The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index; 22 of the 45 sources its claims cite were checked for support.
The Bifunctional microRNA miR-9/miR-9* Regulates REST and CoREST and Is Downregulated in Huntington's Disease
Open accessAbstract
The transcription factor REST silences neuronal gene expression in non-neuronal cells. In neurons, the protein is sequestered in the cytoplasm in part through binding to huntingtin. Polyglutamine expansions in huntingtin, which causes Huntington's disease (HD), abrogates REST-huntingtin binding. Consequently, REST translocates to the nucleus, occupies RE1 repressor sequences and decreases neuronal gene expression. In this work, we found that levels of several microRNAs (miRNAs) with upstream RE1 sites are decreased in HD patient cortices relative to healthy controls. Interestingly, one of these, the bifunctional brain enriched miR-9/miR-9*, targets two components of the REST complex: miR-9 targets REST and miR-9* targets CoREST. These data provide evidence for a double negative feedback loop between the REST silencing complex and the miRNAs it regulates.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In Huntington’s disease (HD) cortex, several REST-regulated microRNAs are downregulated with disease progression, including the bifunctional miR-9/miR-9*. The authors show that miR-9 targets REST and miR-9* targets CoREST, supporting a double-negative feedback loop between the REST silencing complex and the miRNAs it regulates.
Key findings
- In Brodmann’s area 4 (BA4) cortex, five predicted REST-regulated miRNAs were significantly diminished with increasing HD grade: miR-9 (F(3,22)=9.876, p=0.0003), miR-9* (F(3,22)=6.799, p=0.0021), miR-29b (F(3,22)=3.658, p=0.0281), miR-124a (F(3,16)=7.833, p=0.001), and miR-132 (F(3,22)=7.611, p=0.0011).
- A QPCR miRNA array of 365 mature miRNAs in control and early HD (grades 1 and 2) BA4 cortex found an additional 5 decreased miRNAs; miR-196a and miR-486 were increased by nearly 6-fold and 3-fold, respectively, in HD1 samples relative to controls.
- miR-9 targets REST and miR-9* targets CoREST: pre-miR-9 reduced REST reporter and endogenous REST protein, while pre-miR-9* reduced CoREST reporter and endogenous CoREST protein; target site protectors rescued these effects.
- Reducing REST expression in HEK 293 and NT2 cells enhanced miR-9 expression and processing (p<0.05), providing functional evidence for a negative feedback loop between the REST complex and REST-regulated miRNAs.
Methods
- Postmortem BA4 cortex samples from healthy controls (n=7; ages 46–62) and HD grade 1 (n=7; ages 42–70), grade 2 (n=6; ages 45–78), grade 3 (n=2; ages 60–65), and grade 4 (n=4; ages 53–60); CAG repeat length was 16–21 for controls and 37–46 for HD, with postmortem time 2–20 hrs.
- Mature miRNA expression was measured by quantitative PCR using TaqMan Array Human MiRNA Panel v1.0 or TaqMan MiRNA Assays, normalized to RNU48 and shown as fold change relative to controls.
- Mechanistic validation used HEK 293 and NT2 cells with REST/CoREST 3′ UTR luciferase reporters, mU6 miR-9/9* or pre-miRs, anti-miRs, target site protectors, siRNAs, and Western blots; data were analyzed by one-way ANOVA with Dunnett’s post hoc analysis.
Limitations
- The paper does not state a limitations section.
- Evident from the text: human HD grade 3 (n=2) and grade 4 (n=4) samples were very small, and the human data are cross-sectional postmortem BA4 cortex only, limiting generalization across brain regions and disease stages.
- Evident from the text: target validation relied heavily on HEK 293/NT2 cell lines and reporter assays rather than HD brain tissue, and the authors note it is currently under study whether diminished miRNAs result from or contribute to the dedifferentiation profile in HD cortex.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
23 Own result · 10 No full text of the sources · 10 Own interpretation · 9 Partly supported · 4 Supported · 3 Supported so far · 3 Sources not found · 2 Own method · 1 Couldn’t confirm · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“miR-9-1 and miR-9-3 both have upstream RE1 sequences that is can be occupied by REST (Conaco et al., 2006; Johnson et al., 2008).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > REST and CoREST contain predicted miR-9 and 9* regulatory sites
What the sources say
- Partly supportedcites Conaco et al., 2006 sourceExperimental — accuracy not yet measured
The Results identify miR-9-1 and miR-9-3 among loci near REST-binding sites, and report ChIP evidence that REST occupies RE1 sites associated with the identified miRNA genes (Fig. 1A; page not provided). The text of our copy describes those sites as nearby, but does not establish that the RE1 sequences for both loci are upstream. (LLM, conf=0.83)
- Not checked — no full text of the sourcecites Johnson et al., 2008 source
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.
- 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
“The transcription factor REST silences neuronal gene expression in non-neuronal cells.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Abstract
What the sources say
- Not checked — no full text of the sourcecites Zuccato et al., 2003 source
- Supportedcites Conaco et al., 2006 source
The paper’s opening section states that REST inhibits expression of neuronal genes in nonneuronal cells. The Discussion likewise says that REST binds neuronal genes in those cells and blocks their transcription. (LLM, conf=0.95)
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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Interestingly, genes related to neurogenesis are highly overrepresented amongst the genes changed in expression in the cortex (BA4) of HD patients (Hodges et al., 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Supportedcites Hodges et al., 2006 source
In “Signaling pathways and axonal structural elements show the greatest impact of gene expression changes,” the paper reports over-representation of nodes related to CNS development and neurogenesis in HD BA4, as well as in the caudate. This supports the claim about neurogenesis-related genes among those with changed expression in BA4. (LLM, conf=0.94)
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.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Once in the nucleus, REST can bind RE1 consensus sequences and recruit co-repressors including mSin3, the co-repressor of REST (CoREST, also known as RCOR1) and methyl CpG binding protein 2 (MeCP2) (Andres et al., 1999) to inactivate neuron-specific genes (Zuccato et al., 2003; Conaco et al., 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Partly supportedcites Andres et al., 1999 sourceExperimental — accuracy not yet measured
The introduction and Discussion (page not available in our copy) identify REST as a DNA-binding repressor and show that it recruits CoREST to repress neural-specific gene expression. The citation follows a list of three corepressors, but our copy does not identify mSin3 or MeCP2 as REST corepressors; the separately cited clause about gene inactivation is not the issue here. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Zuccato et al., 2003 source
- Supportedcites Conaco et al., 2006 source
The Discussion states that REST binds consensus RE1 sites in neuronal genes and blocks their transcription. The paper also describes silencing through corepressors associated with REST, while the specific list of mSin3, CoREST, and MeCP2 is attached to Andres et al. (1999) in the citing sentence. (LLM, conf=0.92)
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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“We specifically chose Brodmann’s area 4 (BA4) cortex because prior work indicates widespread transcriptional changes in this region in HD patients (Hodges et al., 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
What the sources say
- Supportedcites Hodges et al., 2006 source
In “Regional differences and similarities in gene expression within HD brains” (page not provided), the paper reports altered mRNA expression for 1,482 probe sets in HD BA4 motor cortex compared with controls. That supports the citing sentence’s characterization of substantial transcriptional changes in this region. (LLM, conf=0.92)
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.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“This may reflect a dedifferentiation mediated by aberrant REST localization, since REST mRNA levels do not change significantly in HD (Hodges et al., 2006), as well as global changes in miR-9/9* and miR-124a target levels.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Could not verifycites Hodges et al., 2006 sourceExperimental — accuracy not yet measured
The ‘Regional differences and similarities in gene expression within HD brains’ section reports changes across brain regions, but does not give a result for REST mRNA. Searches for REST, NRSF, and RE1-silencing transcription factor found no passage establishing whether REST mRNA changes significantly in HD. (LLM, conf=0.74)
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.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“One of the molecular phenotypes in HD patients is transcriptional misregulation in striatum and distinct cortical regions (Hodges et al., 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Partly supportedcites Hodges et al., 2006 sourceExperimental — accuracy not yet measured
The Abstract (page not provided) reports altered mRNA expression in the caudate nucleus and motor cortex of human HD brains. It also reports no detected mRNA changes in the prefrontal association cortex, so the claim overstates the evidence if “distinct cortical regions” means multiple affected cortical regions. (LLM, conf=0.85)
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.
- 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
“For miR-139, miR-135b, and miR-212 no significant differences were observed with increasing disease severity, while miR-218 demonstrated a trend toward increasing expression with disease grade (Fig. 1A).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
boostedcorrelational- 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.
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
“Cotransfection of the CoREST 3′ UTR reporter plasmid and 5 or 15 nM pre-miR-9* reduced reporter expression compared to controls (F(2,11) = 41.612, p = 0.0001 and F(2,11) = 7.423, p = 0.0091, respectively), unlike miR-9, (Fig. 3A).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miR-9 targets REST
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.
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 these reporter-based assays, over expression of mU6 miR-9/9*, but not mU6 miR-124a or 132, in HEK 293 cells significantly reduced REST (F(2,12) = 26.006, p = 0.0001) and CoREST (F(2,12) =24.017, p = 0.0001) expression (Fig. 1D,E).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > REST and CoREST contain predicted miR-9 and 9* regulatory sites
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. 15
- Probably not a substantial claim. 16
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The 3′ UTRs of REST (Fig. S2) and CoREST (Fig. S3) contain miRNA recognition elements (MRE) for miR-9, miR-9*, miR-132 and miR-124a (CoREST only) (Wu and Xie, 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > REST and CoREST contain predicted miR-9 and 9* regulatory sites
What the sources say
- Partly supportedcites Wu and Xie, 2006 sourceExperimental — accuracy not yet measured
In Results, under “Evidence for a double-negative feedback loop between REST complex and brain-related miRNAs” (page not available), the paper predicts a miR-9 target site in REST’s longer 3′ UTR and identifies CoREST as a predicted miR-124a target. It lists miR-9* and miR-132 as targeting MeCP2, not REST or CoREST, so it does not support those parts of the claim. (LLM, conf=0.90)
- Not matchedcites TargetScan 4.1
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Could not verifycites Lewis et al., 2003 sourceExperimental — accuracy not yet measured
The paper’s discussion of predicted miRNA–UTR pairs (indexed as Abstract; page unavailable) does not identify REST or CoREST as targets of the specified miRNAs. Searches for REST, CoREST, miR-9*, miR-132, and miR-124a found no passage establishing those particular recognition elements; the supplementary-data passages describe target lists but do not give the relevant entries. (LLM, conf=0.73)
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.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Double negative feedback networks have been reported in other systems where critical balancing of multiple factors is essential (Tsang et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Partly supportedcites Tsang et al., 2007 sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) identifies putative negative autofeedback loops, and the passage on type I circuits (indexed as Abstract; page unavailable) proposes that they help maintain steady protein levels. These passages support a role for feedback in stabilizing regulation, but they do not establish the more specific claim that double-negative feedback networks have been reported in systems requiring a critical balance of multiple factors. (LLM, conf=0.82)
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
Every source the paper cites for this claim was checked and supports it.
In the paper
“REST expression is highest in pluripotent stem cells and decreases upon restriction to neural progenitor cells and subsequently to neurons (Ballas et al., 2005).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Supportedcites Ballas et al., 2005 source
The Discussion states that REST protein is highest in pluripotent ES-cell nuclei and falls to minimal levels as they differentiate into neural progenitors. The Results report that REST is undetectable in cortical progenitors and absent from neuronal-gene chromatin in mature neurons. This progression concerns REST protein; REST mRNA does not show the same decline. (LLM, conf=0.90)
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.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In mouse cortical development, miR-9 appears necessary for appropriate differentiation of Cajal-Retzius cells (Shibata et al., 2008).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Supportedcites Shibata et al., 2008 source
In the section “miR-9 regulates the differentiation of Cajal-Retzius cells” (page unavailable), suppressing miR-9 with an antisense oligonucleotide reduced reelin- and p73-positive Cajal-Retzius cells. This supports the hedged claim that miR-9 is necessary for their appropriate differentiation during mouse cortical development. (LLM, conf=0.93)
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.
- 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
“One putative mechanism underlying the transcriptional changes is aberrant cellular distribution of the transcriptional repressor RE1-silencing transcription factor (REST, also known as neuronal restrictive silencing factor, NRSF) (Lunyak et al., 2002; Zuccato et al., 2003 ; Zuccato et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Not checked — no full text of the sourcecites Lunyak et al., 2002 source
- Not checked — no full text of the sourcecites Zuccato et al., 2003 source
- Supportedcites Zuccato et al., 2007 source
The Introduction says wild-type huntingtin retains REST/NRSF in the cytoplasm, whereas mutant huntingtin is associated with its accumulation in the nucleus and repression of BDNF transcription. The Discussion links this altered distribution to transcriptional dysregulation in Huntington’s disease. (LLM, conf=0.93)
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.
Probably not a substantial claim.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recent studies on the brain enriched miR-9 have revealed its importance in development and lineage commitment (Sempere et al., 2004; Krichevsky et al., 2006).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Partly supportedcites Sempere et al., 2004 sourceExperimental — accuracy not yet measured
In Results and discussion, the paper identifies miR-9 as brain-specific and reports its strong induction during retinoic-acid-induced neuronal differentiation. It concludes that miR-9/miR-9* may play an important role in rodent neurogenesis; it does not establish that miR-9 is important for development or lineage commitment as the citing sentence implies. (LLM, conf=0.85)
- Supportedcites Krichevsky et al., 2006 source
The Abstract reports that brain-specific miR-9 affects neural lineage differentiation in mouse embryonic stem cell-derived cultures. The Discussion identifies miR-9 as a mediator of neurogenesis, while the Summary links these findings to a suggested role in mammalian brain development. (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.
- 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
“Similarly, REST repressor complex binding to RE1 sequences upstream of miRNA transcripts may alter miRNA expression profiles (Conaco et al., 2006; Klein et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Supportedcites Conaco et al., 2006 source
The Results report REST occupancy at RE1 sites associated with several miRNA genes. Changing REST activity altered miR-9, miR-124a, and miR-132 transcript levels, supporting the claim that REST binding may alter miRNA expression profiles. (LLM, conf=0.93)
- Not checked — no full text of the sourcecites Klein et al., 2007 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.
Probably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“REST interacts with CoREST and other transcriptional repressors to regulate neuronal gene expression and lineage commitment through its direct control of both mRNA and, as shown more recently, miRNA transcripts (Vo et al., 2005; Conaco et al., 2006; Mortazavi et al., 2006 ; Visvanathan et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not matchedcites Vo et al., 2005
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Supportedcites Conaco et al., 2006 source
The introductory passage describes REST silencing neuronal genes through associated corepressors, and the Results identify CoREST as a REST corepressor. The Discussion states that REST binds sites in neuronal genes and miR-124a to block their transcription, with their derepression during neurogenesis favoring a neuronal phenotype. No page numbers are available in our copy. (LLM, conf=0.87)
- Partly supportedcites Mortazavi et al., 2006 sourceExperimental — accuracy not yet measured
The introduction says REST recruits CoREST and other cofactors to repress neuronal genes. The section on neuronal transcription factor and microRNA loci says REST represses protein-coding and microRNA genes in stem cells and progenitors, but presents their role in the transition to neurons as a proposed model that may modulate or accelerate that transition. The claim overstates this modeled role in lineage commitment as established. (LLM, conf=0.85)
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.
- Not matched
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The transcriptional repressor REST is mislocalized in brains of patients with HD, with increased nuclear localization and occupancy at RE1 sites compared to healthy controls (Zuccato et al., 2003 ; Zuccato et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Zuccato et al., 2003 source
- Partly supportedcites Zuccato et al., 2007 sourceExperimental — accuracy not yet measured
The section “A global analysis of endogenous REST/NRSF binding in HD human brain” (page unavailable) reports greater REST occupancy at RE1/NRSE sites in cortical samples from patients with HD than in age-matched controls. The paper discusses increased nuclear REST as a proposed explanation, but the passages do not establish increased nuclear localization in patients’ brains compared with controls. (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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Indeed, canonical and non-canonical REST binding motifs have recently been mapped in close proximity to 22 miRNA sites in the human genome, including several of which are located within close proximity to neuron enriched miRNAs (Bruce et al., 2004; Jothi et al., 2008).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Partly supportedcites Bruce et al., 2004 sourceExperimental — accuracy not yet measured
The Discussion reports a genome-wide map of human RE1 sites and notes additional sites that diverge from the consensus. Neither that passage nor the searched passages on microRNA and miRNA report 22 nearby miRNA sites or identify neuron-enriched miRNAs. The paper supports the motif-mapping part, but not the claimed miRNA proximity. (LLM, conf=0.86)
- Partly supportedcites Jothi et al., 2008 sourceExperimental — accuracy not yet measured
The Results (Accuracy of identified binding sites; page unavailable) report canonical NRSF/REST motifs and alternative half-site arrangements at mapped binding sites. The cited paper does not report that these sites lie near 22 miRNA sites or near neuron-enriched miRNAs; those specific parts of the claim are unsupported by our copy. (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.
- 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
“Consistent with these observations, REST levels in HEK 293 cells, which decreased upon mU6 miR-9/9* transfection (Fig. 1D,E) was rescued by TSP+ (Student t-test, p < 0.05), but not a control TSP (TSP Neg; Fig. 2D).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miR-9 targets REST
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 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
“For miR-139, miR-135b, and miR-212 no significant differences were observed with increasing disease severity, while miR-218 demonstrated a trend toward increasing expression with disease grade (Fig. 1A).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
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 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
“Endogenous CoREST protein expression, which was reduced after pre-miR-9* transfection, increased upon cotransfection of TSP+ (Student t-test, p < 0.05) but not TSP Neg (Fig. 3D).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miR-9 targets REST
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 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
“Also, miR-196a and miR-486 were significantly increased by nearly 6 and 3 fold respectively in HD1 samples relative to controls.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
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 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
“Also, we found no change in miR-132 at stages 1 and 2, but significant upregulation later.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
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 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 saw a trend towards increased miR-29a in tissue from early stage HD, followed by diminished levels.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
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.
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 suggest that the miR-9 predicted MREs in the 3′ UTR of REST are functional, in contrast to the miR-9* predicted MREs.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miR-9 targets REST
hedgeddirect- 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
“In zebrafish, miR-9 is important midbrain-hindbrain boundary definition (Leucht et al., 2008).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Leucht et al., 2008 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.
In the paper
“Also, over-expression of miR-124 in non-neuronal cells induces gene expression profiles to a neuronal phenotype (Lim et al., 2005).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Lim et al., 2005 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.
In the paper
“miR-124 promotes neuronal differentiation, in part through targeting of a splicing factor (Makeyev et al., 2007).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Makeyev et al., 2007 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 claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“MiR-132 has been shown to target MeCP2 (Klein et al., 2007), which can interact with REST and CoREST to suppress transcription (Lunyak et al., 2002).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
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
“However, in patients with HD mutant Htt fails to bind REST enabling its nuclear translocation (Zuccato et al., 2003).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Not checked — no full text of the sourcecites Zuccato et al., 2003 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.
In the paper
“Interestingly, and in contrast to our findings, their work showed no change in miR-124a, elevated levels of miR-29a, and decreased levels of miR-132.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
What the sources say
- Not matchedcites Johnson et al., 2008
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: 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
“Our findings, together with recent work showing that REST can be regulated by ubiquitin-mediated proteolysis (Westbrook et al., 2008) underscore the importance of maintaining appropriate levels and intracellular localization (Zuccato et al., 2003) of this repressor complex for appropriate gene transcription and lineage commitment.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
What the sources say
- Not checked — no full text of the sourcecites Westbrook et al., 2008 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.
In the paper
“Consequently, REST translocates to the nucleus, occupies RE1 repressor sequences and decreases neuronal gene expression.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Abstract
What the sources say
- Not checked — no full text of the sourcecites Zuccato et al., 2003 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.
In the paper
“Previous work by Johnson and colleagues measured precursor miRNA levels in HD brain of unknown disease grade (Johnson et al., 2008).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
What the sources say
- Not matchedcites Johnson et al., 2008
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: 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 matched
In the paper
“In mature, healthy neurons, REST is expressed at low levels and primarily sequestered in the cytoplasm in part through interaction with Htt (Zuccato et al., 2003).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Not checked — no full text of the sourcecites Zuccato et al., 2003 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
“This may reflect a dedifferentiation mediated by aberrant REST localization, since REST mRNA levels do not change significantly in HD (Hodges et al., 2006), as well as global changes in miR-9/9* and miR-124a target levels.”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Discussion
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
“Huntington’s Disease (HD) is an autosomal dominant neurodegenerative disease caused by CAG trinucleotide repeat expansion in huntingtin, which encodes Huntingtin (Htt) (The Huntingtons Disease Collaborative Research Group, 1993).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Introduction
What the sources say
- Not matchedcites The Huntingtons Disease Collaborative Research Group, 1993
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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 matched
The paper relies on this without support.
miR-9 and miR-9* are processed from the same primary transcript from three genomic loci (miR-9-1, 9-2, and 9-3).
“MiR-9 and miR-9*, which decreased early in HD (Fig 1A), are processed from the same primary transcript from 3 genomic loci (miR-9-1, 9-2 and 9-3); miR-9-1 and miR-9-3 both have upstream RE1 sequences that is can be occupied by REST (Conaco et al., 2006; Johnson et al., 2008).”
The paper relies on this without support.
The postmortem brain samples from Huntington's disease patients and controls are representative of the disease process and are not confounded by post-mortem interval or other factors.
“Post-mortem time for brain samples was 2 – 20 hrs.”
The paper relies on this without support.
The observed miRNA expression changes in Brodmann's area 4 cortex are attributable to Huntington's disease progression rather than to age, sex, or other demographic differences between groups.
“Tissues were collected from Brodmann’s area 4 (BA4) cortex of healthy control (n = 7; ages 46 – 62) and HD grade 1 (n = 7; ages 42-70), 2 (n = 6; ages 45 -78), 3 (n = 2; ages 60 - 65) and 4 (n = 4; 53 - 60).”
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
“In HD, the dysregulation of miRNAs has been reported in HD in vitro models, transgenic HD animals and human HD brain [12-24].”
From miR-10b-5p expression in Huntington’s disease brain relates to age of onset and the extent of striatal involvement (2015) · cites this paper as [20]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“the miR-9 level was shown to be decreased in the postmortem brains of Huntington's disease patients (Packer et al., 2008)”
From The Brain-Enriched MicroRNA miR-9-3p Regulates Synaptic Plasticity and Memory (2016) · cites this paper as Packer et al., 2008
The cited source says what the claim attributes to it.
In the citing paper
“The physiological importance of miRNAs in nervous system functions and disease states has also been suggested by previous studies of a small number of brainenriched miRNAs (Leucht et al., 2008;Mellios et al., 2008;Packer et al., 2008;Cheng et al., 2009;Schratt, 2009).”
From Comprehensive expression analyses of neural cell-type-specific miRNAs identify new determinants of the specification and maintenance of neuronal phenotypes (2013) · cites this paper as Packer et al., 2008
Statistics that don’t add up
Each reported p-value recomputed from its test statistic and degrees of freedom.
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
“F(3,16) = 7.833, p = 0.001”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
Reported p = .001 · recomputed p = .002
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
“F(2,6) = 16.134, p = 0.0034”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > REST and CoREST contain predicted miR-9 and 9* regulatory sites
Reported p = .0034 · recomputed p = .004
Statistics recomputed
Every reported test result, recomputed from its test statistic and degrees of freedom. A result shows as not adding up only once an independent check has confirmed it.
- Doesn’t add upF(3, 16) = 7.833reported p = .001 · recomputed p = .002
“F(3,16) = 7.833, p = .001”
- Doesn’t add upF(2, 6) = 16.134reported p = .0034 · recomputed p = .004
“F(2,6) = 16.134, p = .0034”
- ConsistentF(3, 22) = 9.876reported p = .0003 · recomputed p < .001
“F(3,22) = 9.876, p = .0003”
- ConsistentF(3, 22) = 6.799reported p = .0021 · recomputed p = .002
“F(3,22) = 6.799, p = .0021”
- ConsistentF(3, 22) = 3.658reported p = .0281 · recomputed p = .028
“F(3,22) = 3.658, p = .0281”
- ConsistentF(2, 6) = 333.08reported p = .0001 · recomputed p < .001
“F(2, 6) = 333.08, p = .0001”
The paper prints p at a floor (such as p < .001)
- ConsistentF(2, 12) = 26.006reported p = .0001 · recomputed p < .001
“F(2,12) = 26.006, p = .0001”
The paper prints p at a floor (such as p < .001)
- ConsistentF(2, 12) = 24.017reported p = .0001 · recomputed p < .001
“F(2,12) =24.017, p = .0001”
- ConsistentF(2, 9) = 35.524reported p < .0001 · recomputed p < .001
“F(2,9) = 35.524, p < .0001”
- ConsistentF(2, 6) = 19.539reported p = .0024 · recomputed p = .002
“F(2,6) = 19.539, p = .0024”
- ConsistentF(2, 9) = 7.552reported p = .0119 · recomputed p = .012
“F(2,9) = 7.552, p = .0119”
- ConsistentF(2, 9) = 38.395reported p < .0001 · recomputed p < .001
“F(2,9) = 38.395, p < .0001”
- ConsistentF(2, 11) = 41.612reported p = .0001 · recomputed p < .001
“F(2,11) = 41.612, p = .0001”
The paper prints p at a floor (such as p < .001)
- ConsistentF(2, 11) = 7.423reported p = .0091 · recomputed p = .009
“F(2,11) = 7.423, p = .0091”
- ConsistentF(2, 9) = 11.173reported p = .0036 · recomputed p = .004
“F(2,9) = 11.173, p = .0036”
- ConsistentF(2, 6) = 32.882reported p = .0006 · recomputed p < .001
“F(2,6) =32.882, p = .0006”
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.
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
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
“We found 5 predicted REST-regulated miRs to be significantly diminished with increasing HD grade: miR-9 (F(3,22) = 9.876, p = 0.0003), miR-9* (F(3,22) = 6.799, p = 0.0021), miR-29b (F(3,22) = 3.658, p = 0.0281), miR-124a (F(3,16) = 7.833, p = 0.001), and miR-132 (F(3,22) = 7.611 p = 0.0011) (Fig. 1A).”
§ The bi-functional microRNA miR-9/miR-9* regulates REST and CoREST and is down-regulated in Huntington’s Disease > Results > miRNA expression changes with HD progression
“Also, we found no change in miR-132 at stages 1 and 2, but significant upregulation later.”
Citations
Cites
Bartel (2004) · doi:10.1016/s0092-8674(04)00045-5 · Cited by 34,714
MACDONALD, M. (1993) · Cell · doi:10.1016/0092-8674(93)90585-e · Cited by 8,366
Prediction of Mammalian MicroRNA Targets
Lewis, B. P., Shih, I.-H., Jones-Rhoades, M. W., Bartel, D. P., & Burge, C. B. (2003) · Cell · doi:10.1016/s0092-8674(03)01018-3 · Cited by 5,199
Microarray analysis shows that some microRNAs downregulate large numbers of target mRNAs
Lim, L. P., Lau, N. C., Garrett-Engele, P., Grimson, A., Schelter, J. M., Castle, J., Bartel, D. P., Linsley, P. S., & Johnson, J. M. (2005) · Nature · doi:10.1038/nature03315 · Cited by 4,755
Sempere, L. F., Freemantle, S., Pitha-Rowe, I., Moss, E., Dmitrovsky, E., & Ambros, V. (2004) · Genome Biology · doi:10.1186/gb-2004-5-3-r13 · Cited by 1,578
Makeyev, E. V., Zhang, J., Carrasco, M. A., & Maniatis, T. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.07.015 · Cited by 1,395
A MicroRNA Feedback Circuit in Midbrain Dopamine Neurons
Kim, J., Inoue, K., Ishii, J., Vanti, W. B., Voronov, S. V., Murchison, E., Hannon, G., & Abeliovich, A. (2007) · Science · doi:10.1126/science.1140481 · Cited by 1,187
Huntingtin interacts with REST/NRSF to modulate the transcription of NRSE-controlled neuronal genes
Zuccato, C., Tartari, M., Crotti, A., Goffredo, D., Valenza, M., Conti, L., Cataudella, T., Leavitt, B. R., Hayden, M. R., Timmusk, T., et al. (2003) · Nature Genetics · doi:10.1038/ng1219 · Cited by 979
REST and Its Corepressors Mediate Plasticity of Neuronal Gene Chromatin throughout Neurogenesis
Ballas, N., Grunseich, C., Lu, D. D., Speh, J. C., & Mandel, G. (2005) · Cell · doi:10.1016/j.cell.2005.03.013 · Cited by 950
Regional and cellular gene expression changes in human Huntington's disease brain
Hodges, A., Strand, A. D., Aragaki, A. K., Kuhn, A., Sengstag, T., Hughes, G., Elliston, L. A., Hartog, C., Goldstein, D. R., Thu, D., et al. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl013 · Cited by 804
Self-citation
Cited by
Sorted by citations
Items 301–400 of 679
The Role of microRNAs in Drug Addiction
Pietrzykowski, A. Z. (2010) · International review of neurobiology · doi:10.1016/s0074-7742(10)91001-5 · Cited by 44
MicroRNA‑124: an emerging therapeutic target in central nervous system disorders
Zhang, W.-H., Jiang, L., Li, M., & Liu, J. (2023) · Experimental Brain Research · doi:10.1007/s00221-022-06524-2 · Cited by 43
Das, E., & Bhattacharyya, N. P. (2014) · FEBS Letters · doi:10.1016/j.febslet.2014.03.015 · Cited by 43
Li, Z., Lu, Y., Xu, X., & Gao, F. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds420 · Cited by 45
Spencer, P. S., Fry, R. C., & Kisby, G. E. (2012) · Frontiers in Genetics · doi:10.3389/fgene.2012.00192 · Cited by 43
Rockowitz, S., & Zheng, D. (2015) · Nucleic Acids Research · doi:10.1093/nar/gkv514 · Cited by 42
Altered Purkinje cell miRNA expression and SCA1 pathogenesis
Rodríguez-Lebrón, E., Liu, G., Keiser, M. S., Behlke, M. A., & Davidson, B. L. (2013) · Neurobiology of Disease · doi:10.1016/j.nbd.2013.01.019 · Cited by 42
Self-citationCirculating miR-9* and miR-384-5p as Potential Indicators for Trimethyltin-induced Neurotoxicity
Ogata, K., Sumida, K., Miyata, K., Kushida, M., Kuwamura, M., & Yamate, J. (2014) · Toxicologic Pathology · doi:10.1177/0192623314530533 · Cited by 42
Liu, X., Wu, Y., Huang, Q., Zou, D., Qin, W., & Chen, Z. (2015) · PLoS ONE · doi:10.1371/journal.pone.0126123 · Cited by 42
MicroRNAs Engage in Complex Circuits Regulating Adult Neurogenesis
Stappert, L., Klaus, F., & Brüstle, O. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00707 · Cited by 45
RNA-Binding Proteins in the Regulation of miRNA Activity: A Focus on Neuronal Functions
Loffreda, A., Rigamonti, A., Barabino, S. M. L., & Lenzken, S. C. (2015) · Biomolecules · doi:10.3390/biom5042363 · Cited by 48
miRNA-Mediated Regulation of Adult Hippocampal Neurogenesis; Implications for Epilepsy
Bielefeld, P., Mooney, C., Henshall, D. C., & Fitzsimons, C. P. (2016) · Brain Plasticity · doi:10.3233/bpl-160036 · Cited by 41
Transcriptomic profiling of platelet senescence and platelet extracellular vesicles
Pienimaeki‐Roemer, A., Konovalova, T., Musri, M. M., Sigrüener, A., Boettcher, A., Meister, G., & Schmitz, G. (2016) · Transfusion · doi:10.1111/trf.13896 · Cited by 41
Mechanistic Insights Into MicroRNA-Induced Neuronal Reprogramming of Human Adult Fibroblasts
Lu, Y.-L., & Yoo, A. S. J. (2018) · Frontiers in Neuroscience · doi:10.3389/fnins.2018.00522 · Cited by 41
Balaraman, S. (2013) · Alcohol research · doi:10.35946/arcr.v35.1.03 · Cited by 40
Wakabayashi, K., Mori, F., Kakita, A., Takahashi, H., Utsumi, J., & Sasaki, H. (2014) · Acta Neuropathologica Communications · doi:10.1186/s40478-014-0173-z · Cited by 41
Comparison of REST Cistromes across Human Cell Types Reveals Common and Context-Specific Functions
Rockowitz, S., Lien, W., Pedrosa, E., Wei, G., Lin, M., Zhao, K., Lachman, H. M., Fuchs, E. V., & Zheng, D. (2014) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1003671 · Cited by 40
Modulation and Evolution of Animal Development through microRNA Regulation of Gene Expression
Kittelmann, S., & McGregor, A. P. (2019) · Genes · doi:10.3390/genes10040321 · Cited by 43
Recapitulating developmental mechanisms for retinal regeneration
Ahmad, I., Teotia, P., Erickson, H. E., & Xia, X. (2019) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2019.100824 · Cited by 42
Choi, I., Woo, J. H., Jou, I., & Joe, E.-H. (2016) · Experimental Neurobiology · doi:10.5607/en.2016.25.1.14 · Cited by 40
miR-200 family controls late steps of postnatal forebrain neurogenesis via Zeb2 inhibition
Beclin, C., Follert, P., Stappers, E., Barral, S., Coré, N., de Chevigny, A., Magnone, V., Lebrigand, K., Bissels, U., Huylebroeck, D., et al. (2016) · Scientific Reports · doi:10.1038/srep35729 · Cited by 45
MiRNAs as major players in brain health and disease: current knowledge and future perspectives
Kapplingattu, S. V., Bhattacharya, S., & Adlakha, Y. K. (2025) · Cell Death Discovery · doi:10.1038/s41420-024-02283-x · Cited by 44
Müller, S. (2014) · Translational Neurodegeneration · doi:10.1186/2047-9158-3-17 · Cited by 39
Argonaute-3 activates the let-7a passenger strand microRNA
Winter, J. J., & Diederichs, S. (2013) · RNA Biology · doi:10.4161/rna.26424 · Cited by 38
Non-Coding RNAs as Potential Neuroprotectants against Ischemic Brain Injury
Kaur, P., Liu, F., Tan, J., Lim, K. J., Sepramaniam, S., Karolina, D. S., Armugam, A., & Jeyaseelan, K. (2013) · Brain Sciences · doi:10.3390/brainsci3010360 · Cited by 38
Kerschbamer, E., & Biagioli, M. (2016) · Frontiers in Neuroscience · doi:10.3389/fnins.2015.00509 · Cited by 39
Sin, O., & Nollen, E. A. A. (2015) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-015-1985-0 · Cited by 43
MicroRNAs in brain development and degeneration
Enciu, A., Popescu, B. O., & Gheorghisan-Galateanu, A. A. (2011) · Molecular Biology Reports · doi:10.1007/s11033-011-0973-1 · Cited by 37
MicroRNAs in central nervous system disorders: current advances in pathogenesis and treatment
Hussein, M., & Magdy, R. (2021) · The Egyptian Journal of Neurology Psychiatry and Neurosurgery · doi:10.1186/s41983-021-00289-1 · Cited by 37
Suster, I., & Feng, Y. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22136765 · Cited by 39
The regulatory roles of microRNAs toward pathogenesis and treatments in Huntington's disease
Tung, C.-W., Huang, P.-Y., Chan, S. C., Cheng, P., & Yang, S. (2021) · Journal of Biomedical Science · doi:10.1186/s12929-021-00755-1 · Cited by 38
MicroRNA-27a reduces mutant hutingtin aggregation in an in vitro model of Huntington's disease
Ban, J.-J., Chung, J.-Y., Lee, M., Im, W., & Kim, M. (2017) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2017.05.040 · Cited by 36
Impact of prenatal environmental stress on cortical development
Ishii, S., & Hashimoto‐Torii, K. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00207 · Cited by 38
A study of neural-related microRNAs in the developing amphioxus
Candiani, S., Moronti, L., Tonelli, D. D. P., Garbarino, G., & Pestarino, M. (2011) · EvoDevo · doi:10.1186/2041-9139-2-15 · Cited by 36
A microRNA negative feedback loop downregulates vesicle transport and inhibits fear memory
Mathew, R. S., Tatarakis, A., Rudenko, A., Johnson-Venkatesh, E. M., Yang, Y. J., Murphy, E. A., Todd, T. P., Schepers, S. T., Siuti, N., Martorell, A. J., et al. (2016) · eLife · doi:10.7554/elife.22467 · Cited by 39
Mechanisms of microRNA-132 in central neurodegenerative diseases: A comprehensive review
Mu, C., Gao, M., Xu, W., Sun, X., Chen, T., Xu, H., & Qiu, H. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.116029 · Cited by 37
MicroRNA Screening and the Quest for Biologically Relevant Targets
Eulálio, A., & Mano, M. (2015) · SLAS DISCOVERY · doi:10.1177/1087057115578837 · Cited by 37
Roese-Koerner, B., Stappert, L., Koch, P., Brüstle, O., & Borghese, L. (2013) · Current Molecular Medicine · doi:10.2174/1566524011313050003 · Cited by 35
MiR-298 Counteracts Mutant Androgen Receptor Toxicity in Spinal and Bulbar Muscular Atrophy
Pourshafie, N., Lee, P. R., Chen, K., Harmison, G. G., Bott, L. C., Katsuno, M., Sobue, G., Burnett, B. G., Fischbeck, K. H., & Rinaldi, C. (2016) · Molecular Therapy · doi:10.1038/mt.2016.13 · Cited by 35
Overexpression of miR-9 in the Nucleus Accumbens Increases Oxycodone Self-Administration
Mavrikaki, M., Anastasiadou, E., Ozdemir, R. A., Potter, D. N., Helmholz, C., Slack, F. J., & Chartoff, E. H. (2019) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyz015 · Cited by 35
Goetzl, L. M., Darbinian, N., & Merabova, N. (2019) · Prenatal Diagnosis · doi:10.1002/pd.5474 · Cited by 35
REST: Transcriptional and Epigenetic Regulator
Bithell, A. (2011) · Epigenomics · doi:10.2217/epi.10.76 · Cited by 35
Vulnerability of microRNA biogenesis in FTD–ALS
Eitan, C., & Hornstein, E. (2016) · Brain Research · doi:10.1016/j.brainres.2015.12.063 · Cited by 38
Targeting Histone Deacetylases for the Treatment of Huntington's Disease
Gray, S. G. (2010) · CNS Neuroscience & Therapeutics · doi:10.1111/j.1755-5949.2010.00184.x · Cited by 34
NRSF: an Angel or a Devil in Neurogenesis and Neurological Diseases
Song, Z., Zhao, D., Zhao, H., & Yang, L. (2014) · Journal of Molecular Neuroscience · doi:10.1007/s12031-014-0474-5 · Cited by 33
The interplay between microRNAs and histone deacetylases in neurological diseases
Bourassa, M. W., & Ratan, R. R. (2014) · Neurochemistry International · doi:10.1016/j.neuint.2014.03.012 · Cited by 34
Mulligan, M. K., DuBose, C., Yue, J., Miles, M. F., Lu, L., & Hamre, K. M. (2013) · Frontiers in Genetics · doi:10.3389/fgene.2013.00126 · Cited by 33
MicroRNAs and Ethanol Toxicity
Miranda, R. C. (2014) · International review of neurobiology · doi:10.1016/b978-0-12-801311-3.00007-x · Cited by 33
P120-catenin regulates REST/CoREST, and modulates mouse embryonic stem cell differentiation
Lee, M., Ji, H. L., Furuta, Y., Park, J., & McCrea, P. D. (2014) · Journal of Cell Science · doi:10.1242/jcs.151944 · Cited by 33
MiR-29b Protects Dorsal Root Ganglia Neurons from Diabetic Rat
Zhang, X., Gong, X., Han, S., & Zhang, Y. (2014) · Cell Biochemistry and Biophysics · doi:10.1007/s12013-014-0029-y · Cited by 33
MicroRNA Biomarkers in Neurodegenerative Diseases and Emerging Nano-Sensors Technology
Shah, P., Cho, S. K., Thulstrup, P. W., Bjerrum, M. J., Lee, P. H., Kang, J., Bhang, Y.-J., & Yang, S. W. (2017) · Journal of Movement Disorders · doi:10.14802/jmd.16037 · Cited by 33
Bergonzoni, G., Döring, J., & Biagioli, M. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.628010 · Cited by 32
Su, X., Shen, B., Wang, K., Song, Q.-X., Yang, X., Wu, D., Shen, H., & Zhu, C. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2022.834620 · Cited by 32
Chen, Y., Zhang, S., Zhao, R., Zhao, Q., & Zhang, T. (2016) · Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics · doi:10.3727/096504016x14791715355957 · Cited by 32
MicroRNAs: a symphony orchestrating evolution and disease dynamics
Quah, S., Subramanian, G., Tan, J. S. L., Utami, K. H., & Sampath, P. (2025) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2024.07.004 · Cited by 31
Astrocyte-to-neuron reprogramming and crosstalk in the treatment of Parkinson's disease
Wang, Y., Xia, Y. F., Kou, L., Yin, S., Chi, X., Li, J., Sun, Y., Wu, J., Zhou, Q., Zou, W., et al. (2023) · Neurobiology of Disease · doi:10.1016/j.nbd.2023.106224 · Cited by 33
Non-Coding RNAs as Sensors of Oxidative Stress in Neurodegenerative Diseases
Gámez‐Valero, A., Guisado-Corcoll, A., Herrero‐Lorenzo, M., Solaguren‐Beascoa, M., & Martí, E. (2020) · Antioxidants · doi:10.3390/antiox9111095 · Cited by 34
Peplow, P., & Martinez, B. (2021) · Neural Regeneration Research · doi:10.4103/1673-5374.310673 · Cited by 32
In vivo delivery of DN:REST improves transcriptional changes of REST-regulated genes in HD mice
Conforti, P., Monteys, A. M., Zuccato, C., Buckley, N. J., Davidson, B. L., & Cattaneo, E. F. (2012) · Gene Therapy · doi:10.1038/gt.2012.84 · Cited by 32
Self-citationTargeting Huntington’s disease through histone deacetylases
Gray, S. G. (2011) · Clinical Epigenetics · doi:10.1007/s13148-011-0025-7 · Cited by 32
Experimental procedures to identify and validate specific mRNA targets of miRNAs
Elton, T. S., & Yalowich, J. C. (2015) · EXCLI journal · doi:10.17179/excli2015-319 · Cited by 32
Ao, R., Wang, Y., Tong, J., & Wang, B. (2016) · Medical Science Monitor · doi:10.12659/msm.897207 · Cited by 30
Epigenetic modulation by small molecule compounds for neurodegenerative disorders
Singh, A. K., Halder-Sinha, S., Clement, J. P., & Kundu, T. K. (2018) · Pharmacological Research · doi:10.1016/j.phrs.2018.04.014 · Cited by 30
Gene regulation in adult neural stem cells. Current challenges and possible applications
Encinas, J. M., & Fitzsimons, C. P. (2017) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2017.07.016 · Cited by 32
miR‐30b protects nigrostriatal dopaminergic neurons from MPP(+)‐induced neurotoxicity via SNCA
Shen, Y., Zhu, Z., Qian, S., Xu, C., & Wang, Y. (2020) · Brain and Behavior · doi:10.1002/brb3.1567 · Cited by 29
Chu, Y., Ko, C., Wang, W., Wang, S., Gean, P., Kuo, Y., & Wang, J. (2015) · Molecular Neurobiology · doi:10.1007/s12035-015-9359-z · Cited by 29
Predicting human microRNA-disease associations based on support vector machine
Jiang, Q., Wang, G., Zhang, T., & Wang, Y. (2010) · IEEE International Conference on Bioinformatics and Biomedicine (BIBM) · doi:10.1109/bibm.2010.5706611 · Cited by 29
Willis, D. E., Wang, M., Brown, E., Fones, L., & Cave, J. W. (2015) · Neuroscience Letters · doi:10.1016/j.neulet.2015.12.003 · Cited by 29
Colicino, E., Giuliano, G., Power, M. C., Lepeule, J., Wilker, E. H., Vokonas, P., Brennan, K. J. M., Fossati, S., Hoxha, M., Spiro, A., et al. (2015) · Environment International · doi:10.1016/j.envint.2015.12.014 · Cited by 29
Neuroendocrine Key Regulator Gene Expression in Merkel Cell Carcinoma
Chteinberg, E., Sauer, C. M., Rennspiess, D., Beumers, L., Schiffelers, L. D., Eben, J., Haugg, A. M., Winnepenninckx, V. J. L., Kurz, A. K., Speel, E. M., et al. (2018) · Neoplasia · doi:10.1016/j.neo.2018.10.003 · Cited by 29
Identification of miR-9 as a negative factor of insulin secretion from beta cells
Hu, D., Wang, Y., Zhang, H., & Kong, D. (2018) · Journal of Physiology and Biochemistry · doi:10.1007/s13105-018-0615-3 · Cited by 28
Histone deacetylase in neuropathology
Gupta, R. V., Ambasta, R. K., & Kumar, P. (2020) · Advances in clinical chemistry · doi:10.1016/bs.acc.2020.09.004 · Cited by 28
Neuronal conversion from glia to replenish the lost neurons
Liang, S., Zhou, J., Yu, X., Lü, S., & Liu, R. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.386400 · Cited by 28
The Role of Epigenetics in Neurodegenerative Diseases
Lovrei, L., Maver, A., Zadel, M., & Peterli, B. (2013) · InTech eBooks · doi:10.5772/54744 · Cited by 31
Nucleic Acids in Human Glioma Treatment: Innovative Approaches and Recent Results
Catuogno, S., Esposito, C. L., Quintavalle, C., Condorelli, G., de Franciscis, V., & Cerchia, L. (2012) · Journal of Signal Transduction · doi:10.1155/2012/735135 · Cited by 28
Steadman, C. R., Labrecque, M. T., Solomon, E. R., Guo, X., & Allan, A. M. (2016) · Neurotoxicology and Teratology · doi:10.1016/j.ntt.2016.10.004 · Cited by 29
Nassar, A., Satarker, S., Gurram, P. C., Upadhya, D., Fayaz, S., & Nampoothiri, M. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03437-1 · Cited by 27
Sibley, C. R., & Wood, M. J. A. (2011) · Journal of Molecular Medicine · doi:10.1007/s00109-011-0781-z · Cited by 28
Sun, L., Yan, M., Hu, X., Peng, L.-W., Che, H., Bao, Y., Guo, F., Liu, T., Chen, X., Zhang, R., et al. (2015) · Molecular Neurodegeneration · doi:10.1186/s13024-015-0032-9 · Cited by 27
Ando, H., Hirose, M., Kurosawa, G., Impey, S., & Mikoshiba, K. (2017) · Scientific Reports · doi:10.1038/s41598-017-12879-2 · Cited by 29
The dynamic recruitment of TRBP to neuronal membranes mediates dendritogenesis during development
Antoniou, A., Khudayberdiev, S., Idziak, A., Bicker, S., Jacob, R., & Schratt, G. M. (2017) · EMBO Reports · doi:10.15252/embr.201744853 · Cited by 27
Tumor and Cerebrospinal Fluid microRNAs in Primary Central Nervous System Lymphomas
Zajdel, M., Rymkiewicz, G., Sromek, M., Cieslikowska, M., Swoboda, P., Kulińczak, M., Goryca, K., Bystydzieński, Z., Błachnio, K., Ostrowska, B., et al. (2019) · Cancers · doi:10.3390/cancers11111647 · Cited by 27
miRNA-Dependent Control of Homeostatic Plasticity in Neurons
Dubes, S., Favereaux, A., Thoumine, O. R., & Letellier, M. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00536 · Cited by 27
Exosomes and MicroRNAs in Biomedical Science
Mirzaei, H., Rahimian, N., Mirzaei, H. R., Nahand, J. S., & Hamblin, M. R. (2022) · Synthesis lectures on biomedical engineering · doi:10.2200/s01171ed1v01y202202bme062 · Cited by 27
Peripheral Biomarkers in Manifest and Premanifest Huntington’s Disease
Morena, E., Romano, C., Marconi, M., Diamant, S., Buscarinu, M. C., Bellucci, G., Romano, S., Scarabino, D., Salvetti, M., & Ristori, G. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076051 · Cited by 27
Mojtahedi, S., Kordi, M. R., Hosseini, S. E., Omran, S. F., & Soleimani, M. (2013) · Cell Biology International · doi:10.1002/cbin.10022 · Cited by 26
Nowek, K., Sun, S. M., Bullinger, L., Bindels, E. M., Exalto, C., Dijkstra, M. K., van Lom, K., Döhner, H., Erkeland, S. J., Löwenberg, B., et al. (2015) · Leukemia · doi:10.1038/leu.2015.183 · Cited by 26
Yang, H., Liu, C., Wang, C.-Y., Zhang, Q., An, J., Zhang, L., & Hao, D. (2015) · Molecular Neurobiology · doi:10.1007/s12035-015-9157-7 · Cited by 26
MiRNA as biomarker for uveitis - A systematic review of the literature
Počkar, S., Petrovič, M. G., Peterlin, B., & Valentinčič, N. V. (2019) · Gene · doi:10.1016/j.gene.2019.02.004 · Cited by 26
The Reelin (RELN) gene is associated with executive function in healthy individuals.
Baune, B. T., Konrad, C., Suslow, T., Domschke, K., Birosova, E., Sehlmeyer, C., & Beste, C. (2010) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2010.08.002 · Cited by 25
MicroRNAs in neurodegenerative disorders
Junn, E., & Mouradian, M. M. (2010) · Cell Cycle · doi:10.4161/cc.9.9.11296 · Cited by 25
Krupp, D. R., Xu, P., Thomas, S., Dellinger, A. E., Etchevers, H., Vekemans, M. J. J., Gilbert, J. R., Speer, M. C., Ashley‐Koch, A. E., & Gregory, S. G. (2012) · Birth Defects Research Part A Clinical and Molecular Teratology · doi:10.1002/bdra.23040 · Cited by 25
Circulating miRNAs: Novel Biomarkers of Acute Coronary Syndrome?
Pleister, A. P., Selemon, H., Elton, S. M., & Elton, T. S. (2013) · Biomarkers in Medicine · doi:10.2217/bmm.13.8 · Cited by 27
Chandrasekaran, S., & Bonchev, D. (2016) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2016.02.001 · Cited by 27
Bache, S., Rasmussen, R. S., Wolcott, Z. C., Rossing, M., Møgelvang, R., Tolnai, D., Hassager, C., Forman, J. L., Køber, L., Nielsen, F. C., et al. (2020) · Translational Stroke Research · doi:10.1007/s12975-020-00793-1 · Cited by 27
Varma-Doyle, A. V., Lukiw, W. J., Zhao, Y., Lovera, J. F., & Devier, D. J. (2020) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2020.117202 · Cited by 26
Yuan, L., Zhang, X., Li, L., Jiang, H., & Chen, J. (2014) · PLoS ONE · doi:10.1371/journal.pone.0115251 · Cited by 24
Non-coding RNAs and their bioengineering applications for neurological diseases
Das, T., Das, T. K., Khodarkovskaya, A., & Dash, S. (2021) · Bioengineered · doi:10.1080/21655979.2021.2003667 · Cited by 24
An emerging role for microRNAs in sexually dimorphic neurobiological systems
Pak, T. R., Rao, Y. S., Prins, S. A., & Mott, N. N. (2013) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-013-1227-y · Cited by 24
Control of cerebral size and thickness
Tuoc, T., Pavlakis, E., Tylkowski, M. A., & Stoykova, A. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1590-7 · Cited by 25
Metadata
- Authors
- Packer, A. N., Xing, Y., Harper, S. Q., Jones, L., & Davidson, B. L.
- Affiliations
- University of Iowa (US)
- Cardiff University (GB)
- Corresponding author
- Davidson, Beverly L.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-12-31
- Volume
- 28
- Issue
- 53
- Pages
- 14341-14346
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3124002
- OpenAlex
- W2001003536
- Semantic Scholar
- 8dce8a39398d97423fda523d757cbefbbd3b6468
- Cited by
- 679
- References
- 29
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 19 · 2023: 35 · 2022: 20 · 2021: 35 · 2020: 30 · 2019: 25 · 2018: 26 · 2017: 38 · 2016: 43 · 2015: 50 · 2014: 68 · 2013: 66 · 2012: 69
- FWCI
- 16.34
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- Funders
- Hereditary Disease Foundation
- National Institutes of Health
- National Institute on Drug Abuse (R21DA025132)
- National Institute of Neurological Disorders and Stroke (P01NS050210)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD044093)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- miR-9, rest, CoREST, Huntington's disease, polyglutamine expansion, huntingtin, microRNA regulation, negative feedback loop, neuronal gene expression
- MeSH terms
- RE1-Silencing Transcription Factor, Aged, Brain, Cell Line, Transformed, DNA-Binding Proteins, Dose-Response Relationship, Drug, Female, Humans, Huntington Disease, Male, Middle Aged, Nerve Tissue Proteins, Postmortem Changes, Repressor Proteins, Transfection, Down-Regulation, Disease Progression, 3' Untranslated Regions, MicroRNAs, Co-Repressor Proteins
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 2026-11-06, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-06 (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 ›
Are you an author, or do you see a problem with this page? Request a review
