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Autophagy is activated for cell survival after endoplasmic reticulum stress
http://hdl.handle.net/10458/2334
http://hdl.handle.net/10458/2334c74f4104-35d1-4db1-8a97-edbe08f63d90
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
9220[1].pdf (746.8 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2009-09-28 | |||||
| タイトル | ||||||
| タイトル | Autophagy is activated for cell survival after endoplasmic reticulum stress | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ | journal article | |||||
| 著者 |
Ogata, Maiko
× Ogata, Maiko× Hino, Shin-ichiro× 斎藤, 敦× Morikawa, Keisuke× 近藤, 慎一× 金本, 聡自× Murakami, Tomohiko× Taniguchi, Manabu× Tanii, Ichiro× Yoshinaga, Kazuya× Shiosaka, Sadao× Hammarback, A. James× Urano, Fumihiko× Imaizumi, Kazunori |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Eukaryotic cells deal with accumulation of unfolded proteins in the endoplasmic reticulum （ER） by the unfolded protein response, involving the induction of molecular chaperones, translational attenuation, and ER-associated degradation, to prevent cell death. Here, we found that the autophagy system is activated as a novel signaling pathway in response to ER stress. Treatment of SK-N-SH neuroblastoma cells with ER stressors markedly induced the formation of autophagosomes, which were recognized at the ultrastructural level. The formation of green fluorescent protein （GFP）-LC3-labeled structures （GFP-LC3 “dots"）, representing autophagosomes, was extensively induced in cells exposed to ER stress with conversion from LC3-I to LC3-II. In IRE1-deficient cells or cells treated with c-Jun N-terminal kinase （JNK） inhibitor, the autophagy induced by ER stress was inhibited, indicating that the IRE1-JNK pathway is required for autophagy activation after ER stress. In contrast, PERK-deficient cells and ATF6 knockdown cells showed that autophagy was induced after ER stress in a manner similar to the wild-type cells. Disturbance of autophagy rendered cells vulnerable to ER stress, suggesting that autophagy plays important roles in cell survival after ER stress. | |||||
| 言語 | en | |||||
| 内容記述 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Copyright © 2009, American Society for Microbiology. All Rights Reserved. | |||||
| 言語 | en | |||||
| 書誌情報 |
en : Molecular and cellular biology 巻 26, 号 24, p. 9220-9231, 発行日 2006-12 |
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| 出版者 | ||||||
| 出版者 | American Society for Microbiology | |||||
| 言語 | en | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 02707306 | |||||
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| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA10620925 | |||||
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| 出版タイプ | VoR | |||||
