Amplification of CRAC current by STIM1 and CRACM1 (Orai1)

被引：470

作者：

Peinelt, Christine

Vig, Monika

Koomoa, Dana L.

Beck, Andreas

Nadler, Monica J. S.

Koblan-Huberson, Murielle

Lis, Annette

Fleig, Andrea

Penner, Reinhold ^{[1
]}

Kinet, Jean-Pierre

机构：

[1] Univ Hawaii, Ctr Biomed Res, Queens Med Ctr, Honolulu, HI 96813 USA

[2] Univ Hawaii, John A Burns Sch Med, Honolulu, HI 96813 USA

[3] Harvard Univ, Sch Med, Boston, MA 02215 USA

[4] Beth Israel Deaconess Med Ctr, Dept Pathol, Boston, MA 02215 USA

来源：

NATURE CELL BIOLOGY | 2006年 / 8卷 / 07期

关键词：

D O I：

10.1038/ncb1435

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Depletion of intracellular calcium stores activates store-operated calcium entry across the plasma membrane in many cells. STIM1, the putative calcium sensor in the endoplasmic reticulum, and the calcium release-activated calcium ( CRAC) modulator CRACM1 ( also known as Orai1) in the plasma membrane have recently been shown to be essential for controlling the store-operated CRAC current ( I-CRAC)(1-4). However, individual overexpression of either protein fails to significantly amplify I-CRAC. Here, we show that STIM1 and CRACM1 interact functionally. Overexpression of both proteins greatly potentiates I-CRAC, suggesting that STIM1 and CRACM1 mutually limit store-operated currents and that CRACM1 may be the long-sought CRAC channel.

引用

页码：771 / U231

页数：6

共 15 条

[1] A mutation in Orai1 causes immune deficiency by abrogating CRAC channel function [J].