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Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics

Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinica...

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Detalles Bibliográficos
Autores principales: Teekakirikul, Polakit, Padera, Robert F., Seidman, J.G., Seidman, Christine E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483129/
https://www.ncbi.nlm.nih.gov/pubmed/23109667
http://dx.doi.org/10.1083/jcb.201207033
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author Teekakirikul, Polakit
Padera, Robert F.
Seidman, J.G.
Seidman, Christine E.
author_facet Teekakirikul, Polakit
Padera, Robert F.
Seidman, J.G.
Seidman, Christine E.
author_sort Teekakirikul, Polakit
collection PubMed
description Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. Studies in these models have provided unexpected insights into the biophysical and biochemical properties of mutated contractile proteins and may help to improve clinical diagnosis and management of patients with HCM.
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spelling pubmed-34831292013-04-29 Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics Teekakirikul, Polakit Padera, Robert F. Seidman, J.G. Seidman, Christine E. J Cell Biol News Hypertrophic cardiomyopathy (HCM) is a common inherited heart disease with serious adverse outcomes, including heart failure, arrhythmias, and sudden cardiac death. The discovery that mutations in sarcomere protein genes cause HCM has enabled the development of mouse models that recapitulate clinical manifestations of disease. Studies in these models have provided unexpected insights into the biophysical and biochemical properties of mutated contractile proteins and may help to improve clinical diagnosis and management of patients with HCM. The Rockefeller University Press 2012-10-29 /pmc/articles/PMC3483129/ /pubmed/23109667 http://dx.doi.org/10.1083/jcb.201207033 Text en © 2012 Teekakirikul et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle News
Teekakirikul, Polakit
Padera, Robert F.
Seidman, J.G.
Seidman, Christine E.
Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title_full Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title_fullStr Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title_full_unstemmed Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title_short Hypertrophic cardiomyopathy: Translating cellular cross talk into therapeutics
title_sort hypertrophic cardiomyopathy: translating cellular cross talk into therapeutics
topic News
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483129/
https://www.ncbi.nlm.nih.gov/pubmed/23109667
http://dx.doi.org/10.1083/jcb.201207033
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