ArticleThe Journal of physiology2014
The contribution of cardiac myosin binding protein-c Ser282 phosphorylation to the rate of force generation and in vivo cardiac contractility.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 32 citations in OpenAlex.
- Differential effects of myosin activators on myocardial contractile function in nonfailing and failing human hearts.American journal of physiology. Heart and circulatory physiology · 2025Article
- cMyBP-C in hypertrophic cardiomyopathy: gene therapy and small-molecule innovations.Frontiers in cardiovascular medicine · 2025Review
- Effect of the Novel Myotrope Danicamtiv on Cross-Bridge Behavior in Human Myocardium.Journal of the American Heart Association · 2023Article
- The contribution of N-terminal truncated cMyBPC to in vivo cardiac function.The Journal of general physiology · 2023Article
- Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022Article
- Article
- cMyBPC phosphorylation modulates the effect of omecamtiv mecarbil on myocardial force generation.The Journal of general physiology · 2021Article
- AAV9 gene transfer of cMyBPC N-terminal domains ameliorates cardiomyopathy in cMyBPC-deficient mice.JCI insight · 2020Article
- Strategies for targeting the cardiac sarcomere: avenues for novel drug discovery.Expert opinion on drug discovery · 2020Review
- Phosphomimetic cardiac myosin-binding protein C partially rescues a cardiomyopathy phenotype in murine engineered heart tissue.Scientific reports · 2019Article
- Regulation of myofilament force and loaded shortening by skeletal myosin binding protein C.The Journal of general physiology · 2019Article
- The HCM-causing Y235S cMyBPC mutation accelerates contractile function by altering C1 domain structure.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Sarcomere-based genetic enhancement of systolic cardiac function in a murine model of dilated cardiomyopathy.International journal of cardiology · 2018Article
- Impact of the Myosin Modulator Mavacamten on Force Generation and Cross-Bridge Behavior in a Murine Model of Hypercontractility.Journal of the American Heart Association · 2018Article
- Dose-Dependent Effects of the Myosin Activator Omecamtiv Mecarbil on Cross-Bridge Behavior and Force Generation in Failing Human Myocardium.Circulation. Heart failure · 2017Article
- Cardiac myosin binding protein-C SerScience advances · 2017Article
- Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.Journal of applied physiology (Bethesda, Md. : 1985) · 2017Article
- β-Adrenergic augmentation of cardiac contractility is dependent on PKA-mediated phosphorylation of myosin-binding protein C and troponin I.The Journal of physiology · 2016Article
- Phosphorylation of cardiac myosin binding protein-C regulates heart contraction and dilatation in vivo during β-adrenergic receptor activation.The Journal of physiology · 2016Article
- Molecule specific effects of PKA-mediated phosphorylation on rat isolated heart and cardiac myofibrillar function.Archives of biochemistry and biophysics · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac myosin binding protein-C phosphorylation plays an important role in modulating cardiac muscle function and accelerating contraction. It has been proposed that Ser282 phosphorylation may serve as a critical molecular switch that regulates the phosphorylation of neighbouring Ser273 and Ser302 residues, and thereby govern myofilament contractile acceleration in response to protein kinase A (PKA). Therefore, to determine the regulatory roles of Ser282 we generated a transgenic (TG) mouse model expressing cardiac myosin binding protein-C with a non-phosphorylatable Ser282 (i.e. serine to alanine substitution, TG(S282A)). Myofibrils isolated from TG(S282A) hearts displayed robust PKA-mediated phosphorylation of Ser273 and Ser302, and the increase in phosphorylation was identical to TG wild-type (TG(WT)) controls. No signs of pathological cardiac hypertrophy were detected in TG(S282A) hearts by either histological examination of cardiac sections or echocardiography. Baseline fractional shortening, ejection fraction, isovolumic relaxation time, rate of pressure development and rate of relaxation (τ) were unaltered in TG(S282A) mice. However, the increase in cardiac contractility as well as the acceleration of pressure development observed in response to β-adrenergic stimulation was attenuated in TG(S282A) mice. In agreement with our in vivo data, in vitro force measurements revealed that PKA-mediated acceleration of cross-bridge kinetics in TG(S282A) myocardium was significantly attenuated compared to TG(WT) myocardium. Taken together, our data suggest that while Ser282 phosphorylation does not regulate the phosphorylation of neighbouring Ser residues and basal cardiac function, full acceleration of cross-bridge kinetics and left ventricular pressure development cannot be achieved in its absence.
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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.