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Decalmodulation of Cav1 channels by CaBPs
Authors:Jason Hardie
Institution:1. Departments of Molecular Physiology and Biophysics;2. Otolaryngology-Head and Neck Surgery and Neurology;3. University of Iowa;4. Iowa City, IA USA
Abstract:Ca2+-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Cav1 and Cav2 channels that is mediated by the Ca2+ sensing protein, calmodulin (CaM), binding to the pore-forming Cav α1 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 Ca2+ binding proteins (CaBPs) that are related to calmodulin. CaBPs are expressed mainly in neural tissues and can antagonize CaM-dependent CDI for Cav1 L-type channels. This review will focus on the roles of CaBPs as Cav1-interacting proteins, and the significance of these interactions for vision, hearing, and neuronal Ca2+ signaling events.
Keywords:Ca2+ channel  calmodulin  inactivation  L-type
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