Evidence map›Paper›PMID 26275053›Full record

ArticlePLoS genetics2015

Runx1 Transcription Factor Is Required for Myoblasts Proliferation during Muscle Regeneration.

Kfir Baruch Umansky, Yael Gruenbaum-Cohen, Michael Tsoory, Ester Feldmesser, Dalia Goldenberg, Ori Brenner, Yoram Groner

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

57 citing papers in PubMed, 88 citations in OpenAlex.

  1. Targeting Runx1 Slows Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  10. Zfp697 is an RNA-binding protein that regulates skeletal muscle inflammation and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  19. Phosphodiesterase 5a Signalling in Skeletal Muscle Pathophysiology.International journal of molecular sciences · 2022
    Article
  20. Review
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

7 authors at 1 institution in 1 country.

Kfir Baruch UmanskyDepartment of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Yael Gruenbaum-CohenDepartment of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Michael TsooryDepartment of Veterinary Resources, The Weizmann Institute of Science, Rehovot, Israel.
Ester FeldmesserGrand Israel National Center for Personalized Medicine (INCPM), The Weizmann Institute of Science, Rehovot, Israel.
Dalia GoldenbergDepartment of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Ori BrennerDepartment of Veterinary Resources, The Weizmann Institute of Science, Rehovot, Israel.
Yoram GronerDepartment of Molecular Genetics, The Weizmann Institute of Science, Rehovot, Israel.
Weizmann Institute of Science · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following myonecrosis, muscle satellite cells proliferate, differentiate and fuse, creating new myofibers. The Runx1 transcription factor is not expressed in naïve developing muscle or in adult muscle tissue. However, it is highly expressed in muscles exposed to myopathic damage yet, the role of Runx1 in muscle regeneration is completely unknown. Our study of Runx1 function in the muscle's response to myonecrosis reveals that this transcription factor is activated and cooperates with the MyoD and AP-1/c-Jun transcription factors to drive the transcription program of muscle regeneration. Mice lacking dystrophin and muscle Runx1 (mdx-/Runx1f/f), exhibit impaired muscle regeneration leading to age-dependent muscle waste, gradual decrease in motor capabilities and a shortened lifespan. Runx1-deficient primary myoblasts are arrested at cell cycle G1 and consequently differentiate. Such premature differentiation disrupts the myoblasts' normal proliferation/differentiation balance, reduces the number and size of regenerating myofibers and impairs muscle regeneration. Our combined Runx1-dependent gene expression, ChIP-seq, ATAC-seq and histone H3K4me1/H3K27ac modification analyses revealed a subset of Runx1-regulated genes that are co-occupied by MyoD and c-Jun in mdx-/Runx1f/f muscle. The data provide unique insights into the transcriptional program driving muscle regeneration and implicate Runx1 as an important participant in the pathology of muscle wasting diseases.

Indexed as

RegenerationAnimalsBase SequenceBinding SitesCell DifferentiationCell ProliferationCells, CulturedConsensus SequenceCore Binding Factor Alpha 2 SubunitFemaleGene ExpressionGene Expression RegulationGenes, junMaleMice, Inbred mdxMuscle, SkeletalCore Binding Factor Alpha 2 SubunitMyoD1 myogenic differentiation proteinMyoD ProteinRunx1 protein, mouse

Identifiers

PMID26275053
PMCPMC4537234
OpenAlexW1586675360

What OpenQuestion holds

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LicenceCC BY
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.