Receptor-interacting protein 1 (RIP1) mediates the activation of proinflammatory cytokines via intermediate induction of IKK complex in NFkB pathways [Ea et al. 2006]. Poly(I-C) treatment stimulated the recruitment of RIP1, TRAF6, and TAK1 to the TLR3 receptor complex in human embryonic kidney HEK293 transfected with FLAG-tagged TLR3 [Cusson-Hermance et al. 2005]. RIP1 was shown to be dispensable for TRIF-dependent activation of IRF3, which occurs in a TRIF/TBK1/IKKi-dependent manner [Cusson-Hermance et al. 2005, Sato et al. 2003]
Fitzgerald, KA, Cusson-Hermance, N, Khurana, S, Kelliher, MA, Lee, TH
Deng, L, Chen, ZJ, Pineda, G, Xia, ZP, Ea, CK
Kawai, T, Takeda, K, Sato, S, Akira, S, Watanabe, Y, Yamamoto, M, Sugiyama, M
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