ReviewExperimental & molecular medicine2023
Etiology of genetic muscle disorders induced by mutations in fast and slow skeletal MyBP-C paralogs.
Review in Experimental & molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 18 citations in OpenAlex.
- Caenorhabditis elegans small heat-shock protein HSP-12.6 has a highly specialized protective function towards muscle thick filaments in vivo.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Subsarcomeric regulation of thin and thick filaments in skeletal muscle myofibrils.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Protein co-expression network analysis explores biological mechanisms associated with meat quality variability in broilers affected by breast myopathies: A focus on wooden breast.Poultry science · 2026Article
- Article
- Myosin Filaments of Vertebrate Skeletal and Cardiac Muscle are Highly Similar, but not Identical.bioRxiv : the preprint server for biology · 2026Article
- Fast Myosin Binding Protein-C Is a Vital Regulator in Young and Aged Fast Skeletal Muscle Homeostasis.Journal of cachexia, sarcopenia and muscle · 2025Article
- In vivo self-renewal and expansion of quiescent stem cells from a non-human primate.Nature communications · 2025Article
- Systemic Changes in Adults With a Fontan Circulation: Insights From the Plasma Proteome.Journal of the American Heart Association · 2025Article
- Nanodomain cAMP signaling in cardiac pathophysiology: potential for developing targeted therapeutic interventions.Physiological reviews · 2025Review
- Myocardial dysfunction caused by MyBPC3 P459fs mutation in hypertrophic cardiomyopathy: evidence from multi-omics approaches and super-resolution imaging.Frontiers in cardiovascular medicine · 2025Article
- Genetic Basis of Hypertrophic Cardiomyopathy in Cats.Current issues in molecular biology · 2024Review
- Compound heterozygous variants in MYBPC1 lead to severe distal arthrogryposis type-1 manifestations.Gene · 2024Article
- Fast myosin binding protein C knockout in skeletal muscle alters length-dependent activation and myofilament structure.Communications biology · 2024Article
- Myosin-binding protein C regulates the sarcomere lattice and stabilizes the OFF states of myosin heads.Nature communications · 2024Article
- Phenotypic spectrum of the first BelgianFrontiers in genetics · 2024Article
- Bringing into focus the central domains C3-C6 of myosin binding protein C.Frontiers in physiology · 2024Review
- Fast myosin binding protein C knockout in skeletal muscle alters length-dependent activation and myofilament structure.bioRxiv : the preprint server for biology · 2023Article
- Myosin-binding protein C forms C-links and stabilizes OFF states of myosin.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Skeletal muscle, a highly complex muscle type in the eukaryotic system, is characterized by different muscle subtypes and functions associated with specific myosin isoforms. As a result, skeletal muscle is the target of numerous diseases, including distal arthrogryposes (DAs). Clinically, DAs are a distinct disorder characterized by variation in the presence of contractures in two or more distal limb joints without neurological issues. DAs are inherited, and up to 40% of patients with this condition have mutations in genes that encode sarcomeric protein, including myosin heavy chains, troponins, and tropomyosin, as well as myosin binding protein-C (MYBPC). Our research group and others are actively studying the specific role of MYBPC in skeletal muscles. The MYBPC family of proteins plays a critical role in the contraction of striated muscles. More specifically, three paralogs of the MYBPC gene exist, and these are named after their predominant expression in slow-skeletal, fast-skeletal, and cardiac muscle as sMyBP-C, fMyBP-C, and cMyBP-C, respectively, and encoded by the MYBPC1, MYBPC2, and MYBPC3 genes, respectively. Although the physiology of various types of skeletal muscle diseases is well defined, the molecular mechanism underlying the pathological regulation of DAs remains to be elucidated. In this review article, we aim to highlight recent discoveries involving the role of skeletal muscle-specific sMyBP-C and fMyBP-C as well as their expression profile, localization in the sarcomere, and potential role(s) in regulating muscle contractility. Thus, this review provides an overall summary of MYBPC skeletal paralogs, their potential roles in skeletal muscle function, and future research directions.
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