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Fig. 1 | Molecular Brain

Fig. 1

From: Biological characteristics of transcription factor RelB in different immune cell types: implications for the treatment of multiple sclerosis

Fig. 1

Canonical and non-canonical NF-κB pathways. The canonical pathway is triggered by various immune receptors, for example, TLRs, TNFR, BCR and TCR. Various receptors activate the IKK complex, resulting in phosphorylation and proteasome-dependent degradation of IκBα, which in turn frees RelA/p50 and promotes its nuclear import. The non-canonical pathway is induced by the TNFSFRs, such as BAFFR, LTβR, CD40 and RANK. Then, downstream molecules NIK and IKKα are activated, leading to p100 processing and the liberation of RelB/p52 heterodimers. Finally, the uncontrolled dimers translocate into nucleus and bind to target genes, triggering their expression

Abbreviations: TLRs: Toll-like receptors; TNFR: tumor necrosis factor receptor; TCR: T cell receptor; BCR: B cell receptor; TNFSFRs: tumor necrosis factor superfamily receptors; BAFFR: B cell activating factor receptor; LTβR: lymphotoxin β receptor; RANK: receptor activator of NF-κB; FN14: fibroblast growth factor-inducible factor 14; IκB: κB inhibitor; IKK: IκB kinase; NIK: NF-κB-inducing kinase

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