坦克结合激酶1
葛兰素史克-3
生物
内部收益率3
激酶
糖原合酶
GSK3B公司
转录因子
细胞生物学
酶
癌症研究
生物化学
丝裂原活化蛋白激酶激酶
蛋白激酶A
基因
作者
Cao Qi Lei,Bo Zhong,Yu Zhang,Jing Zhang,Shuai Wang,Hong Shu
出处
期刊:Immunity
[Elsevier]
日期:2010-12-01
卷期号:33 (6): 878-889
被引量:152
标识
DOI:10.1016/j.immuni.2010.11.021
摘要
Viral infection activates transcription factors IRF3 and NF-κB, which collaborate to induce type I interferons (IFNs). Here, we identified glycogen synthase kinase 3β (GSK3β) as an important regulator for virus-triggered IRF3 and NF-κB activation, IFN-β induction, and cellular antiviral response. Overexpression of GSK3β potentiated virus-induced activation of IRF3 and transcription of the IFNB1 gene, whereas reduced expression or deletion of GSK3β impaired virus-induced IRF3 and NF-κB activation, transcription of the IFNB1 gene, as well as cellular antiviral response. GSK3β physically associated with the kinase TBK1 in a viral infection-dependent manner. GSK3β promoted TBK1 self-association and autophosphorylation at Ser172, which is critical for virus-induced IRF3 activation and IFN-β induction. The effect of GSK3β on virus-induced signaling is independent of its kinase activity. Our findings suggest that GSK3β plays important roles in virus-triggered IRF3 activation by promoting TBK1 activation and provide new insights to the molecular mechanisms of cellular antiviral response.
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