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ウシオダ リョウ
USHIODA RYO
潮田 亮 所属 京都産業大学 生命科学部 先端生命科学科 職種 准教授 |
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| 発行・発表の年月 | 2021/12 |
| 形態種別 | 研究論文 |
| 標題 | Ca2+ imbalance caused by ERdj5 deletion affects mitochondrial fragmentation |
| 執筆形態 | その他 |
| 掲載誌名 | Scientific Reports |
| 出版社・発行元 | Springer Science and Business Media LLC |
| 巻・号・頁 | 11(1) |
| 著者・共著者 | Riyuji Yamashita,Shohei Fujii,Ryo Ushioda,Kazuhiro Nagata |
| 概要 | <title>Abstract</title>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. |
| DOI | 10.1038/s41598-021-99980-9 |
| ISSN | /2045-2322 |
| PermalinkURL | https://www.nature.com/articles/s41598-021-99980-9.pdf |
| researchmap用URL | https://www.nature.com/articles/s41598-021-99980-9 |