Nf-kappab

NF-kappaB is a specific transcription factor that occurs ubiquitously in all cell types and tissues. By binding to certain regulatory sections of DNA, it can influence the transcription of dependent genes. NF-kappaB has numerous target genes and mediates a wide variety of effects(NF-kappaB signaling pathway). NF-kappaB is of great importance for the regulation of the immune response, cell proliferation and apoptosis. The activation of NF-kappaB is considered significant for the development of inflammation, e.g. in the inflammatory induction of dermatitis solaris. Activated and released cytosolic NF-kappaB can migrate into the nucleus, bind to DNA and stimulate the transcription of effector genes.

• 5 subunits of NF-kappaB are currently known (alternative names in brackets):
  • NF-κB1 (p50 or p105)
  • NF-κB2 (p52 or p100)
  • RelA (p65)
  • RelB
  • c-Rel

In some cells, NF-kappaB is always present in the nucleus and is therefore active without the influence of external stimuli. This applies, for example, to 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 in the nucleus. This "remaining in the cytoplasm" is achieved by inhibitory proteins that bind to NF-kappaB and thus deactivate it.

Stimuli that trigger activation of NF-kappaB include UV radiation, growth factors, cytokines (e.g. tumor necrosis factor-α and interleukin-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. NF-kappaB is significantly involved in the inflammatory development of dermatitis solaris after UV exposure.

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