Activation and regulation of store-operated calcium entry.

Activation and regulation of store-operated calcium entry.
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DOI:
10.1111/j.1582-4934.2010.01168.x
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发表时间:
2010-10
影响因子:
5.3
通讯作者:
Putney JW
Putney JW
中科院分区:
医学2区
文献类型:
--
作者:
Smyth JT;Hwang SY;Tomita T;DeHaven WI;Mercer JC;Putney JW

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钙库操纵的钙内流(SOCE)的过程,其中跨质膜的Ca 2+内流被激活,以响应内质网(ER)中细胞内Ca 2+库的耗竭,已被研究超过25年;然而,只有在过去的5年中,我们才能在分子水平上理解这一机制。最近的实验表明,STIM分子作为钙离子传感器内的ER,Ca 2+存储耗尽后,重新排列到非常接近质膜的网站。在这些质膜-ER连接处,STIM与奥赖家族的SOCE通道相互作用并激活该通道。在这篇评论中讨论了导致这些发现的分子和生物物理数据,以及在这个迅速扩大的领域中的一些争议。
The process of store-operated Ca2+ entry (SOCE), whereby Ca2+ influx across the plasma membrane is activated in response to depletion of intracellular Ca2+ stores in the endoplasmic reticulum (ER), has been under investigation for greater than 25 years; however, only in the past 5 years have we come to understand this mechanism at the molecular level. A surge of recent experimentation indicates that STIM molecules function as Ca2+ sensors within the ER that, upon Ca2+ store depletion, rearrange to sites very near to the plasma membrane. At these plasma membrane-ER junctions, STIM interacts with and activates SOCE channels of the Orai family. The molecular and biophysical data that have led to these findings are discussed in this review, as are several controversies within this rapidly expanding field.
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