Evidence map›Paper›PMID 22106411›Full record

ArticleMolecular and cellular biology2012

Protein tyrosine phosphatase-like A regulates myoblast proliferation and differentiation through MyoG and the cell cycling signaling pathway.

Xi Lin, Xiangsheng Yang, Qi Li, Yanlin Ma, Shuang Cui, Dacheng He, Xia Lin, Robert J Schwartz, Jiang Chang

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  6. Life science alliance · 2020
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  16. Genetic deletion of Rnd3 results in aqueductal stenosis leading to hydrocephalus through up-regulation of Notch signaling.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  17. Article
  18. Mechanism of fibrotic cardiomyopathy in mice expressing truncated Rho-associated coiled-coil protein kinase 1.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Xi LinTexas A&M Health Science Center, Institute of Biosciences and Technology, Houston, Texas, USA.
Xiangsheng Yang
Qi Li
Yanlin Ma
Shuang Cui
Dacheng He
Xia Lin
Robert J Schwartz
Jiang Chang
Baylor College of Medicine · USBeijing Normal University · CNTexas A&M Health Science Center · USUniversity of Houston · US

Funding

Fibrogenic Role of ROCK delta1 and Mechanism in Cardiac RemodelingR01HL102314 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$1.8M
Mechanism of SRF-N-mediated Cardiac SuppressionK02HL098956 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2014
$471k
Mechanistic Study of Cleaved Serum Response Factor in Cardiac HypertrophyR21HL094844 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI CHANG, JIANG · 2010 to 2011
$403k
NHLBI NIH HHS K02 HL098956NHLBI NIH HHS K02HL098956NHLBI NIH HHS R01 HL102314NHLBI NIH HHS R01HL102314NHLBI NIH HHS R21 HL094844NHLBI NIH HHS R21HL094844
6 · The paper itself

Abstract

Protein tyrosine phosphatase-like A (PTPLa) has been implicated in skeletal myogenesis and cardiogenesis. Mutations in PTPLa correlated with arrhythmogenic right ventricular dysplasia in humans and congenital centronuclear myopathy with severe hypotonia in dogs. The molecular mechanisms of PTPLa in myogenesis are unknown. In this report, we demonstrate that PTPLa is required for myoblast growth and differentiation. The cells lacking PTPLa remained immature and failed to differentiate into mature myotubes. The repressed MyoG expression was responsible for the impaired myoblast differentiation. Meanwhile, impeded cell growth, with an obvious S-phase arrest and compromised G(2)/M transition, was observed in PTPLa-deficient myoblasts. Further study demonstrated that the upregulation of cyclin D1 and cyclin E2 complexes, along with a compromised G(2)/M transition due to the decreased CDK1 (cyclin-dependent kinase 1) activity and upregulated p21, contributed to the mutant cell S-phase arrest and eventually led to the retarded cell growth. Finally, the transcriptional regulation of the PTPLa gene was explored. We identified PTPLa as a new target gene of the serum response factor (SRF). Skeletal- and cardiac-muscle-specific SRF knockouts resulted in significant decreases in PTPLa expression, suggesting a conserved transcriptional regulation of the PTPLa gene in mice.

Indexed as

Signal TransductionAnimalsCell CycleCell DifferentiationCell LineCell ProliferationGene Expression RegulationMiceMice, KnockoutMuscle, SkeletalMyoblastsMyocardiumMyogeninProtein Tyrosine PhosphatasesSerum Response FactorHacd1 protein, mouseMyogeninMyog protein, mouseProtein Tyrosine PhosphatasesSerum Response Factor

Identifiers

PMID22106411
PMCPMC3255775
OpenAlexW2110117164

What OpenQuestion holds

Textmetadata
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.