Transcription Factor NF-kB, also known as Nuclear Factor kappa B, is a protein complex that plays a crucial role in regulating genes involved in immune response, inflammation, cell survival, and proliferation. It is a transcription factor composed of subunits p50 and p65, among others, encoded by the genes NFKB1 and NFKB2, respectively.
NF-kB operates as a transcription factor by binding to specific DNA sequences called κB sites, found in the promoter region of target genes. Upon activation, NF-kB is released from its inhibitory complex and translocates into the cell nucleus, where it binds to the κB sites and initiates the transcription of downstream genes. The activation of NF-kB can be triggered by various stimuli, such as pro-inflammatory cytokines (e.g., tumor necrosis factor-alpha), pathogen-associated molecular patterns (PAMPs), and stress signals.
The activation of NF-kB is tightly regulated to prevent excessive or prolonged inflammatory responses. In its inactive state, NF-kB is retained in the cytoplasm through its association with inhibitory proteins known as IkBs. Various signaling pathways, such as the canonical and non-canonical pathways, regulate the degradation of IkBs, leading to the subsequent activation and nuclear translocation of NF-kB.
Dysregulation of NF-kB has been implicated in numerous diseases, including chronic inflammation, autoimmune diseases, and cancer. Therapeutic strategies targeting NF-kB signaling are under investigation in the development of drugs to combat these diseases.
