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Figure 1 | Arthritis Research & Therapy

Figure 1

From: Non-canonical NF-κB signaling in rheumatoid arthritis: Dr Jekyll and Mr Hyde?

Figure 1

Overview of nuclear factor-κ B activation pathways. Schematic representation of the canonical and non-canonical nuclear factor (NF)-κB pathways. The canonical NF-κB pathway can be activated by a variety of different stimuli, like tumor necrosis factor-α and lipopolysaccharide (LPS). Activation 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 to induce its degradation, allowing NF-κB dimers (p50-p65) to translocate to the nucleus and bind to DNA to induce NF-κB target gene transcription. The non-canonical pathway (right) is activated by specific stimuli like B cell activating factor, lymphotoxin β, LIGHT and CD40L. NF-κB inducing kinase (NIK) is stabilized and activates and recruits IKKα into the p100 complex to phosphorylate p100, leading to p100 ubiquitination. Processing of p100 generates the p52/RelB NF-κB complex, which is able to translocate to the nucleus and induce gene expression.

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