内部收益率3
干扰素调节因子
信号转导衔接蛋白
IRF7
细胞生物学
IκB激酶
磷酸化
转录因子
RNA解旋酶A
异位表达
坦克结合激酶1
信号转导
特里夫
生物
先天免疫系统
超胸
NF-κB
核糖核酸
解旋酶
基因
蛋白激酶A
生物化学
Toll样受体
受体
丝裂原活化蛋白激酶激酶
同源异型基因
作者
Tiejun Zhao,Yang Long,Qiang Sun,Meztli Arguello,Dean W. Ballard,John Hiscott,Rongtuan Lin
摘要
Intracellular detection of RNA virus infection is mediated by the RNA helicase RIG-I, which is recruited to mitochondria by the adaptor protein MAVS and triggers activation of the transcription factors NF-kappaB, IRF3 and IRF7. Here we demonstrate that virus-induced activation of IRF3 and IRF7 depended on the NF-kappaB modulator NEMO, which acted 'upstream' of the kinases TBK1 and IKKepsilon. IRF3 phosphorylation, formation of IRF3 dimers and DNA binding, as well as IRF3-dependent gene expression, were abrogated in NEMO-deficient cells. IRF3 phosphorylation and interferon production were restored by ectopic expression of NEMO. Thus, NEMO, like MAVS, acts as an adaptor protein that allows RIG-I to activate both the NF-kappaB and IRF signaling pathways.
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