Evidence map›Paper›PMID 28067271›Full record

ArticleNature communications2017

Praja1 E3 ubiquitin ligase promotes skeletal myogenesis through degradation of EZH2 upon p38α activation.

Silvia Consalvi, Arianna Brancaccio, Alessandra Dall'Agnese, Pier Lorenzo Puri, Daniela Palacios

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The roles of E3 ligases in Hepatocellular carcinoma.American journal of cancer research · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Emerging Roles of LncRNAs in the EZH2-regulated Oncogenic Network.International journal of biological sciences · 2021
    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

5 authors at 2 institutions in 2 countries.

Silvia ConsalviLaboratory of Epigenetics and Regenerative Pharmacology, IRCCS Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy.
Arianna BrancaccioLaboratory of Epigenetics and Signal Transduction, IRCCS Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy.
Alessandra Dall'AgneseSanford-Burnham-Prebys Medical Discovery Institute, Development Aging and Regeneration Program, La Jolla 92037, California, USA.
Pier Lorenzo PuriLaboratory of Epigenetics and Regenerative Pharmacology, IRCCS Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy.
Daniela PalaciosLaboratory of Epigenetics and Signal Transduction, IRCCS Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy.
Fondazione Santa Lucia · ITDiscovery Institute · US

Funding

Pathogenic Alterations of the 3D Epigenetic Landscape in Dystrophin-Deficient Skeletal Muscles and Reversal by Dystrophin Re-ExpressionR01AR056712 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI Pier Lorenzo Puri · 2009 to 2026
$7.3M
Signal-dependent switch of SWI/SNF by miRNAs & control of muscle stem cell fateR01AR052779 · NIAMS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI PURI, PIER LORENZO · 2006 to 2015
$4.1M
NIAMS NIH HHS R01 AR052779NIAMS NIH HHS R01 AR056712Worldwide Cancer Research 12-0168
6 · The paper itself

Abstract

Polycomb proteins are critical chromatin modifiers that regulate stem cell differentiation via transcriptional repression. In skeletal muscle progenitors Enhancer of zeste homologue 2 (EZH2), the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), contributes to maintain the chromatin of muscle genes in a repressive conformation, whereas its down-regulation allows the progression through the myogenic programme. Here, we show that p38α kinase promotes EZH2 degradation in differentiating muscle cells through phosphorylation of threonine 372. Biochemical and genetic evidence demonstrates that the MYOD-induced E3 ubiquitin ligase Praja1 (PJA1) is involved in regulating EZH2 levels upon p38α activation. EZH2 premature degradation in proliferating myoblasts is prevented by low levels of PJA1, its cytoplasmic localization and the lower activity towards unphosphorylated EZH2. Our results indicate that signal-dependent degradation of EZH2 is a prerequisite for satellite cells differentiation and identify PJA1 as a new player in the epigenetic control of muscle gene expression.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsCell LineEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticFibroblastsHEK293 CellsHumansMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 14Muscle DevelopmentMuscle, SkeletalPhosphorylationProtein StabilityEnhancer of Zeste Homolog 2 ProteinEzh2 protein, mouseMitogen-Activated Protein Kinase 14Pja1 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID28067271
PMCPMC5423270
OpenAlexW2569474304

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.