Evidence map›Paper›PMID 22847234›Full record

ArticleJournal of molecular cell biology2012

Comparative expression profiling identifies differential roles for Myogenin and p38α MAPK signaling in myogenesis.

Qi-Cai Liu, Xiao-Hui Zha, Hervé Faralli, Hang Yin, Caroline Louis-Jeune, Eusebio Perdiguero, Erinija Pranckeviciene, Pura Muñoz-Cànoves, Michael A Rudnicki, Marjorie Brand and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of molecular cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.1field-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

46 citing papers in PubMed, 77 citations in OpenAlex.

  1. Trial
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  7. Review
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  9. Article
  10. A dysfunctional miR-1-TRPS1-MYOG axis drives ERMS by suppressing terminal myogenic differentiation.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. The synaptosome-associated protein 23 (SNAP23) is necessary for proper myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. The Phosphonate Derivative of CInternational journal of molecular sciences · 2021
    Article
  19. Review
  20. Article
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

12 authors at 5 institutions in 3 countries.

Qi-Cai LiuSprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, ON, Canada K1H 8L6.
Xiao-Hui Zha
Hervé Faralli
Hang Yin
Caroline Louis-Jeune
Eusebio Perdiguero
Erinija Pranckeviciene
Pura Muñoz-Cànoves
Michael A Rudnicki
Marjorie Brand
Carol Perez-Iratxeta
F Jeffrey Dilworth
Ottawa Hospital · CAOttawa Hospital Research InstituteInstitute for Stem Cell Biology and Regenerative Medicine · INPompeu Fabra University · ESUniversity of Ottawa · CA

Funding

GENETIC REGULATION OF SKELETAL MUSCLE REPAIRR01AR044031 · NIAMS · OTTAWA HOSPITAL RESEARCH INSTITUTE · PI RUDNICKI, MICHAEL A · 1996 to 2025
$5.6M
CIHR MOP-93777NIAMS NIH HHS R01 AR044031
6 · The paper itself

Abstract

Skeletal muscle differentiation is mediated by a complex gene expression program requiring both the muscle-specific transcription factor Myogenin (Myog) and p38α MAPK (p38α) signaling. However, the relative contribution of Myog and p38α to the formation of mature myotubes remains unknown. Here, we have uncoupled the activity of Myog from that of p38α to gain insight into the individual roles of these proteins in myogenesis. Comparative expression profiling confirmed that Myog activates the expression of genes involved in muscle function. Furthermore, we found that in the absence of p38α signaling, Myog expression leads to the down-regulation of genes involved in cell cycle progression. Consistent with this, the expression of Myog is sufficient to induce cell cycle exit. Interestingly, p38α-defective, Myog-expressing myoblasts fail to form multinucleated myotubes, suggesting an important role for p38α in cell fusion. Through the analysis of p38α up-regulated genes, the tetraspanin CD53 was identified as a candidate fusion protein, a role confirmed both ex vivo in primary myoblasts, and in vivo during myofiber regeneration in mice. Thus, our study has revealed an unexpected role for Myog in mediating cell cycle exit and has identified an essential role for p38α in cell fusion through the up-regulation of CD53.

Indexed as

AnimalsCell CycleCell DifferentiationCell FusionCell LineCell ProliferationDown-RegulationGene ExpressionMiceMicroRNAsMitogen-Activated Protein Kinase 14Muscle DevelopmentMuscle Fibers, SkeletalMyoblasts, SkeletalMyogeninRegenerationCd53 protein, mouseMicroRNAsMirn20 microRNA, mouseMitogen-Activated Protein Kinase 14MyogeninMyog protein, mouseTetraspanin 25

Identifiers

PMID22847234
PMCPMC4580549
OpenAlexW2100814682

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.