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.
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页数：3
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