Cardiac contractility, motor function, and cross‐bridge kinetics in N47K‐ RLC mutant mice
Author:
Affiliation:
1. Departments of Anatomy and Cell Biology and Internal Medicine University of Iowa IA USA
2. Department of Molecular and Cellular Pharmacology University of Miami Miller School of Medicine FL USA
Funder
National Institutes of Health
American Heart Association
Publisher
Wiley
Subject
Cell Biology,Molecular Biology,Biochemistry
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1111/febs.14096
Reference52 articles.
1. The Molecular Mechanism of Muscle Contraction
2. Three-dimensional structure of myosin subfragment-1: a molecular motor
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4. Regulatory Light Chains of Striated Muscle Myosin. Structure, Function and Malfunction
5. Myosin essential light chain in health and disease
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1. Hypertrophic cardiomyopathy associated E22K mutation in myosin regulatory light chain decreases calcium‐activated tension and stiffness and reduces myofilament Ca 2+ sensitivity;The FEBS Journal;2021-03-10
2. Mavacamten decreases maximal force and Ca2+ sensitivity in the N47K-myosin regulatory light chain mouse model of hypertrophic cardiomyopathy;American Journal of Physiology-Heart and Circulatory Physiology;2021-02-01
3. Hereditary heart disease: pathophysiology, clinical presentation, and animal models of HCM, RCM, and DCM associated with mutations in cardiac myosin light chains;Pflügers Archiv - European Journal of Physiology;2019-01-31
4. Structure and Function of Muscle Cells;Biomechanics, Muscle Fibers, and How to Interface Experimental Apparatus to a Computer;2018
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