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Mechanism of ASC-mediated apoptosis: Bid-dependent apoptosis in type II cells
https://doi.org/10.24517/00027359
https://doi.org/10.24517/00027359e62a051f-ca9a-425c-b661-3f29b0be8c6b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-SUDA-T-1748.pdf (2.1 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||
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| 公開日 | 2017-10-05 | |||||||||||
| タイトル | ||||||||||||
| タイトル | Mechanism of ASC-mediated apoptosis: Bid-dependent apoptosis in type II cells | |||||||||||
| 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 | |||||||||||
| ID登録 | ||||||||||||
| ID登録 | 10.24517/00027359 | |||||||||||
| ID登録タイプ | JaLC | |||||||||||
| 著者 |
Hasegawa, Mizuho
× Hasegawa, Mizuho× Kawase, Kouji× Inohara, Naohiro× Imamura, Ryu× Yeh, Wen-Chen× Kinoshita, Takeshi× Suda, Takashi |
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| 著者別表示 |
今村, 龍
× 今村, 龍
× 木下, 健
× 須田, 貴司
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| 提供者所属 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | 金沢大学がん研究所がん病態制御 | |||||||||||
| 書誌情報 |
Oncogene Volume 巻 26, 号 12, p. 1748-1756, 発行日 2007-03-15 |
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| ISSN | ||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||
| 収録物識別子 | 0950-9232 | |||||||||||
| NCID | ||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||
| 収録物識別子 | AA10687380 | |||||||||||
| DOI | ||||||||||||
| 関連タイプ | isVersionOf | |||||||||||
| 識別子タイプ | DOI | |||||||||||
| 関連識別子 | 10.1038/sj.onc.1209965 | |||||||||||
| 出版者 | ||||||||||||
| 出版者 | Nature Publishing Group | |||||||||||
| 抄録 | ||||||||||||
| 内容記述タイプ | Abstract | |||||||||||
| 内容記述 | Apoptosis-associated speck-like protein containing a CARD (ASC) is an adaptor molecule that mediates apoptotic and inflammatory signals, and implicated in tumor suppression. However, the mechanism of ASC-mediated apoptosis has not been well elucidated. Here, we investigated the molecular mechanisms of ASC-mediated apoptosis in several cell lines using a caspase recruitment domain 12-Nod2 chimeric protein that transduces the signal from muramyl dipeptide into ASC-mediated apoptosis. Experiments using dominant-negative mutants, small-interfering RNAs and peptide inhibitors for caspases indicated that caspase-8 was generally required for ASC-mediated apoptosis, whereas a requirement for caspase-9 depended on the cell type. In addition, caspase-like apoptosis-regulatory protein (CLARP)/Fas-like inhibitor protein, a natural caspase-8 inhibitor, suppressed ASC-mediated apoptosis, and Clarp-/- mouse embryonic fibroblasts were highly sensitive to ASC-mediated apoptosis. Bax-deficient HCT116 cells were resistant to ASC-mediated apoptosis as reported previously, although we failed to observe colocalization of ASC and Bax in cells. Like Fas-ligand-induced apoptosis, the ASC-mediated apoptosis was inhibited by Bcl-2 and/or Bcl-XL in type-II but not type-I cell lines. Bid was cleaved upon ASC activation, and suppression of endogenous Bid expression using small-interfering RNAs in type-II cells reduced the ASC-mediated apoptosis. These results indicate that ASC, like death receptors, mediates two types of apoptosis depending on the cell type, in a manner involving caspase-8. © 2007 Nature Publishing Group All rights reserved. | |||||||||||
| 著者版フラグ | ||||||||||||
| 出版タイプ | AM | |||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||
