ArticleBiochemistry2012
Cardiac myosin binding protein C and its phosphorylation regulate multiple steps in the cross-bridge cycle of muscle contraction.
Article in Biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 39 citations in OpenAlex.
- Opposing Effects of Dietary Nitrate on Muscle Contractile Function in Fast and Slow Human Muscles.Medicine and science in sports and exercise · 2026Trial
- Biomechanical stress unmasks a fibroblast-dependent hypercontractile-disarray phenotype in MYBPC3 truncation HCM.APL bioengineering · 2026Article
- Sex-dependent and muscle-specific progression of the MYBPC1 E248K Myotrem myopathy in response to aging.JCI insight · 2025Article
- Neurophysiology of ACL Injury.Orthopedic reviews · 2025Article
- MYBPC3-c.772G>A mutation results in haploinsufficiency and altered myosin cycling kinetics in a patient induced stem cell derived cardiomyocyte model of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2024Article
- Cardiac myosin-binding protein C N-terminal interactions with myosin and actin filaments: Opposite effects of phosphorylation and M-domain mutations.Journal of molecular and cellular cardiology · 2024Article
- Synthetic growth hormone-releasing hormone agonist ameliorates the myocardial pathophysiology characteristic of heart failure with preserved ejection fraction.Cardiovascular research · 2023Article
- Distinct Mechanisms for Increased Cardiac Contraction Through Selective Alteration of Either Myosin or Troponin Activity.JACC. Basic to translational science · 2022Article
- 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
- Molecular characterization of linker and loop-mediated structural modulation and hinge motion in the C4-C5 domains of cMyBPC.Journal of structural biology · 2022Article
- Nitric oxide and skeletal muscle contractile function.Nitric oxide : biology and chemistry · 2022Review
- Article
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Inhibiting cardiac myeloperoxidase alleviates the relaxation defect in hypertrophic cardiomyocytes.Cardiovascular research · 2022Article
- Development of a Loop-Mediated Isothermal Amplification Assay Coupled With a Lateral Flow Dipstick Test for Detection of Myosin Binding Protein C3Frontiers in veterinary science · 2022Article
- cMyBPC phosphorylation modulates the effect of omecamtiv mecarbil on myocardial force generation.The Journal of general physiology · 2021Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.American journal of physiology. Heart and circulatory physiology · 2019Article
- A post-MI power struggle: adaptations in cardiac power occur at the sarcomere level alongside MyBP-C and RLC phosphorylation.American journal of physiology. Heart and circulatory physiology · 2016Article
- Phosphorylation and calcium antagonistically tune myosin-binding protein C's structure and function.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac myosin binding protein C (c-MyBPC) is a thick filament protein that is expressed in cardiac sarcomeres and is known to interact with myosin and actin. While both structural and regulatory roles have been proposed for c-MyBPC, its true function is unclear; however, phosphorylation has been shown to be important. In this study, we investigate the effect of c-MyBPC and its phosphorylation on two key steps of the cross-bridge cycle using fast reaction kinetics. We show that unphosphorylated c-MyBPC complexed with myosin in 1:1 and 3:1 myosin:c-MyBPC stoichiometries regulates the binding of myosin to actin (K(D)) cooperatively (Hill coefficient, h) (K(D) = 16.44 ± 0.33 μM, and h = 9.24 ± 1.34; K(D) = 11.48 ± 0.75 μM, and h = 3.54 ± 0.67) and significantly decelerates the ATP-induced dissociation of myosin from actin (K(1)k(+2) values of 0.12 ± 0.01 and 0.22 ± 0.01 M(-1) s(-1), respectively, compared with a value of 0.42 ± 0.01 M(-1) s(-1) for myosin alone). Phosphorylation of c-MyBPC abolished the regulation of the association phase (K(1)k(+2) values of 0.32 ± 0.02 and 0.33 ± 0.01 M(-1) s(-1) at 1:1 and 3:1 myosin:c-MyBPC ratios, respectively) and also accelerated the dissociation of myosin from actin (K(1)k(+2) values of 0.23 ± 0.01 and 0.29 ± 0.01 M(-1) s(-1) at a 1:1 and 3:1 myosin:c-MyBPC ratios, respectively) relative to the dissociation of myosin from actin in the presence of unphosphorylated c-MyBPC. These results indicate a direct effect of c-MyBPC on cross-bridge kinetics that is independent of the thin filament that together with its phosphorylation provides a mechanism for fine-tuning cross-bridge behavior to match the contractile requirements of the heart.
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