Intracellular trafficking of TRP channels
Intracellular trafficking of TRP channels
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DOI：
10.1016/j.ceca.2007.01.014
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发表时间：
2007-08-01
期刊：
影响因子：
4
通讯作者：
Boulay, Guylain
中科院分区：
文献类型：
--
作者：
Cayouette, Sylvie;Boulay, Guylain
13年前，有人提出，胞吐插入的存储操作的通道到质膜导致增加的钙离子进入非兴奋细胞后，G蛋白偶联或酪氨酸激酶受体刺激。自从发现TRP通道超家族及其参与受体诱导的Ca 2+内流以来，许多研究表明，TRP超家族的不同成员在刺激时易位到质膜中。虽然TRP通道插入质膜的确切分子机制尚不清楚，但TRP结合蛋白已被证明直接调节这种运输。本文综述了TRP通道转运机制的最新研究进展，重点介绍了TRP结合蛋白的作用。(C)2007爱思唯尔有限公司保留所有权利。
Thirteen years ago, it was suggested that exocytotic insertion of store-operated channels into the plasma membrane lead to increased Ca2+ entry in non-excitable cells upon G protein-coupled or tyrosine kinase receptor stimulation. Since the discovery of the TRP channel superfamily and their involvement in receptor-induced Ca2+ entry, many studies have shown that different members of the TRP superfamily translocate into the plasma membrane upon stimulation. While the exact molecular mechanism by which TRP channels insert into the plasma membrane is unknown, TRP-binding proteins have been shown to directly regulate this trafficking. This review summarizes recent advances related to the mechanism of TRP channel trafficking, focusing on the role of TRP-binding proteins. (C) 2007 Elsevier Ltd. All rights reserved.