Decalmodulation of Cav1 channels by CaBPs.
Decalmodulation of Cav1 channels by CaBPs.
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DOI：
10.1080/19336950.2015.1051273
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Lee A
中科院分区：
文献类型：
--
作者：
Hardie J;Lee A
Ca2+ 依赖性失活 (CDI) 是电压门控 Cav1 和 Cav2 通道的负反馈调节，由 Ca2+ 传感蛋白钙调蛋白 (CaM) 介导，与成孔 Cav α1 亚基结合。 David Yue 和他的同事为我们理解这一过程以及调节 CDI 的因素做出了开创性的贡献。在这方面，重要的是与钙调蛋白相关的 Ca2+ 结合蛋白 (CaBP) 家族的成员。 CaBPs 主要在神经组织中表达，可以拮抗 Cav1 L 型通道的 CaM 依赖性 CDI。本综述将重点关注 CaBP 作为 Cav1 相互作用蛋白的作用，以及这些相互作用对视觉、听力和神经元 Ca2+ 信号传导事件的重要性。
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.