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Authored: Garapati, P V, 2010-08-02, Edited: Garapati, P V, 2010-08-02, Reviewed: Kawai, T, Akira, S, 2010-10-30, TRAF6 is crucial for both RIG-I- and 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 IPS-1, but to converge later at IRF7 in order to co-operatively induce sufficient production of type I IFNs during RLH signaling.
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TRAF6 mediated IRF7 activation
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