Redox regulation of ER and mitochondrial Ca2+ signaling in cell survival and death

被引：39
作者：
Joseph, Suresh K. [1 ]
Booth, David M. [1 ]
Young, Michael P. [1 ]
Hajnoczky, Gyorgy [1 ]
机构：
[1] Thomas Jefferson Univ, Dept Pathol & Cell Biol, MitoCare, Philadelphia, PA 19107 USA
来源：
CELL CALCIUM | 2019年 / 79卷
关键词：
Ca2+; IP3; receptor; Mitochondrial calcium uniporter; Redox regulation; Reactive oxygen species; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; ENDOPLASMIC-RETICULUM STRESS; PROTEIN S-GLUTATHIONYLATION; RELEASE CHANNEL RYR1; OXIDATIVE STRESS; IP3; RECEPTORS; CALCIUM HOMEOSTASIS; CYSTEINE RESIDUES; THIOL REAGENT; MICU1;
D O I：
10.1016/j.ceca.2019.02.006
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Physiological signaling by reactive oxygen species (ROS) and their pathophysiological role in cell death are well recognized. This review focuses on two ROS targets that are key to local Ca2+ signaling at the ER/mitochondrial interface - notably, inositol trisphosphate receptors (IP(3)Rs) and the mitochondrial calcium uniporter (MCU). Both transport systems are central to molecular mechanisms in cell survival and death. Methods for the measurement of the redox state of these proteins and for the detection of ROS nanodomains are described. Recent results on the redox regulation of these proteins are reviewed.
引用
收藏
页码：89 / 97
页数：9
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