NF-κB

NF-κB regulates innate and adaptive immunity, inflammatory responses, immune-cell survival, activation, and differentiation^[1]. Mechanistically, canonical NF-κB signaling depends on phosphorylation-induced proteasomal degradation of IκB proteins, releasing cytosolic NF-κB dimers for transcriptional control^[2]. In inflammation models, NF-κB induces cytokines, chemokines, adhesion molecules, and inflammasome-related responses, linking pathway activation to chronic inflammatory disease and cancer research^[1][3][4]. Compared with related isoforms, mammalian NF-κB includes RelA/p65, RelB, c-Rel, p50/NF-κB1, and p52/NF-κB2, and RelA loss causes embryonic lethality with liver apoptosis, whereas p50 loss produces immune-response defects without developmental abnormalities^[2][5][6]. For experimental applications, NF-κB inhibitors, including IKK-targeting agents and BAY 11-7082, help test pathway dependence in inflammatory signaling, but broad pathway targeting requires careful interpretation because NF-κB also supports normal immune physiology^[4][7].