STIMulating IRE1: How store-operated Ca2+entry intersects with ER proteostasis

被引：0

作者：

Sassano, Maria Livia ^{[1
,2
]}

Van Gorp, Robbe ^{[3
,4
]}

Bultynck, Geert ^{[3
,4
]}

Agostinis, Patrizia ^{[1
,2
]}

机构：

[1] VIB KU Leuven, Ctr Canc Biol, Cell Death Res & Therapy Lab, Leuven, Belgium

[2] Katholieke Univ Leuven, Dept Cellular & Mol Med, Leuven, Belgium

[3] Katholieke Univ Leuven, Dept Cellular & Mol Med, Lab Mol & Cellular Signaling, Leuven, Belgium

[4] Katholieke Univ Leuven, Leuven Kanker Inst LKI, Leuven, Belgium

来源：

CELL CALCIUM | 2025年 / 125卷

关键词：

Unfolded protein response; Store-operated calcium entry; IRE1; STIM1; IP3; receptors;

D O I：

10.1016/j.ceca.2024.102980

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The endoplasmic reticulum (ER) controls intracellular Ca2+ dynamics. Depletion of ER Ca2+ stores results in short-term activation of store-operated Ca2+ entry (SOCE) via STIM1/Orai1 at ER-plasma membrane (ER-PM) contact sites (MCSs) and the long-term activation of the unfolded protein response (UPR), securing ER proteostasis. Recent work by Carreras-Sureda and colleagues describes a bidirectional control between IRE1 and STIM1 within the ER lumen that regulates ER-PM contact assembly and SOCE to sustain T-cell activation and myoblast differentiation.

引用

页数：3

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