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Decalmodulation of Ca(v)1 channels by CaBPs

Ca(2+)-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Ca(v)1 and Ca(v)2 channels that is mediated by the Ca(2+) sensing protein, calmodulin (CaM), binding to the pore-forming Ca(v) α(1) subunit. David Yue and his colleagues made seminal contributions to our understan...

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Detalles Bibliográficos
Autores principales: Hardie, Jason, Lee, Amy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4802809/
https://www.ncbi.nlm.nih.gov/pubmed/26155893
http://dx.doi.org/10.1080/19336950.2015.1051273
Descripción
Sumario:Ca(2+)-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Ca(v)1 and Ca(v)2 channels that is mediated by the Ca(2+) sensing protein, calmodulin (CaM), binding to the pore-forming Ca(v) α(1) subunit. David Yue and his colleagues made seminal contributions to our understanding of this process, as well as factors that regulate CDI. Important in this regard are members of a family of Ca(2+) binding proteins (CaBPs) that are related to calmodulin. CaBPs are expressed mainly in neural tissues and can antagonize CaM-dependent CDI for Ca(v)1 L-type channels. This review will focus on the roles of CaBPs as Ca(v)1-interacting proteins, and the significance of these interactions for vision, hearing, and neuronal Ca(2+) signaling events.