ReviewFrontiers in physiology2016
MYBPC1, an Emerging Myopathic Gene: What We Know and What We Need to Learn.
Review in Frontiers in physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed.
- Human Islet miR-199a-5p and miR-214-3p Associate With Donor Age, BMI, and Sex and Mediate Cellular Aging in Islet-Derived Cells.Acta physiologica (Oxford, England) · 2026Article
- Rejuvenation of white adipose tissue in a longitudinal heterochronic transplantation model.bioRxiv : the preprint server for biology · 2025Article
- Temporal Dynamics of the Plasma Proteomic Landscape Reveals Maladaptation in ME/CFS Following Exertion.Molecular & cellular proteomics : MCP · 2025Article
- The myoblast methylome: multiple types of associations with chromatin and transcription.Epigenetics · 2025Article
- STPath: a generative foundation model for integrating spatial transcriptomics and whole-slide images.NPJ digital medicine · 2025Article
- Single cell transcriptional analysis of human adenoids identifies molecular features of airway microfold cells.Mucosal immunology · 2025Article
- Sex-dependent and muscle-specific progression of the MYBPC1 E248K Myotrem myopathy in response to aging.JCI insight · 2025Article
- Unveiling Key Genes and Crucial Pathways in Goose Muscle Satellite Cell Biology Through Integrated Transcriptomic and Metabolomic Analyses.International journal of molecular sciences · 2025Article
- Genetic and metabolic insights into sexual dimorphism in the flexor carpi radialis of Asiatic toads (Bufo gargarizans) associated with amplexus behavior.BMC genomics · 2025Article
- Long-read sequencing reveals novel transcript diversity inAnimal cells and systems · 2025Article
- The distinctive mechanical and structural signatures of residual force enhancement in myofibers.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Biallelic variants in SNUPN cause a limb girdle muscular dystrophy with myofibrillar-like features.Brain : a journal of neurology · 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
- 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
- Effect of 11-Deoxycorticosterone in the Transcriptomic Response to Stress in Rainbow Trout Skeletal Muscle.Genes · 2023Article
- Transcriptome analysis of mRNAs, lncRNAs, and miRNAs in the skeletal muscle of Tibetan chickens at different developmental stages.Frontiers in physiology · 2023Article
- Article
- Identification of Driver Genes and Interaction Networks Related to Brain Metastasis in Breast Cancer Patients.Disease markers · 2022Article
Corrections and comments
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2 authors.
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Abstract
Myosin Binding Protein-C (MyBP-C) comprises a family of accessory proteins that includes the cardiac, slow skeletal, and fast skeletal isoforms. The three isoforms share structural and sequence homology, and localize at the C-zone of the sarcomeric A-band where they interact with thick and thin filaments to regulate the cycling of actomyosin crossbridges. The cardiac isoform, encoded by MYBPC3, has been extensively studied over the last several decades due to its high mutational rate in congenital hypertrophic and dilated cardiomyopathy. It is only recently, however, that the MYBPC1 gene encoding the slow skeletal isoform (sMyBP-C) has gained attention. Accordingly, during the last 5 years it has been shown that MYBPC1 undergoes extensive exon shuffling resulting in the generation of multiple slow variants, which are co-expressed in different combinations and amounts in both slow and fast skeletal muscles. The sMyBP-C variants are subjected to PKA- and PKC-mediated phosphorylation in constitutive and alternatively spliced sites. More importantly, missense, and nonsense mutations in MYBPC1 have been directly linked with the development of severe and lethal forms of distal arthrogryposis myopathy and muscle tremors. Currently, there is no mammalian animal model of sMyBP-C, but new technologies including CRISPR/Cas9 and xenografting of human biopsies into immunodeficient mice could provide unique ways to study the regulation and roles of sMyBP-C in health and disease.
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