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NF-κB describes a family of inducible transcription factors composed of five structurally related proteins (p50, p52, RelA/p65, RelB, and c-Rel), usually forming various dimeric complexes. In unstimulated cells, NF-κB is sequestered in the cytoplasm by inhibitory IκB proteins. In response to diverse extracellular stimuli (e.g., cytokines, pathogens, stress), the IκB kinase complex (IKK) phosphorylates IκB, leading to its degradation and allowing NF-κB to translocate into the nucleus. In the nucleus, NF-κB binds to κB enhancer elements on DNA, orchestrating the expression of numerous genes involved in immune and inflammatory responses, cell survival, and apoptosis. Both the canonical and noncanonical NF-κB pathways mediate these responses, and dysregulation is implicated in many diseases, including cancer and chronic inflammatory conditions[1][2][4][7].
Inhibition of NF-κB activation (e.g., blocking IκB kinase activity); Stabilization of IκB (preventing NF-κB release); Inhibition of NF-κB nuclear translocation; Inhibition of NF-κB DNA binding/transactivation
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