dc.contributor.author | Urrutia Iñiguez, Janire | |
dc.contributor.author | Aguado Martínez, Alejandra | |
dc.contributor.author | Muguruza Montero, Arantza | |
dc.contributor.author | Núñez Viadero, Eider | |
dc.contributor.author | Malo de la Fuente, Covadonga | |
dc.contributor.author | Casis Sáenz, Oscar | |
dc.contributor.author | Villarroel Muñoz, Álvaro | |
dc.date.accessioned | 2019-03-29T14:09:04Z | |
dc.date.available | 2019-03-29T14:09:04Z | |
dc.date.issued | 2019-01-02 | |
dc.identifier.citation | International Journal of Molecular Sciences 20(2) : (2019) // Article ID 400 | es_ES |
dc.identifier.issn | 1422-0067 | |
dc.identifier.uri | http://hdl.handle.net/10810/32223 | |
dc.description.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. | es_ES |
dc.description.sponsorship | The Department of Industry, Tourism and Trade of the Government of the Autonomous Community of the Basque Country (Elkartek 2017 bG17 kk-2017/000843M50.17.EK.C6) and the Spanish Ministry of Economy, Industry and Competitiveness (BFU2015-66910 and RTI2018-097839) provided financial support for this work. E.N. is supported by a predoctoral grant of the Basque Government. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/BFU2015-66910 | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/RTI2018-097839 | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.subject | calmodulin | es_ES |
dc.subject | ion channels | es_ES |
dc.subject | channelopathies | es_ES |
dc.subject | calcium | es_ES |
dc.subject | cardiac ryanodine receptor | es_ES |
dc.subject | axonal surface expression | es_ES |
dc.subject | st-segment elevation | es_ES |
dc.subject | kcnq2 encephalopathy | es_ES |
dc.subject | ca2+ release | es_ES |
dc.subject | c-terminus | es_ES |
dc.subject | iq motif | es_ES |
dc.subject | mutations | es_ES |
dc.subject | calcium | es_ES |
dc.subject | binding | es_ES |
dc.title | The Crossroad of Ion Channels and Calmodulin in Disease | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.holder | 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). | es_ES |
dc.rights.holder | Atribución 3.0 España | * |
dc.relation.publisherversion | https://www.mdpi.com/1422-0067/20/2/400 | es_ES |
dc.identifier.doi | 10.3390/ijms20020400 | |
dc.departamentoes | Fisiología | es_ES |
dc.departamentoeu | Fisiologia | es_ES |