Evidence map›Paper›PMID 24327761›Full record

ArticleScience signaling2013

Interferon-γ resets muscle cell fate by stimulating the sequential recruitment of JARID2 and PRC2 to promoters to repress myogenesis.

Priya Londhe, Judith K Davie

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. FAPs orchestrate homeostasis of muscle physiology and pathophysiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  6. Immunology of Physical Exercise: IsInternational journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. JMJD family proteins in cancer and inflammation.Signal transduction and targeted therapy · 2022
    Review
  11. All for One and One for All: Regenerating Skeletal Muscle.Cold Spring Harbor perspectives in biology · 2022
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
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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

2 authors at 1 institution in 1 country.

Priya LondheDepartment of Biochemistry and Molecular Biology and Simmons Cancer Institute, Southern Illinois University School of Medicine, Carbondale, IL 62901, USA.
Judith K Davie
Southern Illinois University Carbondale · US

Funding

Understanding the Role of the Class II Activator, CIITA, in Skeletal MuscleR15AR060017 · NIAMS · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI DAVIE, JUDITH KIMBERLY · 2011 to 2011
$393k
NIAMS NIH HHS R15 AR060017PHS HHS RAR060017A
6 · The paper itself

Abstract

The inflammatory cytokine interferon-γ (IFN-γ) orchestrates a diverse array of fundamental physiological processes. IFN-γ and the class II transactivator (CIITA) play essential roles in inhibiting muscle development during the inflammatory response. We describe the mechanism through which IFN-γ and CIITA inhibit myogenesis by repressing gene expression in muscle cells subjected to inflammation. In mice, the presence of increased amounts of circulating IFN-γ resulted in the increased abundance of Polycomb repressive complex 2 (PRC2) in muscle fibers, a tissue in which PRC2 is not normally present in the adult. We showed that CIITA first interacted with the Jumonji family protein JARID2, a noncatalytic subunit of PRC2, which caused an RNA polymerase II (RNAPII), phosphorylated at serine-5, to pause at target promoters. Additional subunits of the PRC2 complex, including the catalytic subunit EZH2, were then recruited in a JARID2-dependent manner that was concurrent with the loss of RNAPII and the methylation of Lys(27) of histone H3 (H3K27), which is associated with gene repression. IFN-γ and CIITA act to both promote the abundance of PRC2 subunits, which are not normally present during muscle differentation, and recruit the PRC2 complex to block myogenesis. Together, these data indicate that increased amounts of IFN-γ reset myogenic cell fate through a multistep mechanism that culminates in the recruitment of PRC2 to silence muscle-specific genes.

Indexed as

AnimalsBlotting, WesternCell LineEnhancer of Zeste Homolog 2 ProteinGene ExpressionHEK293 CellsHistonesHumansInterferon-gammaMethylationMuscle DevelopmentMyoblastsMyogeninNuclear ProteinsPhosphorylationPolycomb Repressive Complex 2Enhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseHistonesInterferon-gammaJarid2 protein, mouseMHC class II transactivator proteinMyogeninNuclear ProteinsPolycomb Repressive Complex 2RNA Polymerase IISerineTrans-Activators

Identifiers

PMID24327761
PMCPMC4000160
OpenAlexW2063962835

What OpenQuestion holds

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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.