Mechanistic complexity of contractile dysfunction in hypertrophic cardiomyopathy
Author:
Affiliation:
1. University of Washington, Seattle, WA
Abstract
Funder
National Institutes of Health
Publisher
Rockefeller University Press
Subject
Physiology
Link
http://rupress.org/jgp/article-pdf/150/8/1051/1236628/jgp_201812091.pdf
Reference24 articles.
1. The familial hypertrophic cardiomyopathy-associated myosin mutation R403Q accelerates tension generation and relaxation of human cardiac myofibrils;Belus;J. Physiol.,2008
2. Sex dimorphisms of crossbridge cycling kinetics in transgenic hypertrophic cardiomyopathy mice;Birch;Am. J. Physiol. Heart Circ. Physiol.,2016
3. Increase in tension-dependent ATP consumption induced by cardiac troponin T mutation;Chandra;Am. J. Physiol. Heart Circ. Physiol.,2005
4. Troponin I Mutations R146G and R21C Alter Cardiac Troponin Function, Contractile Properties, and Modulation by Protein Kinase A (PKA)-mediated Phosphorylation;Cheng;J. Biol. Chem.,2015
5. Effects of Cardiac Troponin I Mutation P83S on Contractile Properties and the Modulation by PKA-Mediated Phosphorylation;Cheng;J. Phys. Chem. B.,2016
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1. Identification of three novel pathogenic mutations in sarcomere genes associated with familial hypertrophic cardiomyopathy based on multi-omics study;Clinica Chimica Acta;2021-09
2. Novel frameshift variant in MYL2 reveals molecular differences between dominant and recessive forms of hypertrophic cardiomyopathy;PLOS Genetics;2020-05-26
3. Novel frameshift variant in MYL2 reveals molecular differences between dominant and recessive forms of hypertrophic cardiomyopathy;2019-10-13
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