Nf-kappab

In some cells, NF-kappaB is always present in the nucleus and thus active without the influence of external stimuli. This concerns for example B-lymphocytes and dendritic cells. In most other cells, however, NF-kappaB is inactive in the cytoplasm and therefore has no access to the DNA located in the nucleus. This "staying behind in the cytoplasm" is achieved by inhibitory proteins that bind to NF-kappaB and thus deactivate it. Among the stimuli that trigger the activation of NF-kappaB are UV rays, growth factors, cytokines (e.g. tumour necrosis factor-α and IL-1beta), bacterial and viral antigens (e.g. lipopolysaccharides, double-stranded RNA). Such stimulation causes a change in the activity of cellular signaling pathways, which are often mediated by phosphorylation. Among the signalling pathways important for NF-kappaB, the MAP kinase signalling pathway is also important. The activated and released NF-kappaB can now migrate into the nucleus, bind to DNA and stimulate the transcription of effector genes. NF-kappaB plays a major role in the development of sunburn after UV exposure.

Another example of genes regulated by NF-kappaB is the cyclooxygenase 2 gene (see cyclooxygenases below). It is likely that cyclooxygenase 2 is increasingly transcribed by NF-kappaB.