Nuclear factor-kappa B (NF-κB) signalling is a transcriptional regulatory pathway that plays important roles in regulating various cellular processes, particularly within the immune system. This pathway leads to the activation of the NF-κB transcription factor and is important in modulating immune responses, inflammation and cell survival via changes in gene expression. NF-κB itself comprises a family of structurally related transcription factors, including p65 (RelA), p50, p52, c-Rel, and RelB which can form various homo- and heterodimers. NF-κB signalling is activated in response to stimuli including pro-inflammatory cytokines (e.g., TNF-α, IL-1β), microbial products, and cellular stress. These trigger the activation of upstream signalling pathways, including the IκB kinase (IKK) complex. The IKK complex phosphorylates the inhibitor of κB (IκB) proteins, IκBα, which normally acts to sequester NF-κB in the cytoplasm. Phosphorylated IκB is subsequently targeted for ubiquitination and proteasomal degradation via the E3 ligase SCFβ-TrCP (Skp1-Cullin1-F-box protein β-Transducin repeat-containing protein). Following IκB degradation, the active NF-κB dimers (e.g., p50: p65) are released from IκB and translocate to the nucleus, allowing NF-κB to function as a transcription factor. In the nucleus, NF-κB binds to specific DNA sequences called κB sites within the promoters of target genes. This binding leads to the transcriptional activation of genes encoding various proteins including pro-inflammatory cytokines, chemokines, cell adhesion molecules, and anti-apoptotic proteins. NF-κB signalling is tightly regulated to prevent excessive or sustained activation. Negative regulators, such as IκB proteins and the deubiquitinase A20, inhibit the pathway, maintaining a balance in immune responses and preventing chronic inflammation. Once the signalling stimulus is removed, the process of NF-κB activation is terminated. Newly synthesized IκBα molecules enter the nucleus, bind to NF-κB, and export it back to the cytoplasm, effectively silencing its transcriptional activity. NF-κB signalling controls the expression of many genes involved in the immune system, including cytokines (such as TNF-α and IL-6), chemokines, cell adhesion molecules, and immune cell surface receptors. These gene products contribute to the recruitment and activation of immune cells, facilitating the body's response to infections and pathogens. NF-κB signalling therefore plays an important role in the regulation of inflammation. When tissues are injured or infected, NF-κB activation promotes the recruitment of immune cells to the site of injury or infection. Whilst acute inflammation is a protective response, chronic inflammation is often associated with various diseases, including autoimmune disorders and cancer. NF-κB signalling is also involved in promoting cell survival by regulating the expression of anti-apoptotic genes. It helps cells withstand stressful conditions and can also be activated in response to DNA damage or oxidative stress to prevent apoptosis (programmed cell death). NF-κB signalling also plays a role in development and tissue homeostasis, influencing cell differentiation, tissue regeneration, and organ development during embryogenesis. Dysregulated NF-κB signaling is implicated in cancer. It can promote cell proliferation, angiogenesis (formation of new blood vessels), and metastasis (the spread of cancer to other tissues). In cancer cells, NF-κB activation can also confer resistance to apoptosis and chemotherapy. We offer a comprehensive product range of research tools for studying the NFkB pathway, including NF-kB p65 antibodies, TMEM173 antibodies, IKB alpha antibodies, NF-kB p65 ELISA Kits, and IKB alpha ELISA Kits. Explore our full NFkB pathway product range below and discover more, for less.