TRAF6 介导的 IRF7 激活
中文名称
通路描述
TRAF6 对于 DDX58（RIG-I）和 IFIH1（MDA5）介导的抗病毒反应至关重要。TRAF6 缺失导致病毒复制增强，并在感染 RNA 病毒后显著减少 I 型干扰素和 IL6 的产生。在缺乏 TRAF6 的情况下，RLH 信号中 NF-kB 和 IRF7 的激活，但非 IRF3 的激活，显著受损。TRAF6 诱导的 IRF 激活可能主要针对 IRF7，而 TRAF3 被认为可激活 IRF3 和 IRF7。这些结果强烈表明，TRAF6-和 TRAF3 依赖的通路可能在线粒体抗病毒信号蛋白 MAVS（IPS-1）处分叉，但在 IRF7 处汇合，以在 RLH 信号中协同诱导足够的 I 型干扰素产生。
英文描述
TRAF6 mediated IRF7 activation TRAF6 is crucial for both DDX58 (RIG-I)- and IFIH1 (MDA5)-mediated antiviral responses. The absence of TRAF6 resulted in enhanced viral replication and a significant reduction in the production of type I IFNs and IL6 after infection with RNA virus. Activation of NF-kB and IRF7, but not that of IRF3, was significantly impaired during RIG-like helicases (RLHs) signaling in the absence of TRAF6. TRAF6-induced activation of IRF is likely to be specific for IRF7, while TRAF3 is thought to activate both IRF3 and IRF7. These results strongly suggest that the TRAF6- and TRAF3-dependent pathways are likely to bifurcate at mitochondrial antiviral-signaling protein MAVS (IPS-1), but to converge later at IRF7 in order to co-operatively induce sufficient production of type I IFNs during RLH signaling.
所含基因
28 个基因