Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts-Reference-Cited by-同舟云学术

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Cardiac myosin heavy chain isoform exchange alters the phenotype of cTnT-related cardiomyopathies in mouse hearts

Published:2010-05 Issue:5 Volume:48 Page:979-988
ISSN:0022-2828
Container-title:Journal of Molecular and Cellular Cardiology
language:en
Short-container-title:Journal of Molecular and Cellular Cardiology

Author:

Rice Ron,Guinto Pia,Dowell-Martino Candice,He Huamei,Hoyer Kirsten,Krenz Maike,Robbins Jeffrey,Ingwall Joanne S.,Tardiff Jil C.

Funder

National Heart, Lung, and Blood Institute

Publisher

Elsevier BV

Subject

Cardiology and Cardiovascular Medicine,Molecular Biology

Reference32 articles.

1. Hypertrophic cardiomyopathy;Elliott;Lancet,2004

2. Mutations in the genes for cardiac troponin T and alpha-tropomyosin in hypertrophic cardiomyopathy;Watkins;N Engl J Med,1995

3. Sudden death due to troponin T mutations;Moolman;J Am Coll Cardiol,1997

4. Codon 102 of the cardiac troponin T gene is a putative hot spot for mutations in familial hypertrophic cardiomyopathy;Forissier;Circulation,1996

5. Changes in the chemical and dynamic properties of cardiac troponin T cause discrete cardiomyopathies in transgenic mice;Ertz-Berger;Proc Natl Acad Sci USA,2005

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1. Altered coronary artery function, arteriogenesis and endothelial YAP signaling in postnatal hypertrophic cardiomyopathy;Frontiers in Physiology;2023-03-31

2. Mechanical dysfunction of the sarcomere induced by a pathogenic mutation in troponin T drives cellular adaptation;Journal of General Physiology;2021-04-15

3. Complexity in genetic cardiomyopathies and new approaches for mechanism-based precision medicine;Journal of General Physiology;2021-01-29

4. Mechanical dysfunction induced by a hypertrophic cardiomyopathy mutation is the primary driver of cellular adaptation;2020-05-05

5. Hypertrophic cardiomyopathy mutations increase myofilament Ca2+ buffering, alter intracellular Ca2+ handling, and stimulate Ca2+-dependent signaling;Journal of Biological Chemistry;2018-07

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