Evidence map›Paper›PMID 21868385›Full record

ArticleThe Journal of biological chemistry2011

miR-155 inhibits expression of the MEF2A protein to repress skeletal muscle differentiation.

Hee Young Seok, Mariko Tatsuguchi, Thomas E Callis, Aibin He, William T Pu, Da-Zhi Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
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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 3 institutions in 1 country.

Hee Young SeokDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115; Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599.
Mariko TatsuguchiDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115.
Thomas E CallisDepartment of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599.
Aibin HeDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115.
William T PuDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115.
Da-Zhi WangDepartment of Cardiology, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts 02115; Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599. Electronic address: dwang@enders.tch.harvard.edu.
Boston Children's Hospital · USHarvard University · USUniversity of North Carolina at Chapel Hill · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNAs (miRNAs) are 21-23-nucleotide non-coding RNAs. It has become more and more evident that this class of small RNAs plays critical roles in the regulation of gene expression at the post-transcriptional level. MEF2A is a member of the MEF2 (myogenic enhancer factor 2) family of transcription factors. Prior report showed that the 3'-untranslated region (3'-UTR) of the Mef2A gene mediated its repression; however, the molecular mechanism underlying this intriguing observation was unknown. Here, we report that MEF2A is repressed by miRNAs. We identify miR-155 as one of the primary miRNAs that significantly represses the expression of MEF2A. We show that knockdown of the Mef2A gene by siRNA impairs myoblast differentiation. Similarly, overexpression of miR-155 leads to the repression of endogenous MEF2A expression and the inhibition of myoblast differentiation. Most importantly, reintroduction of MEF2A in miR-155 overexpressed myoblasts was able to partially rescue the miR-155-induced myoblast differentiation defect. Our data therefore establish miR-155 as an important regulator of MEF2A expression and uncover its function in muscle gene expression and myogenic differentiation.

Indexed as

3' Untranslated RegionsAnimalsCell DifferentiationChlorocebus aethiopsCOS CellsGene Expression RegulationHumansMEF2 Transcription FactorsMiceMicroRNAsMuscle, SkeletalMyoblasts, SkeletalMyogenic Regulatory Factors3' Untranslated RegionsMef2a protein, mouseMEF2 Transcription FactorsMicroRNAsMirn155 microRNA, mouseMyogenic Regulatory Factors

Identifiers

PMID21868385
PMCPMC3195620
OpenAlexW2030551062

What OpenQuestion holds

Textmetadata
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.