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论文题目: Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria
英文论文题目: Tom70 Mediates Sendai Virus-Induced Apoptosis on Mitochondria
第一作者: Wei, B; Cui, Y; Huang, YF; Liu, H; Li, L; Li, M; Ruan, KC; Zhou, Q; Wang, C
英文第一作者: Wei, B; Cui, Y; Huang, YF; Liu, H; Li, L; Li, M; Ruan, KC; Zhou, Q; Wang, C
联系作者: Zhou, Q (reprint author), Chongqing Med Univ, Coll Lab Med, Div Mol Nephrol, Chongqing, Peoples R China.
英文联系作者: Zhou, Q (reprint author), Chongqing Med Univ, Coll Lab Med, Div Mol Nephrol, Chongqing, Peoples R China.
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发表年度: 2015
卷: 89
期: 7
页码: 3804-3818
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.
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.
刊物名称: JOURNAL OF VIROLOGY
英文刊物名称: JOURNAL OF VIROLOGY
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学科: Virology
英文学科: Virology
影响因子: 4.439
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论文类别: Article
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