Evidence map›Paper›PMID 24984191›Full record

ArticleTranslational psychiatry2014

Transcriptional targets of the schizophrenia risk gene MIR137.

A L Collins, Y Kim, R J Bloom, S N Kelada, P Sethupathy, P F Sullivan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Translational psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Review
  5. The evolutionarily conserved miRNA-137 targets the neuropeptide hypocretin/orexin and modulates the wake to sleep ratio.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  12. The role of polygenic risk score gene-set analysis in the context of the omnigenic model of schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
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  15. A comprehensive review of the genetic and biological evidence supports a role for MicroRNA-137 in the etiology of schizophrenia.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2018
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

A L CollinsDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Y KimDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
R J BloomDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
S N KeladaDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
P SethupathyDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
P F Sullivan1] Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA [2] Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWAS) have strongly implicated MIR137 (the gene encoding the microRNA miR-137) in schizophrenia. A parsimonious hypothesis is that a pathway regulated by miR-137 is important in the etiology of schizophrenia. Full evaluation of this hypothesis requires more definitive knowledge about biological targets of miR-137, which is currently lacking. Our goals were to expand knowledge of the biology of miR-137 by identifying its empirical targets, and to test whether the resulting lists of direct and indirect targets were enriched for genes and pathways involved in risk for schizophrenia. We overexpressed miR-137 in a human neural stem cell line and analyzed gene expression changes at 24 and 48 h using RNA sequencing. Following miR-137 overexpression, 202 and 428 genes were differentially expressed after 24 and 48 h. Genes differentially expressed at 24 h were enriched for transcription factors and cell cycle genes, and differential expression at 48 h affected a wider variety of pathways. Pathways implicated in schizophrenia were upregulated in the 48 h findings (major histocompatibility complex, synapses, FMRP interacting RNAs and calcium channels). Critically, differentially expressed genes at 48 h were enriched for smaller association P-values in the largest published schizophrenia GWAS. This work provides empirical support for a role of miR-137 in the etiology of schizophrenia.

Indexed as

Cell LineGene ExpressionGenome-Wide Association StudyHumansMicroRNAsNeural Stem CellsSchizophreniaSequence Analysis, RNATranscription FactorsMicroRNAsMIRN137 microRNA, humanTranscription Factors

Identifiers

PMID24984191
PMCPMC4080323
OpenAlexW1970654007

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.