Transcription factor p65 (nuclear factor NF-κB p65 subunit) (RelA (p65))

RelA (p65) is one of five principal NF-κB transcription factor subunits in mammals, forming homo- and heterodimers (most commonly p65/p50) that bind DNA at κB sites to regulate gene expression in response to inflammatory, immune, and proliferative stimuli.\nNormally held inactive in the cytoplasm associated with inhibitors (IκB family), p65-containing NF-κB complexes are activated by kinases such as IKK, which trigger phosphorylation and degradation of IκBs and allow nuclear translocation. Once in the nucleus, p65 regulates hundreds of genes driving inflammatory and immune responses, cell survival/apoptosis, and cell proliferation.\nDysregulation of p65 activity is implicated in diseases such as cancer, chronic inflammation, autoimmune disorders, and neurodegeneration. Select upstream kinase inhibitors, proteasome inhibitors, or genetic/pharmacological suppression of NF-κB are being explored for therapeutic intervention, though systemic blockade can result in significant adverse effects due to NF-κB's broad role in physiology

Other names

RelAp65NF-κB p65 subunitNFKB3nuclear factor NF-kappa-B p65 subunitv-rel avian reticuloendotheliosis viral oncogene homolog A

Inhibition of IκB kinase (IKK) prevents phosphorylation and degradation of IκBα, keeping NF-κB in the cytosol; Proteasome inhibition (prevents degradation of IκB and NF-κB pathway activation); Direct binding or suppression of NF-κB DNA binding/transcriptional activity