Evidence map›Paper›PMID 23138569›Full record

ArticleCell and tissue research2013

M-cadherin-inhibited phosphorylation of ß-catenin augments differentiation of mouse myoblasts.

Yan Wang, Junaith S Mohamed, Stephen E Alway

Open access · greenAbstract read
In one paragraph

Article in Cell and tissue research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Molecular regulation of myocyte fusion.Current topics in developmental biology · 2024
    Review
  7. Article
  8. Review
  9. The role of SIRT1 in skeletal muscle function and repair of older mice.Journal of cachexia, sarcopenia and muscle · 2019
    Article
  10. Frontiers in cellular and infection microbiology · 2019
    Article
  11. Article
  12. Article
  13. Article
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

3 authors at 1 institution in 1 country.

Yan WangLaboratory of Muscle Biology and Sarcopenia, Department of Exercise Physiology, and Center for Cardiovascular and Respiratory Sciences, Robert C. Byrd Health Sciences Center, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Junaith S Mohamed
Stephen E Alway
West Virginia University · US

Funding

THE ROLE OF HEF1 PROTEIN IN INVASION OF METASTATIC BREAST CANCERP20RR016440 · NCRR · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2001 to 2010
$22.8M
West Virginia Flow Cytometry Core FacilityP30GM103488 · NIGMS · WEST VIRGINIA UNIVERSITY · PI CUFF, CHRISTOPHER F · 2012 to 2016
$4.8M
Id2 REGULATION OF MUSCLE HYPERTROPHY IN AGINGR01AG021530 · NIA · WEST VIRGINIA UNIVERSITY · PI ALWAY, STEPHEN E · 2004 to 2007
$1.0M
NCRR NIH HHS P20 RR016440NIA NIH HHS R01 AG021530NIA NIH HHS R01AG021530NIGMS NIH HHS P30 GM103488
6 · The paper itself

Abstract

β-Catenin is essential for muscle development because it regulates both cadherin-mediated cell-cell adhesion and canonical Wingless and Int1 (Wnt) signaling. The phosphorylation of β-catenin by glycogen synthase kinase-3β (GSK-3β) at serine31/37/threonine41 regulates its stability and its role in canonical Wnt signaling. In this study, we have investigated whether the N-terminal phosphorylation of β-catenin is regulated by M-cadherin, and whether this regulation mediates the role of M-cadherin in myogenic differentiation. Our data show that the knockdown of M-cadherin expression by RNA interference (RNAi) in C2C12 myoblasts significantly increases the phosphorylation of β-catenin at Ser33/37/Thr41 and decreases the protein abundance of ser37/thr41-unphosphorylated active β-catenin. Furthermore, M-cadherin RNAi promotes TCF/LEF transcription activity but also blunts the initiation of the myogenic progress by Wnt pathway activator lithium chloride or Wnt-3a treatment. Knockdown of β-catenin expression by RNAi decreases myogenic induction in myoblasts. Forced expression of a phosphorylation-resistant β-catenin plasmid (S33Y-β-catenin) fails to enhance myogenic differentiation, but it partially rescues C2C12 cells from M-cadherin RNAi-induced apoptosis. These data show, for the first time, that M-cadherin-mediated signaling attenuates β-catenin phosphorylation at Ser31/37/Thr41 by GSK-3β, and that this regulation has a positive effect on myogenic differentiation induced by canonical Wnt signaling.

Indexed as

AnimalsApoptosisbeta CateninCadherinsCell CountCell DifferentiationCell FusionDown-RegulationFibrosisGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMiceMuscle DevelopmentMutant ProteinsMyoblastsPhenotypebeta CateninCadherinsGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseM-cadherinMutant ProteinsTCF Transcription Factors

Identifiers

PMID23138569
PMCPMC3558526
OpenAlexW2084289492

What OpenQuestion holds

Textmetadata
LicenceTDM
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.