ArticleThe Journal of general physiology2003
Effect of MyBP-C binding to actin on contractility in heart muscle.
Article in The Journal of general physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 137 citations in OpenAlex.
- The genetic landscape of pediatric postural orthostatic tachycardia syndrome.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Article
- Pulsatile Myofilament Activity in Myotrem Myopathy Associated with Myogenic Tremor.International journal of molecular sciences · 2025Article
- CaJournal of molecular and cellular cardiology · 2025Article
- Article
- The D75N and P161S Mutations in the C0-C2 Fragment of cMyBP-C Associated with Hypertrophic Cardiomyopathy Disturb the Thin Filament Activation, Nucleotide Exchange in Myosin, and Actin-Myosin Interaction.International journal of molecular sciences · 2024Article
- Etiology of genetic muscle disorders induced by mutations in fast and slow skeletal MyBP-C paralogs.Experimental & molecular medicine · 2023Review
- Transcriptome Profile Identifies Actin as an Essential Regulator of Cardiac Myosin Binding Protein C3 Hypertrophic Cardiomyopathy in a Zebrafish Model.International journal of molecular sciences · 2022Article
- Small Angle X-ray Diffraction as a Tool for Structural Characterization of Muscle Disease.International journal of molecular sciences · 2022Review
- Phosphorylation of cardiac myosin-binding protein-C contributes to calcium homeostasis.The Journal of biological chemistry · 2020Article
- Genetic, clinical, molecular, and pathogenic aspects of the South Asian-specific polymorphic MYBPC3Biophysical reviews · 2020Review
- Human cardiac myosin-binding protein C restricts actin structural dynamics in a cooperative and phosphorylation-sensitive manner.The Journal of biological chemistry · 2019Article
- Sarcomere length-dependent effects on CaThe Journal of general physiology · 2019Article
- Structure before function: myosin binding protein-C slow is a structural protein with regulatory properties.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Hypertrophic cardiomyopathy and the myosin mesa: viewing an old disease in a new light.Biophysical reviews · 2018Review
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Cardiac Myosin Binding Protein-C Autoantibodies are Potential Early Indicators of Cardiac Dysfunction and Patient Outcome in Acute Coronary Syndrome.JACC. Basic to translational science · 2017Article
- Phosphorylation of cardiac myosin binding protein C releases myosin heads from the surface of cardiac thick filaments.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- In vivo definition of cardiac myosin-binding protein C's critical interactions with myosin.Pflugers Archiv : European journal of physiology · 2016Article
- The cMyBP-C HCM variant L348P enhances thin filament activation through an increased shift in tropomyosin position.Journal of molecular and cellular cardiology · 2016Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In contrast to skeletal muscle isoforms of myosin binding protein C (MyBP-C), the cardiac isoform has 11 rather than 10 fibronectin or Ig modules (modules are identified as C0 to C10, NH2 to COOH terminus), 3 phosphorylation sites between modules C1 and C2, and 28 additional amino acids rich in proline in C5. Phosphorylation between C1 and C2 increases maximum Ca-activated force (Fmax), alters thick filament structure, and increases the probability of myosin heads on the thick filament binding to actin on the thin filament. Unphosphorylated C1C2 fragment binds to myosin, but phosphorylation inhibits the binding. MyBP-C also binds to actin. Using two types of immunoprecipitation and cosedimentation, we show that fragments of MyBP-C containing C0 bind to actin. In low concentrations C0-containing fragments bind to skinned fibers when the NH2 terminus of endogenous MyBP-C is bound to myosin, but not when MyBP-C is bound to actin. C1C2 fragments bind to skinned fibers when endogenous MyBP-C is bound to actin but not to myosin. Disruption of interactions of endogenous C0 with a high concentration of added C0C2 fragments produces the same effect on contractility as extraction of MyBP-C, namely decrease in Fmax and increase in Ca sensitivity. These results suggest that cardiac contractility can be regulated by shifting the binding of the NH2 terminus of MyBP-C between actin and myosin. This mechanism may have an effect on diastolic filling of the heart.
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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.