ArticleMolecular and cellular biology2006
Regulation of the M-cadherin-beta-catenin complex by calpain 3 during terminal stages of myogenic differentiation.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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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.
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.
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Who cites it
33 citing papers in PubMed, 58 citations in OpenAlex.
- Calpainopathy (limb-girdle muscular dystrophy type R1): clinical features, diagnostic approaches, and biotechnological treatment methods.Journal of neuromuscular diseases · 2025Review
- Article
- Article
- The double homeodomain protein DUX4c is associated with regenerating muscle fibers and RNA-binding proteins.Skeletal muscle · 2023Article
- CAPN3: A muscle‑specific calpain with an important role in the pathogenesis of diseases (Review).International journal of molecular medicine · 2021Review
- Current and Future Therapeutic Strategies for Limb Girdle Muscular Dystrophy Type R1: Clinical and Experimental Approaches.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- A Small-Molecule Approach to Restore a Slow-Oxidative Phenotype and Defective CaMKIIβ Signaling in Limb Girdle Muscular Dystrophy.Cell reports. Medicine · 2020Article
- Calcium Mechanisms in Limb-Girdle Muscular Dystrophy withInternational journal of molecular sciences · 2019Review
- The Trithorax protein Ash1L promotes myoblast fusion by activating Cdon expression.Nature communications · 2018Article
- Overexpression of the double homeodomain protein DUX4c interferes with myofibrillogenesis and induces clustering of myonuclei.Skeletal muscle · 2018Article
- Cathepsin S Contributes to the Pathogenesis of Muscular Dystrophy in Mice.The Journal of biological chemistry · 2016Article
- Calpain-3 impairs cell proliferation and stimulates oxidative stress-mediated cell death in melanoma cells.PloS one · 2015Article
- The N- and C-terminal autolytic fragments of CAPN3/p94/calpain-3 restore proteolytic activity by intermolecular complementation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Transiently active Wnt/β-catenin signaling is not required but must be silenced for stem cell function during muscle regeneration.Stem cell reports · 2014Article
- PLEIAD/SIMC1/C5orf25, a novel autolysis regulator for a skeletal-muscle-specific calpain, CAPN3, scaffolds a CAPN3 substrate, CTBP1.Journal of molecular biology · 2013Article
- A New Insight into the Role of Calpains in Post-mortem Meat Tenderization in Domestic Animals: A review.Asian-Australasian journal of animal sciences · 2013Review
- Calpain induces N-terminal truncation of β-catenin in normal murine liver development: diagnostic implications in hepatoblastomas.The Journal of biological chemistry · 2012Article
- Satellite cell senescence underlies myopathy in a mouse model of limb-girdle muscular dystrophy 2H.The Journal of clinical investigation · 2012Article
- Toxoplasma gondii down modulates cadherin expression in skeletal muscle cells inhibiting myogenesis.BMC microbiology · 2011Article
- Segregation of myoblast fusion and muscle-specific gene expression by distinct ligand-dependent inactivation of GSK-3β.Cellular and molecular life sciences : CMLS · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The cysteine protease calpain 3 (CAPN3) is essential for normal muscle function, since mutations in CAPN3 cause limb girdle muscular dystrophy type 2A. Previously, we showed that myoblasts isolated from CAPN3 knockout (C3KO) mice were able to fuse to myotubes; however, sarcomere formation was disrupted. In this study we further characterized morphological and biochemical features of C3KO myotubes in order to elucidate a role for CAPN3 during myogenesis. We showed that cell cycle withdrawal occurred normally in C3KO cultures, but C3KO myotubes have an increased number of myonuclei per myotube. We found that CAPN3 acts during myogenesis to specifically control levels of membrane-associated but not cytoplasmic beta-catenin and M-cadherin. CAPN3 was able to cleave both proteins, and in the absence of CAPN3, M-cadherin and beta-catenin abnormally accumulated at the membranes of myotubes. Given the role of M-cadherin in myoblast fusion, this finding suggests that the excessive myonuclear index of C3KO myotubes was due to enhanced fusion. Postfusion events, such as beta1D integrin expression and myofibrillogenesis, were suppressed in C3KO myotubes. These data suggest that the persistence of fusion observed in C3KO cells inhibits subsequent steps of differentiation, such as integrin complex rearrangements and sarcomere assembly.
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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.