ArticleBiophysical journal2003
Mechanical defects of muscle fibers with myosin light chain mutants that cause cardiomyopathy.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Heterogeneous Dysregulation of Myosin Super-Relaxation and Energetics in Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2025Article
- Programmed Exercise Attenuates Familial Hypertrophic Cardiomyopathy in Transgenic E22K MiceFrontiers in cardiovascular medicine · 2022Article
- From Genetic Mutations to Molecular Basis of Heart Failure Treatment: An Overview of the Mechanism and Implication of the Novel Modulators for Cardiac Myosin.International journal of molecular sciences · 2021Review
- Myosin lever arm orientation in muscle determined with high angular resolution using bifunctional spin labels.The Journal of general physiology · 2019Article
- Hereditary heart disease: pathophysiology, clinical presentation, and animal models of HCM, RCM, and DCM associated with mutations in cardiac myosin light chains.Pflugers Archiv : European journal of physiology · 2019Review
- Molecular genetics and pathogenesis of cardiomyopathy.Journal of human genetics · 2016Review
- Three distinct actin-attached structural states of myosin in muscle fibers.Biophysical journal · 2012Article
- Proteomic analysis of metabolic, cytoskeletal and stress response proteins in human heart failure.Journal of cellular and molecular medicine · 2012Article
- Interplay of troponin- and Myosin-based pathways of calcium activation in skeletal and cardiac muscle: the use of W7 as an inhibitor of thin filament activation.Biophysical journal · 2004Article
Corrections and comments
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1 author at 1 institution in 1 country.
Funding
Abstract
Familial hypertrophic cardiomyopathy is a disease caused by single mutations in several sarcomeric proteins, including the human myosin ventricular regulatory light chain (vRLC). The effects of four of these mutations (A13T, F18L, E22K, and P95A) in vRLC on force generation were determined as a function of Ca(2+) concentration. The endogenous RLC was removed from skinned rabbit psoas muscle fibers, and replaced with either rat wildtype vRLC or recombinant rat vRLC (G13T, F18L, E22K, and P95A). Compared to fibers with wildtype rat vRLC, the E22K mutant increased Ca sensitivity of force generation, whereas the G13T and F18L mutants decreased the Ca sensitivity, and the P95A mutant had no significant effect. None of the RLC mutants affected the maximal tension (observed at saturating Ca(2+) concentrations), except for F18L, which decreased the maximal tension to 69 +/- 10% of the wildtype value. Of the mutant RLCs, only F18L decreased the cooperativity of activation of force generation. These results suggest that the primary cause of familial hypertrophic cardiomyopathy, in some cases, is perturbation in the Ca sensitivity of force generation, in which Ca-sensitizing or Ca-desensitizing effects can lead to similar disease phenotypes.
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