The Crossroad of Ion Channels and Calmodulin in Disease

Calmodulin (CaM) is the principal Ca(2+) sensor in eukaryotic cells, orchestrating the activity of hundreds of proteins. Disease causing mutations at any of the three genes that encode identical CaM proteins lead to major cardiac dysfunction, revealing the importance in the regulation of excitabilit...

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Detalles Bibliográficos
Autores principales: Urrutia, Janire, Aguado, Alejandra, Muguruza-Montero, Arantza, Núñez, Eider, Malo, Covadonga, Casis, Oscar, Villarroel, Alvaro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359610/
https://www.ncbi.nlm.nih.gov/pubmed/30669290
http://dx.doi.org/10.3390/ijms20020400
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author Urrutia, Janire
Aguado, Alejandra
Muguruza-Montero, Arantza
Núñez, Eider
Malo, Covadonga
Casis, Oscar
Villarroel, Alvaro
author_facet Urrutia, Janire
Aguado, Alejandra
Muguruza-Montero, Arantza
Núñez, Eider
Malo, Covadonga
Casis, Oscar
Villarroel, Alvaro
author_sort Urrutia, Janire
collection PubMed
description Calmodulin (CaM) is the principal Ca(2+) sensor in eukaryotic cells, orchestrating the activity of hundreds of proteins. Disease causing mutations at any of the three genes that encode identical CaM proteins lead to major cardiac dysfunction, revealing the importance in the regulation of excitability. In turn, some mutations at the CaM binding site of ion channels cause similar diseases. Here we provide a summary of the two sides of the partnership between CaM and ion channels, describing the diversity of consequences of mutations at the complementary CaM binding domains.
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spelling pubmed-63596102019-02-06 The Crossroad of Ion Channels and Calmodulin in Disease Urrutia, Janire Aguado, Alejandra Muguruza-Montero, Arantza Núñez, Eider Malo, Covadonga Casis, Oscar Villarroel, Alvaro Int J Mol Sci Review Calmodulin (CaM) is the principal Ca(2+) sensor in eukaryotic cells, orchestrating the activity of hundreds of proteins. Disease causing mutations at any of the three genes that encode identical CaM proteins lead to major cardiac dysfunction, revealing the importance in the regulation of excitability. In turn, some mutations at the CaM binding site of ion channels cause similar diseases. Here we provide a summary of the two sides of the partnership between CaM and ion channels, describing the diversity of consequences of mutations at the complementary CaM binding domains. MDPI 2019-01-18 /pmc/articles/PMC6359610/ /pubmed/30669290 http://dx.doi.org/10.3390/ijms20020400 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Urrutia, Janire
Aguado, Alejandra
Muguruza-Montero, Arantza
Núñez, Eider
Malo, Covadonga
Casis, Oscar
Villarroel, Alvaro
The Crossroad of Ion Channels and Calmodulin in Disease
title The Crossroad of Ion Channels and Calmodulin in Disease
title_full The Crossroad of Ion Channels and Calmodulin in Disease
title_fullStr The Crossroad of Ion Channels and Calmodulin in Disease
title_full_unstemmed The Crossroad of Ion Channels and Calmodulin in Disease
title_short The Crossroad of Ion Channels and Calmodulin in Disease
title_sort crossroad of ion channels and calmodulin in disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6359610/
https://www.ncbi.nlm.nih.gov/pubmed/30669290
http://dx.doi.org/10.3390/ijms20020400
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