期刊
IMMUNITY
卷 29, 期 4, 页码 538-550出版社
CELL PRESS
DOI: 10.1016/j.immuni.2008.09.003
关键词
-
类别
资金
- Chinese 973 program [2006CB504301, 2009CB522506]
- National Natural Science Foundation of China [30630019, 30700431]
- Chinese 863 program [2006AA02A306]
Viral infection triggers activation of transcription factors such as NF-kappa B and IRF3, which collaborate to induce type I interferons (IFNs) and elicit innate antiviral response. Here, we identified MITA as a critical mediator of virus-triggered type I IFN signaling by expression cloning. Overexpression of MITA activated IRF3, whereas knockdown of MITA inhibited virus-triggered activation of IRF3, expression of type I IFNs, and cellular antiviral response. MITA was found to localize to the outer membrane of mitochondria and to be associated with VISA, a mitochondrial protein that acts as an adaptor in virus-triggered signaling. MITA also interacted with IRF3 and recruited the kinase TBK1 to the VISA-associated complex. MITA was phosphorylated by TBK1, which is required for MITA-mediated activation of IRF3. Our results suggest that MITA is a critical mediator of virus-triggered IRF3 activation and IFN expression and further demonstrate the importance of certain mitochondrial proteins in innate antiviral immunity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据