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Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin

It has been known for several decades that mutations in genes that encode for proteins involved in the control of actomyosin interactions such as the troponin complex, tropomyosin and MYBP-C and thus regulate contraction can lead to hereditary hypertrophic cardiomyopathy. In recent years, it has bec...

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Detalles Bibliográficos
Autor principal: Ehler, Elisabeth
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082317/
https://www.ncbi.nlm.nih.gov/pubmed/29869751
http://dx.doi.org/10.1007/s12551-018-0428-1
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author Ehler, Elisabeth
author_facet Ehler, Elisabeth
author_sort Ehler, Elisabeth
collection PubMed
description It has been known for several decades that mutations in genes that encode for proteins involved in the control of actomyosin interactions such as the troponin complex, tropomyosin and MYBP-C and thus regulate contraction can lead to hereditary hypertrophic cardiomyopathy. In recent years, it has become apparent that actin-binding proteins not directly involved in the regulation of contraction also can exhibit changed expression levels, show altered subcellular localisation or bear mutations that might lead to hereditary cardiomyopathies. The aim of this review is to look beyond the troponin/tropomyosin mechanism and to give an overview of the different types of actin-associated proteins and their potential roles in cardiomyocytes. It will then discuss recent findings relevant to their involvement in heart disease.
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spelling pubmed-60823172018-08-22 Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin Ehler, Elisabeth Biophys Rev Review It has been known for several decades that mutations in genes that encode for proteins involved in the control of actomyosin interactions such as the troponin complex, tropomyosin and MYBP-C and thus regulate contraction can lead to hereditary hypertrophic cardiomyopathy. In recent years, it has become apparent that actin-binding proteins not directly involved in the regulation of contraction also can exhibit changed expression levels, show altered subcellular localisation or bear mutations that might lead to hereditary cardiomyopathies. The aim of this review is to look beyond the troponin/tropomyosin mechanism and to give an overview of the different types of actin-associated proteins and their potential roles in cardiomyocytes. It will then discuss recent findings relevant to their involvement in heart disease. Springer Berlin Heidelberg 2018-06-05 /pmc/articles/PMC6082317/ /pubmed/29869751 http://dx.doi.org/10.1007/s12551-018-0428-1 Text en © The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Ehler, Elisabeth
Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title_full Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title_fullStr Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title_full_unstemmed Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title_short Actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
title_sort actin-associated proteins and cardiomyopathy—the ‘unknown’ beyond troponin and tropomyosin
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082317/
https://www.ncbi.nlm.nih.gov/pubmed/29869751
http://dx.doi.org/10.1007/s12551-018-0428-1
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