Salido Ginés M, Sage Stewart O, Rosado Juan A
Department of Physiology (Cell Physiology Research Group), University of Extremadura, Cáceres 10071, Spain.
Biochim Biophys Acta. 2009 Feb;1793(2):223-30. doi: 10.1016/j.bbamcr.2008.11.001. Epub 2008 Nov 12.
Store-operated calcium entry (SOCE) is a major mechanism for Ca(2+) influx. Since SOCE was first proposed two decades ago many techniques have been used in attempting to identify the nature of store-operated Ca(2+) (SOC) channels. The first identified and best-characterised store-operated current is I(CRAC), but a number of other currents activated by Ca(2+) store depletion have also been described. TRPC proteins have long been proposed as SOC channel candidates; however, whether any of the TRPCs function as SOC channels remains controversial. This review attempts to provide an overview of the arguments in favour and against the role of TRPC proteins in the store-operated mechanisms of agonist-activated Ca(2+) entry.
store-operated calcium entry (SOCE)是Ca(2+)内流的主要机制。自二十年前首次提出SOCE以来,许多技术已被用于试图确定储存操纵性Ca(2+)(SOC)通道的性质。第一个被鉴定且特征最明确的储存操纵性电流是I(CRAC),但也有一些其他由Ca(2+)储存耗竭激活的电流被描述过。TRPC蛋白长期以来一直被认为是SOC通道的候选者;然而,是否有任何TRPCs充当SOC通道仍存在争议。本综述试图概述支持和反对TRPC蛋白在激动剂激活的Ca(2+)内流的储存操纵机制中作用的观点。