ArticleThe Journal of biological chemistry2015
Autolytic activation of calpain 3 proteinase is facilitated by calmodulin protein.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Defining Haplosufficiency in Autosomal Recessive Limb-Girdle Muscular Dystrophy Using Molecular Markers in Disease Carriers.Neurology. Genetics · 2026Article
- Quantification of a serum titin fragment reflects dystrophin restoration in mdx mice and disease severity in patients with dystrophinopathies.Journal of neuromuscular diseases · 2026Article
- RecurrentInternational journal of molecular sciences · 2025Article
- Effects of one-week intake of different edible oils on the urinary proteome of rats.Frontiers in nutrition · 2025Article
- A Patient with Calpainopathy Carrying Compound Heterozygous Mutations of a De Novo Pathogenic Variant of c.1333G>A and a Novel Variant of c.1331C>T in CAPN3.Internal medicine (Tokyo, Japan) · 2024Article
- Article
- 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
- Calpainopathy: Description of a Novel Mutation and Clinical Presentation with Early Severe Contractures.Genes · 2020Article
- Molecular Insights into Muscle Homeostasis, Atrophy and Wasting.Current genomics · 2018Review
- A mechanosensitive CaNature communications · 2017Article
- Failure to up-regulate transcription of genes necessary for muscle adaptation underlies limb girdle muscular dystrophy 2A (calpainopathy).Human molecular genetics · 2016Article
- Titin, a Central Mediator for Hypertrophic Signaling, Exercise-Induced Mechanosignaling and Skeletal Muscle Remodeling.Frontiers in physiology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Calpains are broadly distributed, calcium-dependent enzymes that induce limited proteolysis in a wide range of substrates. Mutations in the gene encoding the muscle-specific family member calpain 3 (CAPN3) underlie limb-girdle muscular dystrophy 2A. We have shown previously that CAPN3 knockout muscles exhibit attenuated calcium release, reduced calmodulin kinase (CaMKII) signaling, and impaired muscle adaptation to exercise. However, neither the precise role of CAPN3 in these processes nor the mechanisms of CAPN3 activation in vivo have been fully elucidated. In this study, we identify calmodulin (CaM), a known transducer of the calcium signal, as the first positive regulator of CAPN3 autolytic activity. CaM was shown to bind CAPN3 at two sites located in the C2L domain. Biochemical studies using muscle extracts from transgenic mice overexpressing CAPN3 or its inactive mutant revealed that CaM binding enhanced CAPN3 autolytic activation. Furthermore, CaM facilitated CAPN3-mediated cleavage of its in vivo substrate titin in tissue extracts. Therefore, these studies reveal a novel interaction between CAPN3 and CaM and identify CaM as the first positive regulator of CAPN3 activity.
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Registered trials
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