【bio-news】细胞抗病毒天然免疫研究新进展
Viral infection triggers activation of transcription factors such as NF-κB 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.
http://www.immunity.com/content/article/abstract?uid=PIIS1074761308004068
[标签:content1][标签:content2]
阅读本文的人还阅读：
【Cancer cell】肝脏及肝癌
【bio-news】美研究显示：
【科普】研究显示男性秃
美联邦机构出巨资支持中
【drug-news】新研究发现使
作者:admin@医学,生命科学 2011-02-20 05:11
医学,生命科学网
