Putney J W, McKay R R
Calcium Regulation Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA.
Bioessays. 1999 Jan;21(1):38-46. doi: 10.1002/(SICI)1521-1878(199901)21:1<38::AID-BIES5>3.0.CO;2-S.
In the phospholipase C signaling system, Ca(2+) is mobilized from intracellular stores by an action of inositol 1,4,5-trisphosphate. The depletion of intracellular calcium stores activates a calcium entry mechanism at the plasma membrane called capacitative calcium entry. The signal for activating the entry is unknown but likely involves either the generation or release, or both, from the endoplasmic reticulum of some diffusible signal. Recent research has focused on mammalian homologues of the Drosophila TRP protein as potential candidates for capacitative calcium entry channels. This review summarizes current knowledge about the nature of capacitative calcium entry signals, as well as the potential role of mammalian TRP proteins as capacitative calcium entry channel molecules.
在磷脂酶C信号系统中,肌醇1,4,5 -三磷酸的作用使Ca(2+)从细胞内储存库中释放出来。细胞内钙储存的耗尽激活了质膜上一种称为容量性钙内流的钙进入机制。激活该内流的信号尚不清楚,但可能涉及某种可扩散信号从内质网的产生或释放,或两者兼而有之。最近的研究集中在果蝇TRP蛋白的哺乳动物同源物上,将其作为容量性钙内流通道的潜在候选者。这篇综述总结了关于容量性钙内流信号性质的当前知识,以及哺乳动物TRP蛋白作为容量性钙内流通道分子的潜在作用。