The Crossroad of Ion Channels and Calmodulin in Disease

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Date
2019-01-02
Author
Urrutia Iñiguez, Janire
Aguado Martínez, Alejandra
Muguruza Montero, Arantza
Núñez Viadero, Eider ORCID
Malo de la Fuente, Covadonga
Casis Sáenz, Oscar ORCID
Villarroel Muñoz, Álvaro
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International Journal of Molecular Sciences 20(2) : (2019) // Article ID 400
URI
http://hdl.handle.net/10810/32223
Abstract
Calmodulin (CaM) is the principal Ca2+ 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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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
Except where otherwise noted, this item's license is described as This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).