Kiselyov K, Shin D M, Kim J Y, Yuan J P, Muallem S
Department of Biological Sciences University of Pittsburgh, Pittsburgh, PA 15260, USA.
Handb Exp Pharmacol. 2007(179):559-74. doi: 10.1007/978-3-540-34891-7_33.
TRP channels, in particular the TRPC and TRPV subfamilies, have emerged as important constituents of the receptor-activated Ca2+ influx mechanism triggered by hormones, growth factors, and neurotransmitters through activation ofphospholipase C (PLC). Several TRPC channels are also activated by passive depletion of endoplasmic reticulum (ER) Ca2+. Although in several studies the native TRP channels faithfully reproduce the respective recombinant channels, more often the properties of Ca2+ entry and/or the store-operated current are strikingly different from that of the TRP channels expressed in the same cells. The present review aims to discuss this disparity in the context of interaction of TRPC channels with auxiliary proteins that may alter the permeation and regulation of TRPC channels.
瞬时受体电位（TRP）通道，特别是TRPC和TRPV亚家族，已成为由激素、生长因子和神经递质通过激活磷脂酶C（PLC）触发的受体激活的Ca2+内流机制的重要组成部分。几种TRPC通道也可通过内质网（ER）Ca2+的被动耗竭而被激活。尽管在一些研究中，天然TRP通道忠实地重现了各自的重组通道，但Ca2+内流和/或储存操纵电流的特性往往与在同一细胞中表达的TRP通道有显著差异。本综述旨在讨论TRPC通道与辅助蛋白相互作用的背景下的这种差异，这些辅助蛋白可能会改变TRPC通道的通透和调节。
