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  • 标题:Ca 2+ imbalance caused by ERdj5 deletion affects mitochondrial fragmentation
  • 本地全文:下载
  • 作者:Riyuji Yamashita ; Shohei Fujii ; Ryo Ushioda
  • 期刊名称:Scientific Reports
  • 电子版ISSN:2045-2322
  • 出版年度:2021
  • 卷号:11
  • DOI:10.1038/s41598-021-99980-9
  • 语种:English
  • 出版社:Springer Nature
  • 摘要:The endoplasmic reticulum (ER) is the organelle responsible for the folding of secretory/membrane proteins and acts as a dynamic calcium ion (Ca 2+) 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 Ca 2+ pump on the ER membrane. These results highlighted the importance of the regulation of redox activity in both Ca 2+ and protein homeostasis in the ER. Here, we show that the deletion of ERdj5 causes an imbalance in intracellular Ca 2+ 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 Ca 2+ is essential for the maintenance of mitochondrial homeostasis involved in cellular senescence.
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