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Title: Nfkb2  
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Subject: RELB, NFKB1, Common variable immunodeficiency, Transcription factors, NeuroD
Collection: Transcription Factors
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Nuclear factor of kappa light polypeptide gene enhancer in B-cells 2 (p49/p100)

PDB rendering based on 1a3q.
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols  ; CVID10; H2TF1; LYT-10; LYT10; NF-kB2; p105; p52
External IDs ChEMBL: GeneCards:
RNA expression pattern
Species Human Mouse
RefSeq (mRNA)
RefSeq (protein)
Location (UCSC)
PubMed search

Nuclear factor NF-kappa-B p100 subunit is a protein that in humans is encoded by the NFKB2 gene.[1] NFKB 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. NFKB 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. For reviews, see Chen et al. (1999) and Baldwin (1996).[supplied by OMIM][2]


  • Interactions 1
  • CVID Link 2
  • See also 3
  • References 4
  • Further reading 5
  • External links 6


NFKB2 has been shown to interact with NFKBIE,[3] BCL3,[4][5] MAP3K8,[6] BTRC,[7][8] RELA,[6][9] RELB,[4][6] NFKB1,[6] REL[6][9] and TSC22D3.[10]


Mutation of the NFKB2 gene has been linked to Common variable immunodeficiency (CVID) as the cause of the disease. Other genes might also be responsible. The frequency of NFKB2 mutation in CVID population is yet to be established.[11]

See also


  1. ^ Schmid RM, Perkins ND, Duckett CS, Andrews PC, Nabel GJ (Sep 1991). "Cloning of an NF-kappa B subunit which stimulates HIV transcription in synergy with p65". Nature 352 (6337): 733–6.  
  2. ^ "Entrez Gene: NFKB2 nuclear factor of kappa light polypeptide gene enhancer in B-cells 2 (p49/p100)". 
  3. ^ Li, Z; Nabel G J (Oct 1997). "A new member of the I kappaB protein family, I kappaB epsilon, inhibits RelA (p65)-mediated NF-kappaB transcription". Mol. Cell. Biol. (UNITED STATES) 17 (10): 6184–90.  
  4. ^ a b Thornburg, Natalie J; Pathmanathan Rajadurai, Raab-Traub Nancy (Dec 2003). "Activation of nuclear factor-kappaB p50 homodimer/Bcl-3 complexes in nasopharyngeal carcinoma". Cancer Res. (United States) 63 (23): 8293–301.  
  5. ^ Bours, V; Franzoso G; Azarenko V; Park S; Kanno T; Brown K; Siebenlist U (Mar 1993). "The oncoprotein Bcl-3 directly transactivates through kappa B motifs via association with DNA-binding p50B homodimers". Cell (UNITED STATES) 72 (5): 729–39.  
  6. ^ a b c d e Bouwmeester, Tewis; Bauch Angela, Ruffner Heinz, Angrand Pierre-Olivier, Bergamini Giovanna, Croughton Karen, Cruciat Cristina, Eberhard Dirk, Gagneur Julien, Ghidelli Sonja, Hopf Carsten, Huhse Bettina, Mangano Raffaella, Michon Anne-Marie, Schirle Markus, Schlegl Judith, Schwab Markus, Stein Martin A, Bauer Andreas, Casari Georg, Drewes Gerard, Gavin Anne-Claude, Jackson David B, Joberty Gerard, Neubauer Gitte, Rick Jens, Kuster Bernhard, Superti-Furga Giulio (Feb 2004). "A physical and functional map of the human TNF-alpha/NF-kappa B signal transduction pathway". Nat. Cell Biol. (England) 6 (2): 97–105.  
  7. ^ Fong, Abraham; Sun Shao-Cong (Jun 2002). "Genetic evidence for the essential role of beta-transducin repeat-containing protein in the inducible processing of NF-kappa B2/p100". J. Biol. Chem. (United States) 277 (25): 22111–4.  
  8. ^ Vatsyayan, Jaya; Qing Guoliang; Xiao Gutian; Hu Jing (Sep 2008). "SUMO1 modification of NF-kappaB2/p100 is essential for stimuli-induced p100 phosphorylation and processing". EMBO Rep. (England) 9 (9): 885–90.  
  9. ^ a b Scheinman, R I; Beg A A; Baldwin A S (Oct 1993). "NF-kappa B p100 (Lyt-10) is a component of H2TF1 and can function as an I kappa B-like molecule". Mol. Cell. Biol. (UNITED STATES) 13 (10): 6089–101.  
  10. ^ Ayroldi, E; Migliorati G; Bruscoli S; Marchetti C; Zollo O; Cannarile L; D'Adamio F; Riccardi C (Aug 2001). "Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor kappaB". Blood (United States) 98 (3): 743–53.  
  11. ^ Chen, Karin; Emily M. Coonrod, Attila Kumánovics, Zechariah F. Franks, Jacob D. Durtschi, Rebecca L. Margraf, Wilfred Wu, Nahla M. Heikal, Nancy H. Augustine, Perry G. Ridge, Harry R. Hill, Lynn B. Jorde, Andrew S. Weyrich, Guy A. Zimmerman, Adi V. Gundlapalli, John F. Bohnsack, Karl V. Voelkerding (17 October 2013). "Germline Mutations in NFKB2 Implicate the Noncanonical NF-κB Pathway in the Pathogenesis of Common Variable Immunodeficiency.". The American Journal of Human Genetics.  

Further reading

  • Schreck R, Albermann K, Baeuerle PA (1993). "Nuclear factor kappa B: an oxidative stress-responsive transcription factor of eukaryotic cells (a review).". Free Radic. Res. Commun. 17 (4): 221–37.  
  • Baldwin AS (1996). "The NF-kappa B and I kappa B proteins: new discoveries and insights.". Annu. Rev. Immunol. 14 (1): 649–83.  
  • Chen F, Castranova V, Shi X, Demers LM (1999). "New insights into the role of nuclear factor-kappaB, a ubiquitous transcription factor in the initiation of diseases.". Clin. Chem. 45 (1): 7–17.  
  • Bottex-Gauthier C, Pollet S, Favier A, Vidal DR (2002). "[The Rel/NF-kappa-B transcription factors: complex role in cell regulation]". Pathol. Biol. 50 (3): 204–11.  
  • Garg A, Aggarwal BB (2002). "Nuclear transcription factor-kappaB as a target for cancer drug development.". Leukemia 16 (6): 1053–68.  

External links

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