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. 2015 Dec 18;8:77. doi: 10.3389/fnmol.2015.00077

FIGURE 1.

FIGURE 1

Schematic representation of the canonical and non-canonical nuclear factor (NF)-κB activation pathways. The canonical NF-κB pathway (upper) can be activated by a wide range of various stimuli, including tumor necrosis factor (TNF)-α, interlukin (IL)-1, lipopolysaccharide (LPS), and Toll-like receptors ligand (such as CD40L). Initiation of the canonical pathway via Toll-like receptor or cytokine receptor signaling depends on the inhibitor of κB kinase (IKK) complex, which is composed of the kinases IKKα and IKKβ, and the regulatory subunit IKKγ (NEMO). Activated IKK phosphorylates the inhibitory subunit IκBα leading to its degradation. The released NF-κB dimers (p50-p65) translocate to the nucleus and bind to κB site of chromosome to induce transcription of NF-κB targeted genes. The non-canonical pathway (lower) is activated by specific stimuli including B cell activating factor (BAF) belonging to the TNF family receptor, LPS, lymphotoxin (LT) α1β2, receptor activator of NF-κB (RANK), and CD40L. NF-κB inducing kinase (NIK) is stabilized. When stimulated, NIK is activated and recruits IKKα to the p100 complex to phosphorylate p100, leading to p100 ubiquitination. P52, the processing product of p100, generates the activated p52/RelB NF-κB complex, which is able to translocate to the nucleus and induce the downstream gene expressions.