ArticleJournal of molecular and cellular cardiology2010
Single molecule kinetics in the familial hypertrophic cardiomyopathy D166V mutant mouse heart.
Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- The co-segregation of the MYL2 R58Q mutation in Chinese hypertrophic cardiomyopathy family and its pathological effect on cardiomyopathy disarray.Molecular genetics and genomics : MGG · 2019Article
- 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
- 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
- Effect of a myosin regulatory light chain mutation K104E on actin-myosin interactions.American journal of physiology. Heart and circulatory physiology · 2015Article
- Impact of familial hypertrophic cardiomyopathy-linked mutations in the NH2 terminus of the RLC on β-myosin cross-bridge mechanics.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Phosphorylation of cMyBP-C affects contractile mechanisms in a site-specific manner.Biophysical journal · 2014Article
- Diversity and similarity of motor function and cross-bridge kinetics in papillary muscles of transgenic mice carrying myosin regulatory light chain mutations D166V and R58Q.Journal of molecular and cellular cardiology · 2013Article
- Discrete effects of A57G-myosin essential light chain mutation associated with familial hypertrophic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2013Article
- Regulatory light chain mutants linked to heart disease modify the cardiac myosin lever arm.Biochemistry · 2013Article
- The effect of myosin RLC phosphorylation in normal and cardiomyopathic mouse hearts.Journal of cellular and molecular medicine · 2012Article
- Myosin regulatory light chain mutation found in hypertrophic cardiomyopathy patients increases isometric force production in transgenic mice.The Biochemical journal · 2012Article
- Cross-bridge kinetics in myofibrils containing familial hypertrophic cardiomyopathy R58Q mutation in the regulatory light chain of myosin.Journal of theoretical biology · 2011Article
- Myosin cross-bridges do not form precise rigor bonds in hypertrophic heart muscle carrying troponin T mutations.Journal of molecular and cellular cardiology · 2011Article
- In the thick of it: HCM-causing mutations in myosin binding proteins of the thick filament.Circulation research · 2011Review
- Evidence for pre- and post-power stroke of cross-bridges of contracting skeletal myofibrils.Biophysical journal · 2011Article
- Single-molecule fluorescence characterization in native environment.Biophysical reviews · 2010Article
- Familial hypertrophic cardiomyopathy can be characterized by a specific pattern of orientation fluctuations of actin molecules .Biochemistry · 2010Article
- Kinetics of a single cross-bridge in familial hypertrophic cardiomyopathy heart muscle measured by reverse Kretschmann fluorescence.Journal of biomedical opticsArticle
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
One of the sarcomeric mutations associated with a malignant phenotype of familial hypertrophic cardiomyopathy (FHC) is the D166V point mutation in the ventricular myosin regulatory light chain (RLC) encoded by the MYL2 gene. In this report we show that the rates of myosin cross-bridge attachment and dissociation are significantly different in isometrically contracting cardiac myofibrils from right ventricles of transgenic (Tg)-D166V and Tg-WT mice. We have derived the myosin cross-bridge kinetic rates by tracking the orientation of a fluorescently labeled single actin molecule. Orientation (measured by polarized fluorescence) oscillated between two states, corresponding to the actin-bound and actin-free states of the myosin cross-bridge. The rate of cross-bridge attachment during isometric contraction decreased from 3 s(-1) in myofibrils from Tg-WT to 1.4 s(-1) in myofibrils from Tg-D166V. The rate of detachment decreased from 1.3 s(-1) (Tg-WT) to 1.2 s(-1) (Tg-D166V). We also showed that the level of RLC phosphorylation was largely decreased in Tg-D166V myofibrils compared to Tg-WT. Our findings suggest that alterations in the myosin cross-bridge kinetics brought about by the D166V mutation in RLC might be responsible for the compromised function of the mutated hearts and lead to their inability to efficiently pump blood.
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