ArticleThe Journal of physiology2013
Length dependence of striated muscle force generation is controlled by phosphorylation of cTnI at serines 23/24.
Article in The Journal of physiology, 2013. 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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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Cardiac myosin-binding protein-C acts as a tunable load sensor to regulate afterload dependence of ventricular function.American journal of physiology. Heart and circulatory physiology · 2025Article
- Troponin I Tyrosine Phosphorylation Beneficially Accelerates Diastolic Function.Circulation research · 2024Article
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- N-terminal truncated cardiac troponin I enhances Frank-Starling response by increasing myofilament sensitivity to resting tension.The Journal of general physiology · 2023Article
- Sarcomere length affects Ca2+ sensitivity of contraction in ischemic but not non-ischemic myocardium.The Journal of general physiology · 2023Article
- The lack of Troponin I Ser-23/24 phosphorylation is detrimental to in vivo cardiac function and exacerbates cardiac disease.Journal of molecular and cellular cardiology · 2023Article
- Molecular regulation of stretch activation.American journal of physiology. Cell physiology · 2022Article
- Reduced preload increases Mechanical Control (strain-rate dependence) of Relaxation by modifying myosin kinetics.Archives of biochemistry and biophysics · 2021Article
- Cardiac MyBP-C phosphorylation regulates the Frank-Starling relationship in murine hearts.The Journal of general physiology · 2021Article
- Site-specific acetyl-mimetic modification of cardiac troponin I modulates myofilament relaxation and calcium sensitivity.Journal of molecular and cellular cardiology · 2020Article
- Regulation of Myofilament Contractile Function in Human Donor and Failing Hearts.Frontiers in physiology · 2020Article
- Regulating myofilament power: The determinant of health.Archives of biochemistry and biophysics · 2019Review
- The force and stiffness of myosin motors in the isometric twitch of a cardiac trabecula and the effect of the extracellular calcium concentration.The Journal of physiology · 2018Article
- The continuing evolution of cardiac troponin I biomarker analysis: from protein to proteoform.Expert review of proteomics · 2017Review
- The Frank-Starling Law: a jigsaw of titin proportions.Biophysical reviews · 2017Review
- Myosin filament activation in the heart is tuned to the mechanical task.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Restrictive Cardiomyopathy Troponin I R145W Mutation Does Not Perturb Myofilament Length-dependent Activation in Human Cardiac Sarcomeres.The Journal of biological chemistry · 2016Article
- Molecule specific effects of PKA-mediated phosphorylation on rat isolated heart and cardiac myofibrillar function.Archives of biochemistry and biophysics · 2016Article
- Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility.Archives of biochemistry and biophysics · 2016Review
- Myosin light chain phosphorylation enhances contraction of heart muscle via structural changes in both thick and thin filaments.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
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3 authors at 2 institutions in 1 country.
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Abstract
According to the Frank-Starling relationship, greater end-diastolic volume increases ventricular output. The Frank-Starling relationship is based, in part, on the length-tension relationship in cardiac myocytes. Recently, we identified a dichotomy in the steepness of length-tension relationships in mammalian cardiac myocytes that was dependent upon protein kinase A (PKA)-induced myofibrillar phosphorylation. Because PKA has multiple myofibrillar substrates including titin, myosin-binding protein-C and cardiac troponin I (cTnI), we sought to define if phosphorylation of one of these molecules could control length-tension relationships. We focused on cTnI as troponin can be exchanged in permeabilized striated muscle cell preparations, and tested the hypothesis that phosphorylation of cTnI modulates length dependence of force generation. For these experiments, we exchanged unphosphorylated recombinant cTn into either a rat cardiac myocyte preparation or a skinned slow-twitch skeletal muscle fibre. In all cases unphosphorylated cTn yielded a shallow length-tension relationship, which was shifted to a steep relationship after PKA treatment. Furthermore, exchange with cTn having cTnI serines 23/24 mutated to aspartic acids to mimic phosphorylation always shifted a shallow length-tension relationship to a steep relationship. Overall, these results indicate that phosphorylation of cTnI serines 23/24 is a key regulator of length dependence of force generation in striated muscle.
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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.