Effects of Two Hypertrophic Cardiomyopathy Mutations in α-Tropomyosin, Asp175Asn and Glu180Gly, on Ca2+Regulation of Thin Filament Motility
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Molecular Biology,Biochemistry,Biophysics
Reference33 articles.
1. α-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: A disease of the sarcomere
2. Codon 102 of the Cardiac Troponin T Gene Is a Putative Hot Spot for Mutations in Familial Hypertrophic Cardiomyopathy
3. Mutations in the Genes for Cardiac Troponin T and α-Tropomyosin in Hypertrophic Cardiomyopathy
4. Mutations in the cardiac myosin binding protein–C gene on chromosome 11 cause familial hypertrophic cardiomyopathy
5. Cardiac myosin binding protein–C gene splice acceptor site mutation is associated with familial hypertrophic cardiomyopathy
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1. Myosin-1C differentially displaces tropomyosin isoforms altering their inhibition of motility;Journal of Biological Chemistry;2024-08
2. Motility Assay to Probe the Calcium Sensitivity of Myosin and Regulated Thin Filaments;Methods in Molecular Biology;2023-12-02
3. Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy;International Journal of Molecular Sciences;2022-02-16
4. The effects of the tropomyosin cardiomyopathy mutations on the calcium regulation of actin-myosin interaction in the atrium and ventricle differ;Biochemical and Biophysical Research Communications;2022-01
5. Cardiomyopathic troponin mutations predominantly occur at its interface with actin and tropomyosin;Journal of General Physiology;2021-01-25
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