Tumor Necrosis Factor Alpha & Nuclear Factor Kappa B

Tumor necrosis factor alpha (TNF-α) is a pleiotropic cytokine produced primarily by macrophages, T-lymphocytes, and NK cells. It exists as a homotrimer and exerts its biological activities through TNFR1 and TNFR2. TNF-α is a master regulator of inflammation, apoptotic and necrotic cell death, and plays major roles in autoimmune diseases, septic shock, and cancer. Targeting TNF-α clinically with biologic agents is a mainstay in the treatment of many chronic inflammatory diseases. Nuclear factor kappa B (NF-κB) is a family of inducible transcription factors that regulate the expression of genes involved in inflammation, immune responses, cell proliferation, and survival. Normally held inactive in the cytoplasm by IκB proteins, NF-κB is released and translocates to the nucleus in response to diverse signals, such as TNF-α. Its activity is a major mediator of inflammatory and immune gene expression, making it an important target in autoimmunity, cancer, and chronic inflammatory diseases. Although TNF-α activates NF-κB signaling, 'Tumor Necrosis Factor Alpha & Nuclear Factor Kappa B' is not a single canonical target. They are distinct molecules with separate canonical names, abbreviations, molecular functions, and therapeutic implications, and must be handled separately in structured databases.

Other names

TNFcachectinTNFαtumor necrosis factorNF-kappaBNFKBnuclear factor NF-kappa-B

TNF-α inhibitors block the interaction of TNF-α with TNFR1/2, or cause apoptosis of TNF-α producing cells. NF-κB inhibitors typically prevent degradation of IκB (the NF-κB inhibitor), block DNA binding, or trap NF-κB in cytoplasm. While distinct, TNF-α activates NF-κB signaling.