期刊
SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-99980-9
关键词
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资金
- Japan Society for the Promotion of Science (JSPS) [24227009]
- JSPS KAKENHI [JP18H04002, JP18K06140, JP15H01545, JP18H04871, JP21H05268]
- Takeda Science Foundation
- CREST
- AMED [JP21gm1410008]
- Research Program for CORE lab of Five-star Alliance in NJRC Mater. Dev
ERdj5 in the endoplasmic reticulum plays a crucial role in regulating intracellular calcium levels, affecting mitochondrial homeostasis and cellular senescence.
The endoplasmic reticulum (ER) is the organelle responsible for the folding of secretory/membrane proteins and acts as a dynamic calcium ion (Ca2+) store involved in various cellular signalling pathways. Previously, we reported that the ER-resident disulfide reductase ERdj5 is involved in the ER-associated degradation (ERAD) of misfolded proteins in the ER and the activation of SERCA2b, a Ca2+ pump on the ER membrane. These results highlighted the importance of the regulation of redox activity in both Ca2+ and protein homeostasis in the ER. Here, we show that the deletion of ERdj5 causes an imbalance in intracellular Ca2+ homeostasis, the activation of Drp1, a cytosolic GTPase involved in mitochondrial fission, and finally the aberrant fragmentation of mitochondria, which affects cell viability as well as phenotype with features of cellular senescence. Thus, ERdj5-mediated regulation of intracellular Ca2+ is essential for the maintenance of mitochondrial homeostasis involved in cellular senescence.
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