ArticleHuman molecular genetics2008
Novel role of calpain-3 in the triad-associated protein complex regulating calcium release in skeletal muscle.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 99 citations in OpenAlex.
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- Left ventricular myocardial molecular profile of human diabetic ischaemic cardiomyopathy.EMBO molecular medicine · 2025Article
- Calpainopathy (limb-girdle muscular dystrophy type R1): clinical features, diagnostic approaches, and biotechnological treatment methods.Journal of neuromuscular diseases · 2025Review
- Anti-ALDOA antibody: a novel diagnostic-associated autoantibody in myasthenia gravis.Frontiers in neurology · 2025Article
- Muscular Dystrophies.Advances in experimental medicine and biology · 2025Review
- Dantrolene-Responsive Muscle Stiffness in a Patient With a Normal Neurologic Exam and EMG: A Case Report.Case reports in neurological medicine · 2025Article
- Loss of Calpain 3 dysregulates store-operated calcium entry and its exercise response in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Human calpain-3 and its structural plasticity: dissociation of a homohexamer into dimers on binding titin.bioRxiv : the preprint server for biology · 2024Article
- A knock down strategy for rapid, generic, and versatile modelling of muscular dystrophies in 3D-tissue-engineered-skeletal muscle.Skeletal muscle · 2024Article
- Loss of calpain 3 dysregulates store-operated calcium entry and its exercise response in mice.bioRxiv : the preprint server for biology · 2024Article
- Calpain-3 Is Not a Sodium Dependent Protease and Simply Requires Calcium for Activation.International journal of molecular sciences · 2023Article
- Cas9-induced single cut enables highly efficient and template-free repair of a muscular dystrophy causing founder mutation.Molecular therapy. Nucleic acids · 2023Article
- Skeletal and cardiac muscle calcium transport regulation in health and disease.Bioscience reports · 2022Review
- Article
- Targeting the Ubiquitin-Proteasome System in Limb-Girdle Muscular Dystrophy With CAPN3 Mutations.Frontiers in cell and developmental biology · 2022Article
- CAPN3: A muscle‑specific calpain with an important role in the pathogenesis of diseases (Review).International journal of molecular medicine · 2021Review
- Molecular and cellular basis of genetically inherited skeletal muscle disorders.Nature reviews. Molecular cell biology · 2021Review
- Systemic delivery of AAVrh74.tMCK.hCAPN3 rescues the phenotype in a mouse model for LGMD2A/R1.Molecular therapy. Methods & clinical development · 2021Article
- Preferent Diaphragmatic Involvement in TK2 Deficiency: An Autopsy Case Study.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Calpain-3 (CAPN3) is a non-lysosomal cysteine protease that is necessary for normal muscle function, as mutations in CAPN3 result in an autosomal recessive form of limb girdle muscular dystrophy type 2A. To elucidate the biological roles of CAPN3 in skeletal muscle, we performed a search for potential substrates and interacting partners. By yeast-two-hybrid analysis we identified the glycolytic enzyme aldolase A (AldoA) as a binding partner of CAPN3. In co-expression studies CAPN3 degraded AldoA; however, no accumulation of AldoA was observed in total extracts from CAPN3-deficient muscles suggesting that AldoA is not an in vivo substrate of CAPN3. Instead, we found CAPN3 to be necessary for recruitment of AldoA to one specific location, namely the triads, which are structural components of muscle responsible for calcium transport and excitation-contraction coupling. Both aldolase and CAPN3 are present in the triad-enriched fraction and are able to interact with ryanodine receptors (RyR) that form major calcium release channels. Levels of triad-associated AldoA and RyR were decreased in CAPN3-deficient muscles compared with wild-type. Consistent with these observations we found calcium release to be significantly reduced in fibers from CAPN3-deficient muscles. Together, these data suggest that CAPN3 is necessary for the structural integrity of the triad-associated protein complex and that impairment of calcium transport is a phenotypic feature of CAPN3-deficient muscle.
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