ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Deletion of 1-43 amino acids in cardiac myosin essential light chain blunts length dependency of Ca(2+) sensitivity and cross-bridge detachment kinetics.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Dual effect of N-terminal deletion of cardiac myosin essential light chain in mitigating cardiomyopathy.iScience · 2024Article
- Mechanisms of Frank-Starling law of the heart and stretch activation in striated muscles may have a common molecular origin.Journal of muscle research and cell motility · 2021Article
- Insights into myosin regulatory and essential light chains: a focus on their roles in cardiac and skeletal muscle function, development and disease.Journal of muscle research and cell motility · 2020Article
- Thick Filament Protein Network, Functions, and Disease Association.Comprehensive Physiology · 2018Review
- Cardiomyopathy-related mutation (A30V) in mouse cardiac troponin T divergently alters the magnitude of stretch activation in α- and β-myosin heavy chain fibers.American journal of physiology. Heart and circulatory physiology · 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
- Interplay between the effects of a Protein Kinase C phosphomimic (T204E) and a dilated cardiomyopathy mutation (K211Δ or R206W) in rat cardiac troponin T blunts the magnitude of muscle length-mediated crossbridge recruitment against the β-myosin heavy chain background.Journal of muscle research and cell motility · 2016Article
- Interplay Between the Effects of Dilated Cardiomyopathy Mutation (R206L) and the Protein Kinase C Phosphomimic (T204E) of Rat Cardiac Troponin T Are Differently Modulated by α- and β-Myosin Heavy Chain Isoforms.Journal of the American Heart Association · 2016Article
- Article
- Ventricular myosin modifies in vitro step-size when phosphorylated.Journal of molecular and cellular cardiology · 2014Article
- Remodeling of the heart in hypertrophy in animal models with myosin essential light chain mutations.Frontiers in physiology · 2014Article
- Length-dependent changes in contractile dynamics are blunted due to cardiac myosin binding protein-C ablation.Frontiers in physiology · 2014Article
- Interplay between the overlapping ends of tropomyosin and the N terminus of cardiac troponin T affects tropomyosin states on actin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
- Discrete effects of A57G-myosin essential light chain mutation associated with familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2013Article
- 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.Journal of muscle research and cell motility · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The role of cardiac myosin essential light chain (ELC) in the sarcomere length (SL) dependency of myofilament contractility is unknown. Therefore, mechanical and dynamic contractile properties were measured at SL 1.9 and 2.2 μm in cardiac muscle fibers from two groups of transgenic (Tg) mice: 1) Tg-wild-type (WT) mice that expressed WT human ventricular ELC and 2) Tg-Δ43 mice that expressed a mutant ELC lacking 1-43 amino acids. In agreement with previous studies, Ca(2+)-activated maximal tension decreased significantly in Tg-Δ43 fibers. pCa(50) (-log(10) [Ca(2+)](free) required for half maximal activation) values at SL of 1.9 μm were 5.64 ± 0.02 and 5.70 ± 0.02 in Tg-WT and Tg-Δ43 fibers, respectively. pCa(50) values at SL of 2.2 μm were 5.70 ± 0.01 and 5.71 ± 0.01 in Tg-WT and Tg-Δ43 fibers, respectively. The SL-mediated increase in the pCa(50) value was statistically significant only in Tg-WT fibers (P < 0.01), indicating that the SL dependency of myofilament Ca(2+) sensitivity was blunted in Tg-Δ43 fibers. The SL dependency of cross-bridge (XB) detachment kinetics was also blunted in Tg-Δ43 fibers because the decrease in XB detachment kinetics was significant (P < 0.001) only at SL 1.9 μm. Thus the increased XB dwell time at the short SL augments Ca(2+) sensitivity at short SL and thus blunts SL-mediated increase in myofilament Ca(2+) sensitivity. Our data suggest that the NH(2)-terminal extension of cardiac ELC not only augments the amplitude of force generation, but it also may play a role in mediating the SL dependency of XB detachment kinetics and myofilament Ca(2+) sensitivity.
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