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. 2021 Nov 30;53(11):1697–1705. doi: 10.1038/s12276-021-00712-w

Fig. 3. IKK and TBK1 functions in the liver.

Fig. 3

Canonical NF-κB signaling is mediated by the IKKα/IKKβ/IKKγ complex upon proinflammatory cytokine (TNF-α or IL-1β) or lipopolysaccharide stimulus. This complex induces the phosphorylation-mediated degradation of IκB, which leads to NF-κB activation. Furthermore, LTβ, CD40L, and BAFF stimulate NIK phosphorylation, thereby promoting IKKα phosphorylation and downstream signaling via the RelB:p52 complex. On the other hand, TBK1 is phosphorylated via STING or MAVS activation upon viral infection, which promotes IRF3 activation for the type I IFN response. Additionally, inactive TBK1 promotes FA oxidation in hepatocytes.