ArticleJournal of cell science2011
Suppression of GSK-3β activation by M-cadherin protects myoblasts against mitochondria-associated apoptosis during myogenic differentiation.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Omega-3 fatty acid supplementation does not attenuate declines in skeletal muscle mitochondrial area in young, healthy females during immobilization.Physiological reports · 2026Article
- Planar cell polarity protein Vangl2 interacts with M-cadherin and stabilizes its cell surface expression in mouse C2C12 myoblasts.Frontiers in cell and developmental biology · 2026Article
- Development of an anti-CDH15/M-cadherin monoclonal antibody CaBiochemistry and biophysics reports · 2025Article
- Epigenetics of Skeletal Muscle-Associated Genes in theEpigenomes · 2020Article
- Diarylheptanoid 1-(4-hydroxyphenyl)-7-phenyl-(6E)-6-hepten-3-one enhances C2C12 myoblast differentiation by targeting membrane estrogen receptors and activates Akt-mTOR and p38 MAPK-NF-κB signaling axes.Journal of natural medicines · 2019Article
- Supplementation of Saponins from Leaves ofAntioxidants (Basel, Switzerland) · 2019Article
- Excess active P13K rescues huntingtin-mediated neuronal cell death but has no effect on axonal transport defects.Apoptosis : an international journal on programmed cell death · 2019Article
- A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation.PloS one · 2019Article
- Effects of hindlimb suspension and reloading on gastrocnemius and soleus muscle mass and function in geriatric mice.Experimental gerontology · 2019Article
- A tale of two niches: differential functions for VCAM-1 in satellite cells under basal and injured conditions.American journal of physiology. Cell physiology · 2017Article
- Epigallocatechin-3-gallate increases autophagy signaling in resting and unloaded plantaris muscles but selectively suppresses autophagy protein abundance in reloaded muscles of aged rats.Experimental gerontology · 2017Article
- Angiotensin-II-induced Muscle Wasting is Mediated by 25-Hydroxycholesterol via GSK3β Signaling Pathway.EBioMedicine · 2017Article
- Cardiac and mitochondrial dysfunction following acute pulmonary exposure to mountaintop removal mining particulate matter.American journal of physiology. Heart and circulatory physiology · 2015Article
- Inhibition of glycogen synthase kinase-3β attenuates glucocorticoid-induced suppression of myogenic differentiation in vitro.PloS one · 2014Article
- Netrin-1 protects hypoxia-induced mitochondrial apoptosis through HSP27 expression via DCC- and integrin α6β4-dependent Akt, GSK-3β, and HSF-1 in mesenchymal stem cells.Cell death & disease · 2013Article
- M-cadherin-inhibited phosphorylation of ß-catenin augments differentiation of mouse myoblasts.Cell and tissue research · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis occurs concurrently with differentiation of muscle progenitor cells (MPCs) before they fuse to form myotubes. Dysregulated apoptosis in MPCs contributes to the low regeneration capability in aged muscle and decreases the survival rate of donor cells in stem cell-based therapies for muscular dystrophies. This study investigated the role of the M-cadherin/PI3K/Akt/GSK-3β signaling pathway in regulating apoptosis during differentiation of MPCs. Disruption of M-cadherin-dependent cell-cell adhesion by M-cadherin RNA interference in confluent C2C12 myoblasts sensitized the cells to mitochondria-associated intrinsic apoptosis induced by cell confluence or serum starvation. Further investigation of this pathway revealed that M-cadherin-mediated signaling suppressed GSK-3β activation by enhancing the PI3K/AKT-dependent inhibitory phosphorylation of Ser9 in GSK-3β. Overexpression of wild-type GSK-3β in confluent C2C12 myoblasts exacerbated the apoptosis, whereas chemical inhibition of GSK-3β using TDZD-8, or forced expression of constitutively active Akt (myrAkt), or a kinase-deficient GSK-3β mutant [GSK-3β(K85R)], attenuated apoptosis and rescued the impaired myogenic differentiation that is caused by M-cadherin RNA interference. These data suggest that M-cadherin-mediated signaling prevents acceleration of mitochondria-associated intrinsic apoptosis in MPCs by suppressing GSK-3β activation during myogenic differentiation.
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Registered trials
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.