Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria
文献类型：期刊论文
| 作者 | Wei, B; Cui, Y; Huang, YF; Liu, H; Li, L; Li, M; Ruan, KC; Zhou, Q; Wang, C |
| 刊名 | JOURNAL OF VIROLOGY
 |
| 出版日期 | 2015 |
| 卷号 | 89期号:7页码:3804-3818 |
| 通讯作者 | Zhou, Q (reprint author), Chongqing Med Univ, Coll Lab Med, Div Mol Nephrol, Chongqing, Peoples R China.,zhouqin@cqmu.edu.cn ; cwang01@sibcb.ac.cn |
| 英文摘要 | Virus infection triggers immediate innate immune responses. Apoptosis represents another effective means to restrict virus invasion, besides robust expression of host cytokines and chemokines. IRF3 was recently demonstrated to be indispensable for Sendai virus (SeV)-induced apoptosis, but the underlying mechanism is not fully understood. Here we report that a dynamic protein complex, Tom70/Hsp90/IRF3/Bax, mediates SeV-induced apoptosis. The cytosolic proapoptotic protein Bax interacts specifically with IRF3 upon virus infection. The mitochondrial outer membrane protein Tom70 recruits IRF3 to mitochondria via Hsp90. Consequently, the relocation of Bax onto mitochondria induces the leakage of cytochrome c into the cytosol and initiates the corresponding apoptosis. Interestingly, IKK-i is essential for this apoptosis, whereas TBK1 is dispensable. Collectively, our study characterizes a novel protein complex that is important for SeV-induced apoptosis. IMPORTANCE Apoptosis is an effective means of sacrificing virus-infected cells and restraining the spread of virus. In this study, we demonstrate that IRF3 associates with Bax upon virus infection. Tom70 recruits this protein complex to the mitochondrial outer membrane through Hsp90, which thus induces the release of cytochrome c into the cytosol, initiating virus-induced apoptosis. Interestingly, IKK-i plays an essential role in this activation. This study uncovers a novel mechanism of SeV-induced apoptosis. |
| 学科主题 | Virology |
| 类目[WOS] | Virology |
| 关键词[WOS] | INTERFERON REGULATORY FACTOR-3 ; ANTIVIRAL SIGNALING PROTEIN ; HEPATITIS-C-VIRUS ; NF-KAPPA-B ; ADAPTER PROTEIN ; INNATE IMMUNITY ; NS1 PROTEIN ; ACTIVATION ; PATHWAY ; BCL-2 |
| 收录类别 | SCI |
| 语种 | 英语 |
| WOS记录号 | WOS:000352216100029 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.143/handle/331003/82]  |
| 专题 | 上海生化细胞研究所_上海生科院生化细胞研究所 |
| 推荐引用方式 GB/T 7714 | Wei, B,Cui, Y,Huang, YF,et al. Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria[J]. JOURNAL OF VIROLOGY,2015,89(7):3804-3818. |
| APA | Wei, B.,Cui, Y.,Huang, YF.,Liu, H.,Li, L.,...&Wang, C.(2015).Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria.JOURNAL OF VIROLOGY,89(7),3804-3818. |
| MLA | Wei, B,et al."Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria".JOURNAL OF VIROLOGY 89.7(2015):3804-3818. |
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