Embryonic fibroblast cells from TBK1-deficient mice show decreased IRF3 activation and IFN induction by poly IC, while IKKi-deficient cells show normal IRF3 activation. However, the activation of IRF3 is totally abolished in TBK1 and IKKi double-deficient cells, indicating that the functions of TBK1 and IKKi are redundant in mouse embryo fibroblast cells.[Hemmi et al 2004].
TBK1/IKKi interact with SIKE (Suppressor of IKK epsilon), which was shown to act as an inhibitor of TBK1/IKKi-mediated type I IFN production, but not NF-kB activation signaling[Huang J et al 2005].
Dötsch, V, Rozenknop, A, Rogov, V, Nordmeier, RD, Ikeda, F, Akira, S, Dikic, I, Hecker, CM, Hofmann, K
Fitzgerald, KA, Rowe, DC, McWhirter, SM, Golenbock, DT, Maniatis, T, Rosains, J
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