生物
TLR3型
特里夫
信号转导衔接蛋白
干扰素调节因子
信号转导
细胞生物学
干扰素
转录因子
内部收益率3
抄写(语言学)
病毒学
先天免疫系统
Toll样受体
受体
基因
遗传学
哲学
语言学
作者
Liang‐Guo Xu,Yan‐Yi Wang,Ke-Jun Han,Lianyun Li,Zhonghe Zhai,Hong‐Bing Shu
出处
期刊:Molecular Cell
[Elsevier]
日期:2005-09-01
卷期号:19 (6): 727-740
被引量:1741
标识
DOI:10.1016/j.molcel.2005.08.014
摘要
Viral infection or stimulation of TLR3 triggers signaling cascades, leading to activation of the transcription factors IRF-3 and NF-kappaB, which collaborate to induce transcription of type I interferon (IFN) genes. In this study, we identified a protein termed VISA (for virus-induced signaling adaptor) as a critical component in the IFN-beta signaling pathways. VISA recruits IRF-3 to the cytoplasmic viral dsRNA sensor RIG-I. Depletion of VISA inhibits virus-triggered and RIG-I-mediated activation of IRF-3, NF-kappaB, and the IFN-beta promoter, suggesting that VISA plays a central role in virus-triggered TLR3-independent IFN-beta signaling. Our data also indicate that VISA interacts with TRIF and TRAF6 and mediates bifurcation of the TLR3-triggered NF-kappaB and IRF-3 activation pathways. These findings suggest that VISA is critically involved in both virus-triggered TLR3-independent and TLR3-mediated antiviral IFN signaling.
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