Schematic model for the activation of NFKB signaling pathways

Schematic model for the activation of NF-κB signaling pathways. In the canonical NF-κB pathway, stimulation of pro-inflammatory receptors activates the IKK complex (comprised of IKKα, IKKβ and IKKγ) leading to the phos-phorylation of IKBCX and its proteasomal degradation. This induces the translocation of p65/p50 dimers into the nucleus where the dimer binds to the promoter regions of a subset of target genes. In the noncanonical NF-κB pathway, stimulation of BAFF-R, CD40, and lymphotoxina-β receptor (LTβR) leads to the stabilization of NIK and results in the activation of the IKKα homo-dimers. Active IKKα, in turn, induces the phosphorylation of the NF-κB family member NF-κB2/p100 leading to its processing by the proteasome to generate p52. This allows the translocation of the p52/Rel B dimer into nucleus where it regulates the transcription of target genes. For details, see text.

Publication

The complex interplay between autophagy and NF-κB signaling pathways in cancer cells. (2011) Aurore Trocoli, et al. Am J Cancer Res. 2011;1(5):629-649. Figure: F2. All organisms Drosophila melanogaster Danio rerio Homo sapiens

Disease mentions