摘要

Ca2+-dependent inactivation (CDI) is a negative feedback regulation of voltage-gated Ca(v)1 and Ca(v)2 channels that is mediated by the Ca2+ sensing protein, calmodulin (CaM), binding to the pore-forming Ca-v (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 Ca2+ 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 Ca2+ signaling events.

  • 出版日期2016-1-2