【摘要】干扰素规章的因素(IRF)3在病毒或细菌的侵略期间为chemokines和cytokines的transcriptional正式就职是批评的。kinases坦克有约束力的kinase(TBK)1并且IkappaBkinase(IKK)蔚罐头phosphorylateIRF3和玩的C终端部分在IRF3激活的重要角色。在这研究,我们显示出那另外一个kinase,c-Jun-NH2-terminalkinase(JNK),它的N终端丝氨酸上的phosphorylatesIRF3173残余,和TAK1能经由JNK刺激IRF3phosphorylation。没有影响C终端phosphorylat
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