Carcinogenesis and Neoplasia ... a Companion Site.


NF-κB is an important regulator of cell proliferation, cellular survival, and the inflammatory and immune responses. Within the nucleus, the NF-κB transcription factor promotes the expression of specific genes regulated by NF-κB DNA-binding sites.

The enzyme IκB kinase (IKK) stimulates phosphorylation of two serine residues in the regulatory domain of Inhibitor of kappa B (IκB), targetting the IκB molecules for ubiquitin/proteasome degradation, and releasing NF-κB from inhibition as cytoplasm-sequestered NF-κB dimers.

Many tumor types have chronically active NF-κB, resulting from:
mutations in genes encoding the NF-κB transcription factors themselves, or
mutations in genes that control NF-κB activity

Several viruses, including HIV/AIDS, control the expression of viral genes through viral binding sites for NF-κB, thus contributing to viral replication or viral pathogenicity. For HIV-1, activation of NF-κB could be related to activation of the virus from a latent, inactive state.

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