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Advances in understanding the activation mechanism of store-operated Ca2+ channels

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Author:: No author available

Journal Title:: WORLD CHINESE JOURNAL OF DIGESTOLOGY

Issue:: 17

DOI:: 10.3969/j.issn.1009-3079.2007.17.001

Key Word:: 钙池操纵的Ca2+通道;钙内流因子模型;构象耦联模型

Abstract：钙池操纵的Ca2+通道(store-operated Ca2+ channels,SOC)是非兴奋细胞Ca2+内流的主要通道之一,参与多种病理和生理过程,在钙信号通路的研究中,SOC的激活机制一直是人们关注的焦点之一,迄今为止,钙内流因子模型(Ca2+influx factor model,CIF model)和构象耦联模型(conformational coupling model)受到广泛关注.部分学者已经从很多不同类型的细胞中提取出CIF,并证实钙非依赖性的磷脂酶A2(Ca2+-independent phospholipase A2,iPLA2)作为CIF的底物,在某些类型细胞的SOC激活过程中发挥重要作用,并进一步提出了ERCIF-iPLA2-CaM-LysoPLs-SOC通路模型.瞬时受体电位(transient receptor potential,TRP)通道蛋白与l,4,5-磷酸肌醇受体(inositol 1,4,5trisphosphate receptor, IP3R)的结构连接作为构象耦联模型的基础已被广泛证实,随着对IP3R,Ryanodine受体、肌动蛋白等在钙信号通路中所发挥作用的深入研究,构象耦联模型将得到不断补充和完善.SOC激活机制的破解,将对进一步完善非兴奋细胞的钙通道特性及其调节机制理论带来重大突破.

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