Evidence map›Paper›PMID 20026657›Full record

ArticleThe Journal of cell biology2009

p38-{gamma}-dependent gene silencing restricts entry into the myogenic differentiation program.

Mark A Gillespie, Fabien Le Grand, Anthony Scimè, Shihuan Kuang, Julia von Maltzahn, Vanessa Seale, Ana Cuenda, Jeffrey A Ranish, Michael A Rudnicki

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

64 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Muscle cell-derived Ccl8 is a negative regulator of skeletal muscle regeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  6. Article
  7. Review
  8. P38 kinase in gastrointestinal cancers.Cancer gene therapy · 2023
    Review
  9. Review
  10. Review
  11. Regulation of muscle stem cell fate.Cell regeneration (London, England) · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. p38 MAPK Pathway in the Heart: New Insights in Health and Disease.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. The p38 Pathway: From Biology to Cancer Therapy.International journal of molecular sciences · 2020
    Review
  19. Article
  20. p38γ MAPK contributes to left ventricular remodeling after pathologic stress and disinhibits calpain through phosphorylation of calpastatin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article

4 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Mark A GillespieThe Sprott Centre for Stem Cell Research, Ottawa Health Research Institute, Ontario, Canada.
Fabien Le Grand
Anthony Scimè
Shihuan Kuang
Julia von Maltzahn
Vanessa Seale
Ana Cuenda
Jeffrey A Ranish
Michael A Rudnicki
Stem Cell Network · CAConsejo Superior de Investigaciones Científicas · ESInstitute for Systems Biology · USUniversity of Ottawa · CA

Funding

Canadian Institutes of Health Research MOP12080
6 · The paper itself

Abstract

The mitogen-activated protein kinase p38-gamma is highly expressed in skeletal muscle and is associated with the dystrophin glycoprotein complex; however, its function remains unclear. After induced damage, muscle in mice lacking p38-gamma generated significantly fewer myofibers than wild-type muscle. Notably, p38-gamma-deficient muscle contained 50% fewer satellite cells that exhibited premature Myogenin expression and markedly reduced proliferation. We determined that p38-gamma directly phosphorylated MyoD on Ser199 and Ser200, which results in enhanced occupancy of MyoD on the promoter of myogenin together with markedly decreased transcriptional activity. This repression is associated with extensive methylation of histone H3K9 together with recruitment of the KMT1A methyltransferase to the myogenin promoter. Notably, a MyoD S199A/S200A mutant exhibits markedly reduced binding to KMT1A. Therefore, p38-gamma signaling directly induces the assembly of a repressive MyoD transcriptional complex. Together, these results establish a hitherto unappreciated and essential role for p38-gamma signaling in positively regulating the expansion of transient amplifying myogenic precursor cells during muscle growth and regeneration.

Indexed as

Gene SilencingAnimalsCell DifferentiationCell LineCell ProliferationEpigenesis, GeneticGene Expression RegulationHistonesMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 12Muscle DevelopmentMuscle, SkeletalMyoD ProteinMyogeninPhosphorylationHistonesMitogen-Activated Protein Kinase 12MyoD1 myogenic differentiation proteinMyoD ProteinMyogenin

Identifiers

PMID20026657
PMCPMC2806273
OpenAlexW2136285175

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.