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Transmission of cell stress from endoplasmic reticulum to mitochondria: Enhanced expression of Lon protease
http://hdl.handle.net/2297/28988
http://hdl.handle.net/2297/28988ae03ee87-ddb1-4bc4-85c2-5d05d2bef5fb
名前 / ファイル | ライセンス | アクション |
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ME-PR-HORI-O-1151.pdf (350.8 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-03 | |||||
タイトル | ||||||
タイトル | Transmission of cell stress from endoplasmic reticulum to mitochondria: Enhanced expression of Lon protease | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Hori, Osamu
× Hori, Osamu× Ichinoda, Fusae× Tamatani, Takashi× Yamaguchi, Atsushi× Sato, Naoya× Ozawa, Kentaro× Kitao, Yasuko× Miyazaki, Mayuki× Harding, Heather P.× Ron, David× Tohyama, Masaya× Stern, David M.× Ogawa, Satoshi |
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書誌情報 |
Journal of Cell Biology 巻 157, 号 7, p. 1151-1160, 発行日 2002-06-24 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0021-9525 | |||||
NCID | ||||||
識別子タイプ | NCID | |||||
関連識別子 | BA0755651X | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1083/jcb.200108103 | |||||
出版者 | ||||||
出版者 | Rockefeller University Press | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The rat homologue of a mitochondrial ATP-dependent protease Lon was cloned from cultured astrocytes exposed to hypoxia. Expression of Lon was enhanced in vitro by hypoxia or ER stress, and in vivo by brain ischemia. These observations suggested that changes in nuclear gene expression (Lon) triggered by ER stress had the potential to impact important mitochondrial processes such as assembly and/or degradation of cytochrome c oxidase (COX). In fact, steady-state levels of nuclear-encoded COX IV and V were reduced, and mitochondrial-encoded subunit II was rapidly degraded under ER stress. Treatment of cells with cycloheximide caused a similar imbalance in the accumulation of COX subunits, and enhanced mRNA for Lon and Yme1, the latter another mitochondrial ATP-dependent protease. Furthermore, induction of Lon or GRP75/mtHSP70 by ER stress was inhibited in PERK (-/-) cells. Transfection studies revealed that overexpression of wild-type or proteolytically inactive Lon promoted assembly of COX II into a COX I-containing complex, and partially prevented mitochondrial dysfunction caused by brefeldin A or hypoxia. These observations demonstrated that suppression of protein synthesis due to ER stress has a complex effect on the synthesis of mitochondrial-associated proteins, both COX subunits and ATP-dependent proteases and/or chaperones contributing to assembly of the COX complex. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |