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Official Full Name
nuclear factor of kappa light polypeptide gene enhancer in B-cells 1
This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene.
NFKB1; p50; KBF1; p105; EBP-1; MGC54151; NFKB-p50; NFkappaB; NF-kappaB; NFKB-p105; DKFZp686C01211; nuclearfactor NF-kappa-Bp105subunit; NF-kappabeta; OTTHUMP00000161765; OTTHUMP00000216418; OTTHUMP00000219572; DNA binding factor KBF1; nuclear factor NF-kappa-B p50 subunit; nuclear factor kappa-B DNA binding subunit; nuclear factor of kappa light polypeptide gene enhancer in B-cells 1; nuclear factor NF-kappa-B p105 subunit; NF kappaB; NF kB1; NFKB p50; DNA-binding factor KBF1; NF-kB1; NF-kappa-B; NF-kB p50 subunit; nuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105)

Cat.No. Product Name Price
AD10736ZHuman NFKB1 adenoviral particlesInquriy
Cat.No. Product Name Price
CLKO-0195NFKB1 KO Cell Lysate-HeLaInquriy

As a pleiotropic transcription factor and an endpoint of a series of signal transduction events, nuclear factor kappa B (NFkB) has been detected in numerous tissues, mainly in the bone marrow, appendix, lymph node, spleen, gall bladder, expressing cytokines, chemokines, growth factors, cell adhesion molecules, and some acute phase proteins in health and in various disease states. NFKB is activated by a wide variety of stimuli such as cytokines, oxidant-free radicals, inhaled particles, ultraviolet irradiation, and bacterial or viral products, getting involve in many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. Nuclear factor kappa B subunit 1 (NFkB1) was first reported as interacting with an 11-bp cis-acting sequence in the immunoglobulin light-chain enhancer. NFkB1 is bound to REL, RELA, or RELB to form the NFKB complex.

Conventional mechanism of gene

NFkB 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. Transcriptional activators or repressors consist of different dimer combinations, respectively. Various mechanisms such as post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors plays an essential role in the regulation of NFkB.

NFkB complexes are held in the cytoplasm and inhibited by I-kappa-B proteins, which inactivate NFkB by trapping it in the cytoplasm. In a conventional activation pathway, phosphorylation of serine residues on the I-kappa-B proteins by I-kappa-B kinases (IKKs) marks them for destruction via the ubiquitination pathway in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. Activated NFKB 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). NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. The NF-kappa-B p50-p50 homodimer is a transcriptional repressor, but can act as a transcriptional activator when associated with BCL3.

Gene function

NFKB1 appears to have dual functions such as cytoplasmic retention of attached NF-kappa-B proteins by p105 and generation of p50 by a cotranslational processing. The proteasome-mediated process ensures the production of both p50 and p105 and preserves their independent function, although processing of NFKB1/p105 also appears to occur post-translationally. p50 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. In a complex with MAP3K8, NFKB1/p105 represses MAP3K8-induced MAPK signaling; active MAP3K8 is released by proteasome-dependent degradation of NFKB1/p105.

The relationships between gene and major human diseases

Inappropriate activation of NF-kappa-B has been reported to link with inflammatory events, including autoimmune arthritis, asthma, septic shock, lung fibrosis, glomerulonephritis, atherosclerosis, and AIDS.

Fig 1. Dysregulation of NFkB pathway [1].

  • NFkB in Autoimmunity [2]

There are a large number of evidences that NF-κB is essential for maintaining immunological tolerance, on account of its actions during thymic selection, both for negative selection of autoreactive T cells, and selection and maintenance of Tregs.

Common NFKB1 polymorphisms have been proven to make a distinction with several autoimmune and inflammatory diseases. More recently, a polymorphism within the NFKB1 locus was shown to segregate with multiple sclerosis. The non-canonical NF-κB pathway appears to be particularly vital for normal mTec function; however, evidence has also emerged for a obvious lymphocyte-intrinsic action of the canonical pathway for maintaining T cell tolerance. Patients with NFKB1 haploinsufficiency also show a defect in Tregs, with a diminution in effector Tregs

  • NFkB with cancer [3]

NF-KB is the master transcriptional regulators of tumor-associated macrophages, which are central regulators of tumour progression and metastasis by matrix metalloproteinases. NF-KB activated in cancer cells by IL-1, TNF-Alfa proinflammatory cytokines, hypoxia, and ROI is expressed by leukocytes as well as the pathogen-associated molecular pattern (PAMP) and STAT-3 transcriptional factor, activated by IL-6 and EGF which in turn up-regulates HIF-1 responsible for cancer cell survival and tumour progression by cell proliferation, angiogenesis, genomic instability through anti-apoptotic activity, epithelial-mesenchymal transition, invasion, and metastasis.

  • NFkB with AIDS [4]

There are some mechanisms by which HIV transcription can be reactivated. In J-Lat 9.2 cells, HIV is integrated in the same orientation as the estrogen-dependent PP5 gene and reactivates upon removal of the hormone. Cytokines and the activation state of the infected T cell also contribute to HIV reactivation via NFkB. Up regulated level of nuclear NFkB bind tightly to DNA, thereby impeding the progress of upstream RNAPII and initiating some transcription from the 5′LTR. Depending on the degree of transcriptional interference, these processes compete with each other, such that low levels of host gene transcription are overcome more rapidly by cellular activation and vice versa.


NFkB is an important transcription factor expressed in human being. It is responsible for regulating gene expression of factors that control cell adhesion, proliferation, inflammation, redox state, and tissue-specific enzymes. Activation of NFkB mediates inflammation in metabolic and age-related diseases. The research of NFkB is meaningful to cure major human disease.


  1. Marfella, R., et al., The possible role of the ubiquitin proteasome system in the development of atherosclerosis in diabetes. Cardiovasc Diabetol, 2007. 6: p. 35.
  2. Miraghazadeh, B. and M.C. Cook, Nuclear Factor-kappaB in Autoimmunity: Man and Mouse. Front Immunol, 2018. 9: p. 613.
  3. Shrihari, T.G., Dual role of inflammatory mediators in cancer. Ecancermedicalscience, 2017. 11: p. 721.
  4. Cary, D.C., K. Fujinaga, and B.M. Peterlin, Molecular mechanisms of HIV latency. J Clin Invest, 2016. 126(2): p. 448-54.

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