Irf3 deficient mice were found to be more vulnerable to virus infection. Mouse cells defective in IRF3 and IRF7 expression totally fail to induce IFN genes in response to viral infection. It was shown on mice and mouse cells that both IRF3 and IRF7 have non redundant and distinct roles (Sato M et al. 2000). IRF3 is expressed at a basal level in normally growing cells and is a major factor in the early induction phase of IFN-alpha/beta production, while the IRF7 gene expression is induced upon IFNs stimulation and IRF7 is involved in the late induction phase.
TBK1-mediated phosphorylation of the adaptor protein TRIF (TICAM1) leads to IRF3 association with TICAM1 in human HEK293T cells suggesting that TICAM1 (TRIF) recruits IRF3 to the activated TLR3 or TLR4 signaling complex through a phosphorylation-dependent mechanism (Liu S et al. 2015).
Hiscott, J, Lin, R, Pitha-Rowe, PM, Heylbroeck, C
Takeuchi, O, Hoshino, K, Sanjo, H, Takeda, K, Sato, S, Yamamoto, M, Kaisho, T, Kawai, T, Hemmi, H
Zhang, Y, Cao, X, Zhao, W, Hou, J, Liu, S, Zheng, Y, Xie, Y, Yu, Y, Feng, G, An, H, Qian, C, Xu, H, Zhou, J
Fitzgerald, KA, Rowe, DC, Latz, E, Barnes, BJ, Golenbock, DT, Pitha-Rowe, PM, Monks, BG, Caffrey, DR, Visintin, A
Fujita, T, Inagaki, F, Takahashi, K, Yoneyama, M, Mori, M, Ito, T
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