The NF-κB family of transcription factors plays critical roles in inflammation, immunity, cell proliferation, differentiation, and survival. NF-κB activation is induced by various stimuli, including bacterial and viral infections, inflammatory cytokines, and antigen receptor engagement. The primary mechanism for regulating NF-κB involves inhibitory IκB proteins, which are phosphorylated and degraded by the IκB kinase (IKK) complex, leading to NF-κB nuclear translocation and gene expression. Additional regulation occurs through post-translational modifications of NF-κB components. NF-κB is involved in immune and inflammatory responses, stress responses, and cell proliferation and apoptosis. It regulates a wide range of target genes, including those involved in immune responses, apoptosis, and development. The NF-κB family consists of five proteins that form various dimers, with p50/65 being the most abundant. The regulation of NF-κB activity is complex, involving multiple post-translational modifications and feedback loops. The IKK complex is central to canonical NF-κB signaling, while the non-canonical pathway involves IKKα and is regulated by NIK. Post-translational modifications, such as phosphorylation, ubiquitination, and acetylation, modulate NF-κB activity. The termination of NF-κB responses involves the resynthesis of IκB proteins and other regulatory mechanisms. Understanding the intricate regulation of NF-κB is crucial for elucidating its role in physiological and pathological processes, and for developing targeted therapies for diseases associated with NF-κB dysregulation.The NF-κB family of transcription factors plays critical roles in inflammation, immunity, cell proliferation, differentiation, and survival. NF-κB activation is induced by various stimuli, including bacterial and viral infections, inflammatory cytokines, and antigen receptor engagement. The primary mechanism for regulating NF-κB involves inhibitory IκB proteins, which are phosphorylated and degraded by the IκB kinase (IKK) complex, leading to NF-κB nuclear translocation and gene expression. Additional regulation occurs through post-translational modifications of NF-κB components. NF-κB is involved in immune and inflammatory responses, stress responses, and cell proliferation and apoptosis. It regulates a wide range of target genes, including those involved in immune responses, apoptosis, and development. The NF-κB family consists of five proteins that form various dimers, with p50/65 being the most abundant. The regulation of NF-κB activity is complex, involving multiple post-translational modifications and feedback loops. The IKK complex is central to canonical NF-κB signaling, while the non-canonical pathway involves IKKα and is regulated by NIK. Post-translational modifications, such as phosphorylation, ubiquitination, and acetylation, modulate NF-κB activity. The termination of NF-κB responses involves the resynthesis of IκB proteins and other regulatory mechanisms. Understanding the intricate regulation of NF-κB is crucial for elucidating its role in physiological and pathological processes, and for developing targeted therapies for diseases associated with NF-κB dysregulation.