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. Author manuscript; available in PMC: 2021 Oct 1.
Published in final edited form as: Transl Res. 2020 May 17;224:55–70. doi: 10.1016/j.trsl.2020.05.001

Figure 1. NIBP/TRAPPC9 function within the NFκB activation pathway.

Figure 1.

NFκB can be activated via three main pathways: the classical/canonical, alternative/non-canonical, and the atypical pathways. The classical pathway involves a three subunit IKK complex composed of IKK1, IKK2, and regulatory subunit IKKγ, IκB proteins, and the NFκB p65/p50 heterodimer. The alternative pathway involves NIK, a two-subunit IKK complex composed of two IKK1 subunits, p100, and the NFκB RelB/p52 heterodimer. NIBP binds directly to IKK2 and NIK and may bridge both classical and alternative activation pathways together. NIBP may be essential for NFκB activation and its dysregulation may be involved in the pathogenesis of various NFκB-associated disorders.

Notes. IL1R, interleukin-1 receptor; TLR, toll-like receptor; TNFR, tumor necrosis factor receptor; BAFFR, B-cell activating factor receptor; NIK, NFκB-inducing kinase; IκB, Inhibitor of NFκB; IKK, IκB kinase; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells.