ArticleJournal of muscle research and cell motility2013
Characterizations of myosin essential light chain's N-terminal truncation mutant Δ43 in transgenic mouse papillary muscles by using tension transients in response to sinusoidal length alterations.
Article in Journal of muscle research and cell motility, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 26 citations in OpenAlex.
- The elementary step that generates force and sinusoidal analysis in striated muscle fibers.Journal of muscle research and cell motility · 2025Review
- Biomechanical evaluation of flash-frozen and cryo-sectioned papillary muscle samples by using sinusoidal analysis: cross-bridge kinetics and the effect of partial CaJournal of muscle research and cell motility · 2024Article
- The effect of gender and obesity in modulating cross-bridge function in cardiac muscle fibers.Journal of muscle research and cell motility · 2022Article
- Hypertrophic cardiomyopathy associated E22K mutation in myosin regulatory light chain decreases calcium-activated tension and stiffness and reduces myofilament CaThe FEBS journal · 2021Article
- Ablation of the N terminus of cardiac essential light chain promotes the super-relaxed state of myosin and counteracts hypercontractility in hypertrophic cardiomyopathy mutant mice.The FEBS journal · 2020Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- The naked mole-rat exhibits an unusual cardiac myofilament protein profile providing new insights into heart function of this naturally subterranean rodent.Pflugers Archiv : European journal of physiology · 2017Article
- Hypercontractile mutant of ventricular myosin essential light chain leads to disruption of sarcomeric structure and function and results in restrictive cardiomyopathy in mice.Cardiovascular research · 2017Article
- Cardiac contractility, motor function, and cross-bridge kinetics in N47K-RLC mutant mice.The FEBS journal · 2017Article
- Comparison of elementary steps of the cross-bridge cycle in rat papillary muscle fibers expressing α- and β-myosin heavy chain with sinusoidal analysis.Journal of muscle research and cell motility · 2016Article
- In vivo myosin step-size from zebrafish skeletal muscle.Open biology · 2016Article
- Molecular and Functional Effects of a Splice Site Mutation in the MYL2 Gene Associated with Cardioskeletal Myopathy and Early Cardiac Death in Infants.Frontiers in physiology · 2016Article
- In vitro and in vivo single myosin step-sizes in striated muscle.Journal of muscle research and cell motility · 2015Article
- Constitutive phosphorylation of cardiac myosin regulatory light chain prevents development of hypertrophic cardiomyopathy in mice.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Novel familial dilated cardiomyopathy mutation in MYL2 affects the structure and function of myosin regulatory light chain.The FEBS journal · 2015Article
- The R21C Mutation in Cardiac Troponin I Imposes Differences in Contractile Force Generation between the Left and Right Ventricles of Knock-In Mice.BioMed research international · 2015Article
- Phosphorylation of cMyBP-C affects contractile mechanisms in a site-specific manner.Biophysical journal · 2014Article
- Cardiac myosin binding protein C phosphorylation affects cross-bridge cycle's elementary steps in a site-specific manner.PloS one · 2014Article
- Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations.Frontiers in physiology · 2014Article
- Discrete effects of A57G-myosin essential light chain mutation associated with familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cross-bridge kinetics were studied at 20 °C in cardiac muscle strips from transgenic (Tg) mice expressing N-terminal 43 amino acid truncation mutation (Δ43) of myosin essential light chain (ELC), and the results were compared to those from Tg-wild type (WT) mice. Sinusoidal length changes were applied to activated skinned papillary muscle strips to induce tension transients, from which two exponential processes were deduced to characterize the cross-bridge kinetics. Their two rate constants were studied as functions of ATP, phosphate (Pi), ADP, and Ca(2+) concentrations to characterize elementary steps of the cross-bridge cycle consisting of six states. Our results demonstrate for the first time that the cross-bridge kinetics of Δ43 are accelerated owing to an acceleration of the rate constant k 2 of the cross-bridge detachment step, and that the number of strongly attached cross-bridges are decreased because of a reduction of the equilibrium constant K 4 of the force generation step. The isometric tension and stiffness of Δ43 are diminished compared to WT, but the force per cross-bridge is not changed. Stiffness measurement during rigor induction demonstrates a reduction in the stiffness in Δ43, indicating that the N-terminal extension of ELC forms an extra linkage between the myosin cross-bridge and actin. The tension-pCa study demonstrates that there is no Ca(2+) sensitivity change with Δ43, but the cooperativity is diminished. These results demonstrate the importance of the N-terminal extension of ELC in maintaining the myosin motor function during force generation and optimal cardiac performance.
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