Evidence map›Paper›PMID 25755281›Full record

ArticleMolecular and cellular biology2015

WNT/β-Catenin Signaling Regulates Multiple Steps of Myogenesis by Regulating Step-Specific Targets.

Akiko Suzuki, Richard C Pelikan, Junichi Iwata

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

48 citing papers in PubMed, 78 citations in OpenAlex.

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  10. Secreted ADAMTS-like 2 promotes myoblast differentiation by potentiating WNT signaling.Matrix biology : journal of the International Society for Matrix Biology · 2023
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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

3 authors at 2 institutions in 1 country.

Akiko SuzukiDepartment of Diagnostic and Biomedical Sciences, The University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA Center for Craniofacial Research, The University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Richard C PelikanCenter for Craniofacial Research, The University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA.
Junichi IwataDepartment of Diagnostic and Biomedical Sciences, The University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA Center for Craniofacial Research, The University of Texas Health Science Center at Houston School of Dentistry, Houston, Texas, USA The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas, USA junichi.iwata@uth.tmc.edu.
The University of Texas Health Science Center at Houston · USUniversity of Houston · US

Funding

Role of WNT Signaling in Craniofacial Muscle DevelopmentR03DE024759 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI IWATA, JUNICHI · 2015 to 2016
$231k
NIDCR NIH HHS R03 DE024759
6 · The paper itself

Abstract

Molecules involved in WNT/β-catenin signaling show specific spatiotemporal expression and play vital roles in myogenesis; however, it is still largely unknown how WNT/β-catenin signaling regulates each step of myogenesis. Here, we show that WNT/β-catenin signaling can control diverse biological processes of myogenesis by regulating step-specific molecules. In order to identify the temporally specific roles of WNT/β-catenin signaling molecules in muscle development and homeostasis, we used in vitro culture systems for both primary mouse myoblasts and C2C12 cells, which can differentiate into myofibers. We found that a blockade of WNT/β-catenin signaling in the proliferating cells decreases proliferation activity, but does not induce cell death, through the regulation of genes cyclin A2 (Ccna2) and cell division cycle 25C (Cdc25c). During muscle differentiation, the inhibition of WNT/β-catenin signaling blocks myoblast fusion through the inhibition of the Fermitin family homolog 2 (Fermt2) gene. Blocking WNT/β-catenin signaling in the well-differentiated myofibers results in the failure of maintenance of their structure by disruption of cadherin/β-catenin/actin complex formation, which plays a crucial role in connecting a myofiber's cytoskeleton to the surrounding extracellular matrix. Thus, our results indicate that WNT/β-catenin signaling can regulate multiple steps of myogenesis, including cell proliferation, myoblast fusion, and homeostasis, by targeting step-specific molecules.

Indexed as

Muscle DevelopmentWnt Signaling PathwayAnimalscdc25 PhosphatasesCell DifferentiationCell LineCell ProliferationCells, CulturedCyclin A2HomeostasisMembrane ProteinsMiceMice, Inbred C57BLMyoblastsTongueCCNA2 protein, mouseCdc25c protein, mousecdc25 PhosphatasesCyclin A2Membrane Proteins

Identifiers

PMID25755281
PMCPMC4405648
OpenAlexW2115629296

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.