Temperature-dependent STIM1 activation induces Ca2+ influx and modulates gene expression

被引：0

作者：

Xiao B. ^{[1
]}

Coste B. ^{[1
]}

Mathur J. ^{[2
]}

Patapoutian A. ^{[1
,2
]}

机构：

[1] Dorris Neuroscience Center, Department of Cell Biology, Scripps Research Institute, San Diego, CA

[2] Genomics Institute, Novartis Research Foundation, San Diego, CA

来源：

Nature Chemical Biology | 2011年 / 7卷 / 6期

基金：

美国国家卫生研究院;

关键词：

D O I：

10.1038/nchembio.558

中图分类号：

学科分类号：

摘要：

Intracellular Ca2+ is essential for diverse cellular functions. Ca2+ entry into many cell types including immune cells is triggered by depleting endoplasmic reticulum (ER) Ca2+, a process termed store-operated Ca2+ entry (SOCE). STIM1 is an ER Ca2+ sensor. Upon Ca2+ store depletion, STIM1 clusters at ERg-plasma membrane junctions where it interacts with and gates Ca2+ -permeable Orai1 ion channels. Here we show that STIM1 is also activated by temperature. Heating cells caused clustering of STIM1 at temperatures above 35 °C without depleting Ca2+ stores and led to Orai1-mediated Ca2+ influx as a heat off-response (response after cooling). Notably, the functional coupling of STIM1 and Orai1 is prevented at high temperatures, potentially explaining the heat off-response. Additionally, physiologically relevant temperature shifts modulate STIM1-dependent gene expression in Jurkat T cells. Therefore, temperature is an important regulator of STIM1 function. © 2011 Nature America, Inc. All rights reserved.

引用

页码：351 / 358

页数：7

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