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Product description: Monoclonal Antibody. Recognizes the Human, Mouse, Rat protein. Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol. NF-kappaB (Nuclear Factor kappa B) is a nuclear transcription factor found in all cell types and is involved in cellular responses to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, and bacterial or viral antigens. NF-kappaB plays a key role in regulating the immune response to infection. Consistent with this role, incorrect regulation of NF-kappaB has been linked to cancer, inflammatory and autoimmune diseases, septic shock, viral infection and improper immune development. There are five members in the NF-kappaB family: NF-kappaB1, NF-kappaB2, RelA (also named p65), RelB, and c-Rel. The most common form of NF-kappaB is the p50/RelA heterodimer, although other forms of NF-kappaB dimers, such as p50/p50, p52/p52, p52/RelA, p50/c-Rel, c-Rel/c-Rel, p52/RelB, and p50/RelB, have also been identified in some types of cells. The primary role of NF-kappaB is to maintain normal cellular functions that range from cell-to-cell communication to cell motility, cell cycle progression, and cell lineage development. The activity of NF-kappaB is tightly regulated by interaction with inhibitory IkappaB proteins. NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. The NF-kappa-B p52-p52 homodimer is a transcriptional repressor. NFKB2 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p100 and generation of p52 by a cotranslational processing. The proteasome-mediated process ensures the production of both p52 and p100 and preserves their independent function. p52 binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. p52 and p100 are respectively the minor and major form; the processing of p100 being relatively poor. Isoform p49 is a subunit of the NF-kappa-B protein complex, which stimulates the HIV enhancer in synergy with p65.
Alternate Names/Synonyms: NFKB2; LYT10
Product Type: Monoclonal Antibody
Isotype: Mouse IgG2b kappa
Immunogen: Recombinant human His-NFkappaB (aa 1-454) protein purified from E. coli.
Applications: ELISA, WB
Species Crossreactivity: Human, Mouse, Rat
Formulation: Liquid. HEPES with 0.15M NaCl, 0.01% BSA, 0.03% sodium azide, and 50% glycerol.
Short Term Storage: +4°C
Long Term Storage: -20°C
Shipping: BLUE ICE
Use & Stability: Stable for at least 1 year after receipt when stored at -20°C.
Literature References: 1) Campbell KJ, Perkins ND. Cell Cycle. (2004) vol.3(7): p.869-72. (General)2) Perkins ND. Trends Cell Biol. (2004) vol.14(2): p.64-9. (General)3) Zanetti M, et al, Ann N Y Acad Sci. (2003) vol.987: p.249-57. (General)
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