NFKB1 Research Reagents

Nuclear factor NF-kappa-B p105 subunit is a protein in humans that is encoded by NFKB1 gene. 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 and the heterodimeric p65-p50 complex appears to be most abundant one. 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.

The following NFKB1 reagents supplied by CUSABIO are manufactured under a strict quality control system. Multiple applications have been validated and solid technical support is offered.

NFKB1 Antibodies

NFKB1 Antibodies for Homo sapiens (Human)

NFKB1 Proteins

NFKB1 Proteins for Gallus gallus (Chicken)

NFKB1 Proteins for Homo sapiens (Human)

NFKB1 Proteins for Mus musculus (Mouse)

NFKB1 Proteins for Rattus norvegicus (Rat)

NFKB1 Proteins for Canis lupus familiaris (Dog) (Canis familiaris)

NFKB1 ELISA Kit

NFKB1 ELISA Kit for Homo sapiens (Human)

NFKB1 ELISA Kit for Mus musculus (Mouse)

NFKB1 ELISA Kit for Rattus norvegicus (Rat)

NFKB1 Background

Nuclear factor NF-kappa-B p105 subunit is a protein in humans that is encoded by the NFKB1 gene [1]. 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 [2]. 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, and the heterodimeric p65-p50 complex appears to be most abundant one [3][4]. 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 [3]. The NFKB1/p105 pathway involves the unprocessed NFKB1/p105 which preferentially binds to a homodimer of processed NFKB1/p50 [4]. The complex is inactive, and ubiquitinylation of p105 followed by destruction is required for the liberation of the processed NFKB dimer [5]. The importance of the NFKB1 function can be seen in mouse models, where NFKB1-null mice display increased inflammation and susceptibility to certain forms of DNA damage, leading to cancer, and a rapid aging phenotype [6].

[1] Meyer R, Hatada EN, et al. Cloning of the DNA-binding subunit of human nuclear factor kappa B: the level of its mRNA is strongly regulated by phorbol ester or tumor necrosis factor alpha [J]. Proc Natl Acad Sci U S A. 1991, 88 (3): 966–70.
[2] Perkins ND. Integrating cell‐signalling pathways with NF‐κB and IKK function. Nat Rev Mol Cell Biol 2007, 8, 49–62.
[3] Moynagh PN. The NF‐κB pathway. J Cell Sci 2005, 118, 4589–4592.
[4] Barkett M and Gilmore TD. Control of apoptosis by Rel/NF-kappaB transcription factors. Oncogene. 18:6910–6924. 1999.
[5] Kravtsova-Ivantsiv Y, Shomer I, et al. KPC1-mediated ubiquitination and proteasomal processing of NF-jB1 p105 to p50 restricts tumor growth. Cell 2015, 161, 333–347.
[6] Tyrell Cartwright, Neil D. Perkins, et al. NFKB1: a suppressor of inflammation, ageing and cancer [J]. FEBS Journal 283 (2016) 1812–1822.

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