Evidence map›Paper›PMID 31243342›Full record

ArticleCell death and differentiation2020

Prmt7 promotes myoblast differentiation via methylation of p38MAPK on arginine residue 70.

Hyeon-Ju Jeong, Sang-Jin Lee, Hye-Jin Lee, Hye-Been Kim, Tuan Anh Vuong, Hana Cho, Gyu-Un Bae, Jong-Sun Kang

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  5. KDM5D histone demethylase mediates p38α inactivation via its enzymatic activity to inhibit cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Epigenetic control of skeletal muscle atrophy.Cellular & molecular biology letters · 2024
    Review
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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

8 authors at 2 institutions in 1 country.

Hyeon-Ju Jeong *Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Sang-Jin Lee *Drug Information Research Institute, College of Pharmacy, Sookmyung Women's University, Seoul, 04310, Republic of Korea.
Hye-Jin LeeDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Hye-Been KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Tuan Anh VuongDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Hana ChoDepartment of Physiology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea.
Gyu-Un BaeDrug Information Research Institute, College of Pharmacy, Sookmyung Women's University, Seoul, 04310, Republic of Korea. gbae@sookmyung.ac.kr.
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Single Cell Network Research Center, Sungkyunkwan University, Suwon, 16419, Republic of Korea. Kangj01@skku.edu.
Sungkyunkwan University · KRSookmyung Women's University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MyoD functions as a master regulator to induce muscle-specific gene expression and myogenic differentiation. Here, we demonstrate a positive role of Protein arginine methyltransferase 7 (Prmt7) in MyoD-mediated myoblast differentiation through p38MAPK activation. Prmt7 depletion in primary or C2C12 myoblasts impairs cell cycle withdrawal and myogenic differentiation. Furthermore, Prmt7 depletion decreases the MyoD-reporter activities and the MyoD-mediated myogenic conversion of fibroblasts. Together with MyoD, Prmt7 is recruited to the Myogenin promoter region and Prmt7 depletion attenuates the recruitment of MyoD and its coactivators. The mechanistic study reveals that Prmt7 methylates p38MAPKα at the arginine residue 70, thereby promoting its activation which in turn enhances MyoD activities. The arginine residue 70 to alanine mutation in p38MAPKα impedes MyoD/E47 heterodimerization and the recruitment of Prmt7, MyoD and Baf60c to the Myogenin promoter resulting in blunted Myogenin expression. In conclusion, Prmt7 promotes MyoD-mediated myoblast differentiation through methylation of p38MAPKα at arginine residue 70.

Indexed as

AnimalsArginineCell DifferentiationMethylationMiceMice, KnockoutMyoblastsp38 Mitogen-Activated Protein KinasesProtein-Arginine N-MethyltransferasesArgininep38 Mitogen-Activated Protein KinasesPRMT7 protein, mouseProtein-Arginine N-Methyltransferases

Identifiers

PMID31243342
PMCPMC7206020
OpenAlexW2954097226

What OpenQuestion holds

Textmetadata
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.