibility; the citing authors’ broader conclusion is their own framing. (LLM, conf=0.91)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe cited sources support only part of this claim — read each source’s verdict below.
In the paper
“it appears to sort cargo into CCPs independently of AP2 (Garuti et al., 2005; Keyel et al., 2006; Maurer and Cooper, 2006).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Introduction
What the sources say
- Partly supportedcites Garuti et al., 2005 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) says Dab-2 may assist LDLR internalization, supporting a possible role in cargo uptake. But the experiments showing LDLR clustering despite disruption of an AP-2 binding site concern ARH, not Dab2; this copy does not establish that Dab2 acts independently of AP-2. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites Keyel et al., 2006 source
- Not checked — no full text of the sourcecites Maurer and Cooper, 2006 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The incorporation of certain cargo/adaptor protein complexes (i.e., transferrin receptor/AP2) into CCPs increases the efficiency of CCP maturation without affecting CCP density or CCP maturation rate (Loerke et al., 2009; Mettlen et al., 2009).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Introduction
What the sources say
- Partly supportedcites Loerke et al., 2009 sourceExperimental — accuracy not yet measured
The Results section, “Cargo Concentration Enhances CCP Maturation Efficiency” (page unavailable), reports that TfnR overexpression increased the productive fraction of CCPs in an AP2-dependent manner and concludes that TfnR is not rate-limiting for vesicle formation. But the productive CCP lifetime decreased slightly in one measured condition, and the available Figure 3 caption identifies a pit-density comparison without stating that density was unchanged. Those unqualified parts of the claim are not fully supported by our copy. (LLM, conf=0.85)
- Partly supportedcites Mettlen et al., 2009 sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) says CCP maturation is sensitive to cargo loading, supporting the general link between cargo incorporation and maturation. It does not report that transferrin receptor/AP-2 incorporation increases maturation efficiency without changing pit density or maturation rate. The Results (page unavailable) instead report that AP-2 depletion reduced the number of CCPs while leaving the proportions and lifetimes of CCP subpopulations unchanged; depletion is not the same manipulation as incorporation. (LLM, conf=0.85)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
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
“Dab2-mCherry colocalized with enhanced GFP (EGFP)–tagged clathrin light chain a (LCa-EGFP; Fig. 1, A–C) and EGFP-tagged σ2 subunit of AP2 (σ2-EGFP; Fig. S2 A) in CCPs at the cell surface.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA 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
“Under these conditions, ARH partially displaces AP2 from CCPs”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“In cells expressing CD8/LDLR, ARH-mCherry displayed nearly identical accumulation kinetics during the first 30–40 s at CCPs as compared with LCa-EGFP (Fig. 8 D, orange lines vs. green lines, respectively).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“However, if we first expressed CD8/LDLR for 2–7 h and then added LmB, ARH redistributed from the nucleus to CCPs (Fig. S3 Fb,c).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe 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 effect of CD8/LDLR overexpression on CCP dynamics was relatively small.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > ARH is AP2 dependent and limiting during CD8/LDLR uptake
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“(ii) ARH, which is lacking NPF motifs, did not induce formation of flat lattices”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“ARH translocated from the nucleus into the cytosol upon CD8/LDLR expression”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 45
- The quote only partly states this claim. 2
- Probably not a substantial claim. 5
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Upon overexpression of CD8/LDLR, ARH-F259A exited the nucleus, but was not recruited into CCPs (Fig. 5 B).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
What the sources say
- Partly supportedcites Mishra et al., 2005 sourceExperimental — accuracy not yet measured
The Results and Discussion report that F259A abolishes ARH binding to AP-2 and that GFP-tagged ARH fragments bearing F259A lose colocalization with AP-2. This supports the AP-2-binding aspect and is consistent with impaired recruitment to coated regions, but our copy does not report ARH-F259A exiting the nucleus upon CD8/LDLR overexpression or directly test its recruitment to CCPs under that condition. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
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
“The number of nonterminal events increased upon mild overexpression of cargo, and clusters of dynamic CCPs were observed.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > CD8/LDLRs and their adaptors increase the size and dynamic behavior of productive CCPs
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“this nucleo-cytoplasmic shuttling did not depend on AP2 binding and/or CCP recruitment, but on a functional PTB domain.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Upon CD8/LDLR expression, ARH exited the nucleus and was recruited to the plasma membrane, where it colocalized with clathrin (Fig. 4 C), and α-adaptin (Fig. 4 D) in diffraction-limited CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CCP localization of ARH is cargo dependent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“However, unlike clathrin, but as for ARH-mCherry, these σ2-EGFP intensities began to decrease before LCa-EGFP.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“(iii) a mix of ARH and Dab2 led to the breakdown of GCCSs”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this 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
“(iv) AP2 complexes are nonuniformly distributed in GCCSs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear? Based: unclearThe quote only partly states this claim.
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
“However, ARH accumulation seemed to reach its maximum in CCPs with lifetimes >80 s, whereas clathrin intensities were higher in longer-lived cohorts.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“GCCS formation was dependent on Dab2 expression, as they were not detected in cells overexpressing CD8/LDLR alone (Fig. S2, E and F; see also Fig. 4, C and D).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“When we coexpressed CD8/LDLR, Dab2-mCherry, and ARH-EGFP in BSC1 cells, both adaptors were recruited to the plasma membrane, where they colocalized (Fig. 4 E). However, in the presence of ARH, Dab2 and CD8/LDLR overexpression failed to generate GCCSs”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CCP localization of ARH is cargo dependent
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“CD8/LDLR overexpression also increased signal intensities of all σ2-EGFP–labeled CCP cohorts (Fig. 8, E and F; red lines and bars, respectively) and prolonged the growth phase to ∼50 s.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“However, despite this dynamic behavior, CCVs were observed to pinch off from the edges of these GCCSs only on rare occasions, indicating that they are not endocytically active (Videos 4 and 5).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Dab2 and CD8/LDLR expression can induce clathrin-coated structures (CCSs) that mimic nonterminal endocytic events
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Consistent with this, ARH-containing CCPs almost always colocalized with AP2 (Fig. 4 D), even though we could readily detect clathrin-labeled CCPs that did not contain AP2 (Fig. S2 E, circles).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“productive CCPs, which ultimately lead to vesicle formation, contribute 50.7 ± 2.0% (mean ± jackknifed cell-to-cell error; Thomson and Chave, 1991) to the total number of CCPs found at the plasma membrane (Fig. 7 A), with early and late abortive CCPs representing 30.7 ± 1.3% and 17.0 ± 1.3%, respectively.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Cargo overexpression prolongs the lifetime of productive CCPs
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
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
“This activity was dependent on its abilities to bind LDLR through its PTB domain and to interact with AP2.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > ARH is AP2 dependent and limiting during CD8/LDLR uptake
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“at the high levels of overexpression achieved upon complete removal of tet, Dab2 was strongly recruited to the plasma membrane and induced the formation of giant clathrin-coated structures (GCCSs).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Increased efficiency of LDLR uptake upon ARH expression was not achieved through an increased CCP density, an increased percentage of productive CCPs, or an increased rate of their maturation.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > ARH is AP2 dependent and limiting during CD8/LDLR uptake
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“The double mutant ARH-S117Y;F165A-mCherry was localized to the nucleus and failed to exit upon CD8/LDLR expression (Fig. 5 C), indicating a role for PTB binding interactions in the nuclear shuttling of ARH.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“When TfnRs were overexpressed, even in the presence of Dab2 (Fig. S2 C), we did not detect an effect on CCP size or the appearance of GCCSs by immunofluorescence.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Although biochemical measurements establish that CD8/LDLR endocytosis is saturable, resulting in a markedly decreased efficiency of CME”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > ARH is AP2 dependent and limiting during CD8/LDLR uptake
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“EM analysis of the ventral surface of cells revealed the appearance of larger flat lattices (Fig. 1 H), up to 500 nm in diameter (Table I), and clusters of CCPs (Fig. 1, F and H; see also Fig. 3 Ba) that were not detected under control conditions.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“EM revealed these to be flat lattices (Table I) and not clusters of CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“Unexpectedly, in cells overexpressing CD8/LDLR, Dab2-p67 induced the formation of GCCSs and colocalized with clathrin heavy chain (CHC; Fig. 2 C).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Increased membrane recruitment of Dab2 is sufficient to induce GCCSs
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“The calculated mean lifetimes were 5.7 ± 0.3 s, 19.1 ± 1.7 s, and 62.8 ± 3.1 s for early abortive, late abortive, and productive CCPs, respectively (Fig. 7 B).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Cargo overexpression prolongs the lifetime of productive CCPs
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“An additional pool of ARH did not alter the lifetimes of productive CCPs (76.3 ± 5.2 s), despite increasing the efficiency of CD8/LDLR endocytosis (Fig. 6 B).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Cargo overexpression prolongs the lifetime of productive CCPs
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“at the low levels of CD8/LDLR expression induced in the presence of 25 ng/ml tet (Fig. S1), CCPs increased in intensity (Fig. 1, E–G), suggesting an increase in CCP size and/or clustering of CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“When CD8/LDLR and ARH were coexpressed, CCPs also grew in size, as detected by increased clathrin intensities and electron microscopy, yet they remained under the light-diffraction limit.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > CD8/LDLRs and their adaptors increase the size and dynamic behavior of productive CCPs
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“In addition, although the relative intensities of these two markers could not be directly compared, an earlier decrease of the ARH-mCherry signals compared with LCa-EGFP signals (Fig. 8 D, arrows) led to a more symmetrical shape of the ARH-mCherry profiles.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“(ii) the competition of ARH and Dab2 for cargo binding, thereby disrupting Dab2 scaffolding of GCCSs”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
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
“We also noted that stable ARH expression altered cell morphology such that the cells displayed a very broad and regular leading edge (Fig. 4 A, Fig. S3 A). These shape changes were accompanied by alterations in the actin cytoskeleton (Fig. S3, A and B), which were reversed upon CD8/LDLR expression, as ARH redistributed to CCPs (Fig. S3 C).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CCP localization of ARH is cargo dependent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Together, these results demonstrate a continuum in the size of CCPs dependent on the expression levels of Dab2 and cargo: both Dab2 and CD8/LDLR overexpression are required for the formation of GCCSs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Relative amounts of Dab2 and CD8/LDLR control CCP size
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“This apparent discrepancy reflects the fact that biochemical assays for ligand uptake measure CME indirectly and the efficiency of CME depends on cargo loading/concentration into CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > ARH is AP2 dependent and limiting during CD8/LDLR uptake
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The efficiency of CME depends on cargo loading/concentration into CCPs.
- Rests on an assumption: Biochemical assays for ligand uptake measure CME indirectly.
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
“Overexpression of a specific receptor and its adaptors alters the relative adaptor composition of CCPs and hence their dynamic behavior.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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, although cargo overexpression is sufficient to trigger nuclear exit, AP2 interactions are required to stabilize ARH in CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“This could potentially bypass the requirement for a threshold amount of AP2 and its associated partners, and hence disrupt signaling to the endocytic restriction/checkpoint.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. 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
“Although endocytosis of CD8/LDLRs was more efficient with increased amounts of ARH, the rescue was incomplete, indicating the existence of other rate-limiting components during uptake of high CD8/LDLR loads.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > ARH partially rescues saturated CME in an AP2-dependent manner
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“However, at higher cargo concentrations, other binding interactions, perhaps involving the remaining NPF motifs on Dab2-p67, are sufficient to stabilize Dab2 at the membrane, leading to the formation of larger CCPs and ultimately GCCSs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Increased membrane recruitment of Dab2 is sufficient to induce GCCSs
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Together, these data indicate that CD8/LDLR overexpression stimulates initiation of CCPs, but does not affect the total number of productive CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Cargo overexpression prolongs the lifetime of productive CCPs
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Together, these observations indicate that ARH interacts with and controls actin dynamics by an as yet unknown mechanism.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CCP localization of ARH is cargo dependent
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A similar dissociation/redistribution has been suggested for AP2 (Rappoport et al., 2005; Saffarian and Kirchhausen, 2008) and was further supported by our analysis of CCP cohorts labeled by σ2-EGFP.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
What the sources say
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“which could account for the destabilization of nascent CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably 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
“Dab2 and ARH compete with each other and with AP2 for binding sites within the same CCPs as evidenced by (i) the strong colocalization of these various adaptors in CCPs, (ii) the competition of ARH and Dab2 for cargo binding, thereby disrupting Dab2 scaffolding of GCCSs, and (iii) the displacement of AP2 by ARH from cargo-laden CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“ARH lacks a recognizable NLS, suggesting that an additional factor might be involved in its nuclear shuttling.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > AP2 binding is required for CCP recruitment of ARH, whereas its nuclear export is passive and AP2 independent
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Dab2-p96 binds to both clathrin and AP2, and localizes to CCPs, whereas Dab2-p67 lacks the main AP2- and clathrin-binding motifs and does not localize to CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > Increased membrane recruitment of Dab2 is sufficient to induce GCCSs
What the sources say
- Not matchedcites Xu et al., 1995
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
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, the absence of ARH from CCPs under control conditions suggests that ARH recruitment is highly regulated and involves a yet-unidentified factor/mechanism.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“ARH can interact directly with both clathrin (He et al., 2002) and AP2 complexes (Mishra et al., 2005)”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Dab2 and ARH are differentially recruited to CCPs, yet compete for occupancy
What the sources say
- Not matchedcites He et al., 2002
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites Mishra et al., 2005 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Not matched
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 Dab2-dependent formation of nonfunctional, flat GCCSs under conditions of high cargo concentrations could reflect an imbalance of protein–protein interactions, possibly involving the disproportionate recruitment, through the multiple NPF motifs found in Dab2, of EH domain–containing proteins (e.g., Eps15, Eps15R, and intersectin) that bind directly or indirectly to clathrin.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Discussion > Adaptor content and the endocytosis checkpoint
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Rests on an assumption: Dab2 contains multiple NPF motifs that recruit EH domain-containing proteins that bind directly or indirectly to clathrin.
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
“Together, these data establish that CD8/LDLR overexpression increases the size of CCPs, and ARH enhances this effect and increases the packaging efficiency of CD8/LDLR into these enlarged CCPs.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 apparently earlier disappearance of adaptors relative to clathrin indicates either their dissociation from CCPs before clathrin and/or a nonuniform redistribution of both ARH and AP2 in the clathrin lattice, resulting in their differential illumination within the TIRF field.”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Results > CD8/LDLRs increase the amount of coat components per CCP
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“there are conflicting reports as to whether LDLR and TfnR are internalized via the same or distinct CCPs (Keyel et al., 2006; Lakadamyali et al., 2006).”
§ Cargo- and adaptor-specific mechanisms regulate clathrin-mediated endocytosis > Introduction
What the sources say
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
The CD8/LDLR chimera is a valid model for LDLR endocytosis and its adaptor-dependent trafficking.
“The CD8/LDLR chimera comprises the extracellular and transmembrane domains of CD8 and the intracellular LDLR tail bearing a FXNPXY motif (Motley et al., 2003).”
The paper relies on this without support.
Fluorescent tags (mCherry, EGFP) do not alter the function of ARH, clathrin, or AP2.
“This expected localization of Dab2-mCherry suggests that the fluorescent tag did not interfere with its function.”
The paper relies on this without support.
Dab2 is recruited to CCPs and can function independently of AP2.
“Dab2, unlike ARH, is recruited to CCPs and can function independently of AP2.”
The paper relies on this without support.
The efficiency of CME depends on cargo loading/concentration into CCPs.
“the efficiency of CME depends on cargo loading/concentration into CCPs.”
The paper relies on this without support.
Biochemical assays for ligand uptake measure CME indirectly.
“biochemical assays for ligand uptake measure CME indirectly”
The paper relies on this without support.
Dab2 contains multiple NPF motifs that recruit EH domain-containing proteins that bind directly or indirectly to clathrin.
“through the multiple NPF motifs found in Dab2, of EH domain–containing proteins (e.g., Eps15, Eps15R, and intersectin) that bind directly or indirectly to clathrin.”
Self-check
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.
Mean CCP area exceeds the stated maximum diameter at low CD8/LDLR expression
MajorThe text says these lattices reached at most 500 nm in diameter, but Table I gives a mean area of 0.45 μm2 for the same condition. Even a circular lattice 500 nm in diameter has an area of only about 0.196 μm2, so the reported mean cannot be below that maximum.
“EM analysis of the ventral surface of cells revealed the appearance of larger flat lattices (Fig. 1 H), up to 500 nm in diameter (Table I)”
“| CD8/LDLR | 25 | Dab2 | 0.45 ± 0.38a | 19 |”
Mean ARH-associated CCP area exceeds the stated maximum diameter
MajorThe stated maximum diameters are 500 nm for flat lattices and 165 nm for curved lattices, yet Table I reports a mean area of 0.89 μm2 for this condition. A 500-nm-diameter circle has an area of only about 0.196 μm2.
“EM analysis showed that the CCPs present in these cells consisted of flat and curved lattices, which remained below the diffraction limit (up to 500-nm and 165-nm diameter, respectively; Fig. S4 D, Table I).”
“| CD8/LDLR | 0 | ARH | 0.89 ± 0.54c | 27 |”
ARH localization is attributed to the wrong figure
MinorThe text cites Figure 3 A and B for nuclear ARH localization, whereas the Figure 4 caption identifies its A and B panels as the ARH-mCherry condition.
“the vast majority of ARH-mCherry was found in the nucleus of BSC1 cells (Fig. 3, A and B).”
“Figure: Figure 4. ARH localization is cargo dependent. BSC1 cells stably expressing ARH-mCherry were infected with adenoviruses coding for CD8/LDLR and cultured in the presence (A and B) or absence (C and D) of tet.”
Text cites a Figure 3 E panel absent from the caption
MinorThe text points to Figure 3 E for exchange kinetics, but the Figure 3 caption enumerates panels only through D.
“Dab2 and clathrin exchanged actively in these structures (Fig. 3 D), albeit with different kinetics (Fig. 3 E; Chetrit et al., 2009).”
“Figure: Figure 3. GCCSs are dynamic and, at moderate CD8/LDLR levels, generate nonterminal endocytic events. BSC1 cells were cultured as described in Fig. 1 and observed by dual-color TIRF-FM (A, Bb, C), electron microscopy (Ba), or spinning disk confocal microscopy (D).”
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Metadata
- Authors
- Mettlen, M., Loerke, D., Yarar, D., Danuser, G., & Schmid, S. L.
- Affiliations
- Scripps Research Institute (US)
- University of Denver (US)
- Corresponding author
- Schmid, Sandra L.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2010-03-15
- Volume
- 188
- Issue
- 6
- Pages
- 919-933
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- PMC
- PMC2845073
- OpenAlex
- W2033344378
- Cited by
- 177
- References
- 42
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 7 · 2023: 6 · 2022: 10 · 2021: 13 · 2020: 12 · 2019: 10 · 2018: 10 · 2017: 10 · 2016: 11 · 2015: 14 · 2014: 10 · 2013: 13 · 2012: 17
- FWCI
- 4.85
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-sa
- Locations
- The Journal of Cell Biology (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- Leukemia and Lymphoma Society
- Thailand Science Research and Innovation
- National Institutes of Health (MH61345)
- National Institute of Mental Health (R01MH061345, MH61345, R37MH061345)
- National Institute of General Medical Sciences (R01GM073165)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Keywords
- clathrin-mediated endocytosis, clathrin-coated pits, LDL receptor, Dab2, receptor internalization
- MeSH terms
- Animals, Cells, Cultured, Chlorocebus aethiops, Clathrin, Coated Pits, Cell-Membrane, Endocytosis, Ligands, Particle Size, Receptors, LDL, Time Factors, Adaptor Proteins, Signal Transducing, Rats
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