Evidence map›Paper›PMID 31044068›Full record

ArticleCell & bioscience2019

Emerin anchors Msx1 and its protein partners at the nuclear periphery to inhibit myogenesis.

Zhangjing Ma, Huiyuan Shi, Yi Shen, Huixia Li, Yu Yang, Jiange Yang, Hui Zhao, Gang Wang, Jingqiang Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. The role of inner nuclear membrane protein emerin in myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Zhangjing Ma *1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Huiyuan Shi *1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Yi Shen1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Huixia Li1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Yu Yang1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Jiange Yang1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Hui ZhaoZhengzhou Revogene Inc, Zhengzhou, 450000 People's Republic of China.
Gang Wang1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.
Jingqiang Wang1State Key Laboratory of Genetic Engineering and Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Zhongshan Hospital, Fudan University, Shanghai, 200438 People's Republic of China.ORCID 0000-0001-9909-6441
Fudan University · CNChinese Academy of Sciences · CNZhengzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPrevious studies have shown that in myogenic precursors, the homeoprotein Msx1 and its protein partners, histone methyltransferases and repressive histone marks, tend to be enriched on target myogenic regulatory genes at the nuclear periphery. The nuclear periphery localization of Msx1 and its protein partners is required for Msx1's function of preventing myogenic precursors from pre-maturation through repressing target myogenic regulatory genes. However, the mechanisms underlying the maintenance of Msx1 and its protein partners' nuclear periphery localization are unknown.

resultsWe show that an inner nuclear membrane protein, Emerin, performs as an anchor settled at the inner nuclear membrane to keep Msx1 and its protein partners Ezh2, H3K27me3 enriching at the nuclear periphery, and participates in inhibition of myogenesis mediated by Msx1. Msx1 interacts with Emerin both in C2C12 myoblasts and mouse developing limbs, which is the prerequisite for Emerin mediating the precise location of Msx1, Ezh2, and H3K27me3. The deficiency of Emerin in C2C12 myoblasts disturbs the nuclear periphery localization of Msx1, Ezh2, and H3K27me3, directly indicating Emerin functioning as an anchor. Furthermore, Emerin cooperates with Msx1 to repress target myogenic regulatory genes, and assists Msx1 with inhibition of myogenesis.

conclusionsEmerin cooperates with Msx1 to inhibit myogenesis through maintaining the nuclear periphery localization of Msx1 and Msx1's protein partners.

Indexed as

EmerinEzh2H3K27me3Msx1MyogenesisNuclear-periphery

Identifiers

PMID31044068
PMCPMC6460851
OpenAlexW2939852171

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.