We constantly strive to ensure we provide our customers with the best antibodies. As a result of this work we offer this antibody in purified format. We are in the process of updating our datasheets. If you have any questions regarding this update, please feel free to contact our technical support team. This product is a high quality NFKB(p100) Antibody (C-term S866/870).

96749 Da

Antigen Cellular Localization: Nucleus. Cytoplasm. Note=Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B)

Rabbit

Human

848-874 aa

This NFKB(p100) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 848-874 amino acids from the C-terminal region of human NFKB(p100).

Rabbit Ig

LYT10

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes 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. In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK- ARNTL/BMAL1 heterodimer.

NF-kappa-B has been detected in numerous cell types thatexpress cytokines, chemokines, growth factors, cell adhesionmolecules, and some acute phase proteins in health and in variousdisease states. NF-kappa-B is activated by a wide variety ofstimuli, such as cytokines, oxidant-free radicals, inhaledparticles, ultraviolet irradiation, and bacterial or viralproducts. Inappropriate activation of NF-kappa-B has been linked toinflammatory events associated with autoimmune arthritis, asthma,septic shock, lung fibrosis, glomerulonephritis, atherosclerosis,and AIDS. In contrast, complete and persistent inhibition ofNF-kappa-B has been linked directly to apoptosis, inappropriateimmune cell development, and delayed cell growth. NFKB1 (MIM164011) and NFKB2 encode p105 and p100 proteins that are processedto produce the active p50 and p52 NF-kappa-B subunits,respectively. However, the p100 and p105 proteins serve regulatoryfunctions and should not be considered exclusively as precursorforms. The most abundant activated form of NF-kappa-B is aheterodimer of the p50 or p52 subunit bound to the RELA subunit(MIM 164014). Other NF-kappa-B complexes, consisting of hetero- andhomodimers of p50, p52, RELA, REL (MIM 164910), and RELB (MIM604758), have also been detected. NF-kappa-B complexes areinhibited by I-kappa-B proteins, NFKBIA (MIM 164008) or NFKBIB (MIM604495), which inactivate NF-kappa-B by trapping it in thecytoplasm. Phosphorylation of serine residues on the I-kappa-Bproteins by the kinases IKBKA (CHUK; MIM 600664) or IKBKB (MIM603258) marks them for destruction via the ubiquitination pathway,thereby allowing activation of the NF-kappa-B complex. Theactivated NF-kappa-B complex translocates into the nucleus andbinds DNA at kappa-B-binding motifs, such as 5-prime GGGRNNYYCC3-prime or 5-prime HGGARNYYCC 3-prime (where H is A, C, or T; R isan A or G purine; and Y is a C or T pyrimidine). For reviews, seeChen et al. (1999) [PubMed 9895331] and Baldwin (1996) [PubMed8717528].

Store at +4°C short term. For long-term storage, aliquot and store at -20°C or below. Stable for 12 months at -20°C. Avoid repeated freeze-thaw cycles.

WB, E

WB~~1:1000

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