| Antigen Alias |
Nuclear factor NF-kappa-B p100 subunit, DNA-binding factor KBF2, H2TF1, Lymphocyte translocation chromosome 10 protein, Nuclear factor of kappa light polypeptide gene enhancer in B-cells 2, Oncogene Lyt-10, Lyt10, Nuclear factor NF-kappa-B p52 subunit, NFK |
| Product description |
NF-kappa-B has been detected in numerous cell types that
express cytokines, chemokines, growth factors, cell adhesion
molecules, and some acute phase proteins in health and in various
disease states. NF-kappa-B is activated by a wide variety of
stimuli, such as cytokines, oxidant-free radicals, inhaled
particles, ultraviolet irradiation, and bacterial or viral
products. Inappropriate activation of NF-kappa-B has been linked to
inflammatory events associated with autoimmune arthritis, asthma,
septic shock, lung fibrosis, glomerulonephritis, atherosclerosis,
and AIDS. In contrast, complete and persistent inhibition of
NF-kappa-B has been linked directly to apoptosis, inappropriate
immune cell development, and delayed cell growth. NFKB1 (MIM
164011) and NFKB2 encode p105 and p100 proteins that are processed
to produce the active p50 and p52 NF-kappa-B subunits,
respectively. However, the p100 and p105 proteins serve regulatory
functions and should not be considered exclusively as precursor
forms. The most abundant activated form of NF-kappa-B is a
heterodimer of the p50 or p52 subunit bound to the RELA subunit
(MIM 164014). Other NF-kappa-B complexes, consisting of hetero- and
homodimers of p50, p52, RELA, REL (MIM 164910), and RELB (MIM
604758), have also been detected. NF-kappa-B complexes are
inhibited by I-kappa-B proteins, NFKBIA (MIM 164008) or NFKBIB (MIM
604495), which inactivate NF-kappa-B by trapping it in the
cytoplasm. Phosphorylation of serine residues on the I-kappa-B
proteins by the kinases IKBKA (CHUK; MIM 600664) or IKBKB (MIM
603258) marks them for destruction via the ubiquitination pathway,
thereby allowing activation of the NF-kappa-B complex. The
activated NF-kappa-B complex translocates into the nucleus and
binds DNA at kappa-B-binding motifs, such as 5-prime GGGRNNYYCC
3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R is
an A or G purine; and Y is a C or T pyrimidine). For reviews, see
Chen et al. (1999) [PubMed 9895331] and Baldwin (1996) [PubMed
8717528].1) Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010) |