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Gene Review

NFKB1  -  nuclear factor of kappa light polypeptide...

Homo sapiens

Synonyms: DNA-binding factor KBF1, EBP-1, KBF1, NF-kB1, NF-kappa-B, ...
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Disease relevance of NFKB1


Psychiatry related information on NFKB1

  • Apart from its role in these events, evidence has begun to accumulate that NF-kappa B is involved in brain function, particularly following injury and in neurodegenerative conditions such as Alzheimer's disease [8].
  • The presence of regulatory sequences for the binding of transcription factors such as NF-kappa B and AP-2, whose activation is associated with the immediate response of the cell to an injury, may be an indication of the important role which HO-1 may play in defense mechanisms against tissue injury [9].
  • Thus this NF-kappa B-like factor may be involved in the mechanism causing AIDS dementia [10].
  • RESULTS: Levels of RNA transcripts encoding the serotonin transporter protein and components of the NF-kappa B transcription factor complex are significantly increased in individuals with bipolar disorder compared with unaffected controls [11].

High impact information on NFKB1


Chemical compound and disease context of NFKB1


Biological context of NFKB1

  • NFKB1 promoter/exon 1 luciferase reporter plasmid constructs containing the -94delATTG allele and transfected into either HeLa or HT-29 cell lines showed less promoter activity than comparable constructs containing the -94insATTG allele [2].
  • Genome-wide screens in IBD families show evidence for linkage on chromosome 4q where NFKB1 maps [2].
  • We sequenced the NFKB1 promoter, exon 1 and all coding exons in 10 IBD probands and two controls, and identified six nucleotide variants, including a common insertion/deletion promoter polymorphism (-94ins/delATTG) [2].
  • We also studied a single nucleotide polymorphism in intron 11 of the NFKB1 gene (rs1020759), which probably lacks any functional role, and found no significant association with the disease [3].
  • The U2 subgroup was associated with overexpression of genes involved in T-cell activation and apoptosis, including NFKB1 and BCL-2 [21].

Anatomical context of NFKB1

  • Antisense oligonucleotides to RelA, but not NFKB1, inhibited phorbol myristate acetate-induced IL-8 production in Jurkat T lymphocytes [1].
  • This response arises from exceedingly low basal expression of the p105/p50 NF-kappaB subunit encoded by the NFKB1 gene in these cell lines [22].
  • The MAD-3 cDNA encodes an I kappa B-like protein that is likely to be involved in regulation of transcriptional responses to NF-kappa B, including adhesion-dependent pathways of monocyte activation [23].
  • Here, we show that NTHi strongly activates NF-kappa B in human epithelial cells via two distinct signaling pathways, NF-kappa B translocation-dependent and -independent pathways [24].
  • Inflammatory stimulation of endothelial cells by tumor necrosis factor alpha (TNF-alpha) involves activation of nuclear factor kappa B (NF-kappa B) and p38 mitogen-activated protein (MAP) kinase signaling pathways [25].

Associations of NFKB1 with chemical compounds

  • However, expression of the death domain of RIP Induces apoptosis, but potently inhibits NF-kappa B activation by TNF [26].
  • Anti-beta(2)-GPI antibody binding has been shown to induce nuclear factor-kappa B (NF-kappa B) translocation leading to a proinflammatory EC phenotype similar to that elicited by interaction with microbial products (lipopolysaccharide [LPS]) and proinflammatory cytokines (interleukin 1 beta [IL-1 beta], tumor necrosis factor alpha [TNF-alpha]) [27].
  • Thus, we have explored the effect of two inhibitors of the NF-kappa B activation, pyrrolidine dithiocarbamate (PDTC) and N-acetylcysteine (NAC), on the production of these cytokines by EC [28].
  • Extracellular SMase does not have access to intracellular sphingomyelin, but treatment of ECs with membrane-permeant ceramide analogues still completely fails to activate NF-kappa B and only activates JNK at late times [29].
  • These data reveal a second mechanism by which NF-kappa B activity may be regulated by DEX [30].
  • Small interfering RNA-mediated knockdown of beclin 1 and atg7 expression, two autophagy-related genes, reduced TNFalpha- and reactive oxygen species-induced apoptosis in cells lacking NF-kappaB activation and in NF-kappaB-competent cells, respectively [31].
  • Overall, our results demonstrate that gossypin inhibits the NF-kappaB activation pathway, which may explain its role in the suppression of inflammation, carcinogenesis, and angiogenesis [32].
  • These effects were not observed in a form of Cezanne that was mutated at the catalytic cysteine residue (Cys209), indicating that the deubiquitinating activity of Cezanne is essential for NF-kappaB regulation [33].
  • In addition LC8 inhibited NF-kappaB activation by other stimuli including interleukin-1beta and lipopolysaccharide, both of which generated reactive oxygen species [34].

Physical interactions of NFKB1

  • Both the NF-IL6 and NF-kappa B binding sites in the IL-6 promoter were required for synergistic activation [35].
  • We show here that NF-kappa B p100 is a component of the previously identified DNA-binding activity H2TF1 [36].
  • In addition, ATFa, ATF2, and ATF3 interact directly with NF-kappa B in vitro, linking two unrelated families of transcription factors in a novel protein-protein interaction [37].
  • We found that the IL-8 NF-kappa B-binding site specifically formed a complex with NF-kappa B-containing nuclear extracts from HTLV-I-infected T-cell lines and freshly isolated leukemic cells from adult T-cell leukemia patients [38].
  • The exposure of MC to AIgA rapidly activated a NF-kappa B complex constituted of p50 and p65 subunits [39].
  • UXT forms a dynamic complex with NF-kappaB and is recruited to the NF-kappaB enhanceosome upon stimulation [40].

Enzymatic interactions of NFKB1

  • In promoter-reporter assay, the luciferase activities of the reporter constructs, including the putative NF-kappa B site deleted and mutated form were significantly reduced after HRG-beta 1 treatment as compared with the 1.5-kb VEGF-C promoter [41].
  • Western blot analyses and electrophoretic mobility shift assays revealed that incubation with TNF alpha induced the expression of phosphorylated inhibitor kappa B (p-I kappa B) and activation of NF-kappa B in endometriotic stromal cells [42].
  • We demonstrate that Ebp1 interacts with and is phosphorylated by the PKR protein kinase [43].
  • A proteasome inhibitor prevents activation of NF-kappa B and stabilizes a newly phosphorylated form of I kappa B-alpha that is still bound to NF-kappa B [44].

Regulatory relationships of NFKB1

  • TNFR1 signaling is also known to activate the transcription factor NF-kappa B and promote survival [45].
  • PKC blockade with H7 does not inhibit activation of these NF-kappa B-like proteins but does inhibit ELAM-1 gene transcription [46].
  • We find that concentrations of TNF that strongly activate NF-kappa B and JNK within 15 minutes do not produce either a measurable decline in sphingomyelin or a measurable generation of ceramide in cultured human umbilical vein ECs at any time examined [29].
  • CD40 induces human multiple myeloma cell migration via phosphatidylinositol 3-kinase/AKT/NF-kappa B signaling [47].
  • Thus, the IL-1 beta gene may be considered as an important additional member of the family of cytokine genes regulated in part by the NF-kappa B/rel family of transcription factors [48].
  • We find that HMGB1 activates the canonical nuclear factor kappaB (NF-kappaB) pathway via extracellular signal-regulated kinase phosphorylation [49].

Other interactions of NFKB1

  • Thus, TNFR1-mediated-signal transduction includes a checkpoint, resulting in cell death (via complex II) in instances where the initial signal (via complex I, NF-kappa B) fails to be activated [45].
  • The death domain of tumor necrosis factor (TNF) receptor-1 (TNFR1) triggers distinct signaling pathways leading to apoptosis and NF-kappa B activation through its interaction with the death domain protein TRADD [26].
  • We show that induction of a trimer of the NFAT and Oct sites is not sensitive to phorbol ester treatment, and that mutations in the NF-kappa B site have no effect on inducibility of the IL-2 promoter [50].
  • Here we report that transient expression of TRAF6 stimulated both ERK and NF kappa B activity in the 293 cell line [51].
  • NF-kappa B and p53 activation was assessed by electromobility shift assays [52].
  • RPS3 knockdown impaired NF-kappaB-mediated transcription of selected p65 target genes but not nuclear shuttling or global protein translation [53].

Analytical, diagnostic and therapeutic context of NFKB1


  1. NF-kappa B subunit-specific regulation of the interleukin-8 promoter. Kunsch, C., Rosen, C.A. Mol. Cell. Biol. (1993) [Pubmed]
  2. Functional annotation of a novel NFKB1 promoter polymorphism that increases risk for ulcerative colitis. Karban, A.S., Okazaki, T., Panhuysen, C.I., Gallegos, T., Potter, J.J., Bailey-Wilson, J.E., Silverberg, M.S., Duerr, R.H., Cho, J.H., Gregersen, P.K., Wu, Y., Achkar, J.P., Dassopoulos, T., Mezey, E., Bayless, T.M., Nouvet, F.J., Brant, S.R. Hum. Mol. Genet. (2004) [Pubmed]
  3. Association of common polymorphisms in inflammatory genes interleukin (IL)6, IL8, tumor necrosis factor alpha, NFKB1, and peroxisome proliferator-activated receptor gamma with colorectal cancer. Landi, S., Moreno, V., Gioia-Patricola, L., Guino, E., Navarro, M., de Oca, J., Capella, G., Canzian, F. Cancer Res. (2003) [Pubmed]
  4. Chronic human immunodeficiency virus type 1 infection stimulates distinct NF-kappa B/rel DNA binding activities in myelomonoblastic cells. Roulston, A., Beauparlant, P., Rice, N., Hiscott, J. J. Virol. (1993) [Pubmed]
  5. Role of the NFKB1 -94ins/delATTG promoter polymorphism in IBD and potential interactions with polymorphisms in the CARD15/NOD2, IKBL, and IL-1RN genes. Glas, J., Török, H.P., Tonenchi, L., Müller-Myhsok, B., Mussack, T., Wetzke, M., Klein, W., Epplen, J.T., Griga, T., Schiemann, U., Lohse, P., Seiderer, J., Schnitzler, F., Brand, S., Ochsenkühn, T., Folwaczny, M., Folwaczny, C. Inflamm. Bowel Dis. (2006) [Pubmed]
  6. Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma. Keats, J.J., Fonseca, R., Chesi, M., Schop, R., Baker, A., Chng, W.J., Van Wier, S., Tiedemann, R., Shi, C.X., Sebag, M., Braggio, E., Henry, T., Zhu, Y.X., Fogle, H., Price-Troska, T., Ahmann, G., Mancini, C., Brents, L.A., Kumar, S., Greipp, P., Dispenzieri, A., Bryant, B., Mulligan, G., Bruhn, L., Barrett, M., Valdez, R., Trent, J., Stewart, A.K., Carpten, J., Bergsagel, P.L. Cancer. Cell (2007) [Pubmed]
  7. Constitutive NF-kappaB activation in colorectal carcinoma plays a key role in angiogenesis, promoting tumor growth. Sakamoto, K., Maeda, S., Hikiba, Y., Nakagawa, H., Hayakawa, Y., Shibata, W., Yanai, A., Ogura, K., Omata, M. Clin. Cancer Res. (2009) [Pubmed]
  8. NF-kappa B: a crucial transcription factor for glial and neuronal cell function. O'Neill, L.A., Kaltschmidt, C. Trends Neurosci. (1997) [Pubmed]
  9. Identification of binding sites for transcription factors NF-kappa B and AP-2 in the promoter region of the human heme oxygenase 1 gene. Lavrovsky, Y., Schwartzman, M.L., Levere, R.D., Kappas, A., Abraham, N.G. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  10. Human neuroblastoma cells produce the NF-kappa B-like HIV-1 transcription activator during differentiation. Kurata, S., Wakabayashi, T., Ito, Y., Miwa, N., Ueno, R., Marunouchi, T., Kurata, N. FEBS Lett. (1993) [Pubmed]
  11. Serial analysis of gene expression in the frontal cortex of patients with bipolar disorder. Sun, Y., Zhang, L., Johnston, N.L., Torrey, E.F., Yolken, R.H. The British journal of psychiatry. Supplement. (2001) [Pubmed]
  12. The NF-kappa B and I kappa B proteins: new discoveries and insights. Baldwin, A.S. Annu. Rev. Immunol. (1996) [Pubmed]
  13. Function and activation of NF-kappa B in the immune system. Baeuerle, P.A., Henkel, T. Annu. Rev. Immunol. (1994) [Pubmed]
  14. Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives. Mattson, M.P. Physiol. Rev. (1997) [Pubmed]
  15. A functional variant of SUMO4, a new I kappa B alpha modifier, is associated with type 1 diabetes. Guo, D., Li, M., Zhang, Y., Yang, P., Eckenrode, S., Hopkins, D., Zheng, W., Purohit, S., Podolsky, R.H., Muir, A., Wang, J., Dong, Z., Brusko, T., Atkinson, M., Pozzilli, P., Zeidler, A., Raffel, L.J., Jacob, C.O., Park, Y., Serrano-Rios, M., Larrad, M.T., Zhang, Z., Garchon, H.J., Bach, J.F., Rotter, J.I., She, J.X., Wang, C.Y. Nat. Genet. (2004) [Pubmed]
  16. Tumor necrosis factor induces lipopolysaccharide tolerance in a human adenocarcinoma cell line mainly through the TNF p55 receptor. Laegreid, A., Thommesen, L., Jahr, T.G., Sundan, A., Espevik, T. J. Biol. Chem. (1995) [Pubmed]
  17. Tyloxapol inhibits NF-kappa B and cytokine release, scavenges HOCI, and reduces viscosity of cystic fibrosis sputum. Ghio, A.J., Marshall, B.C., Diaz, J.L., Hasegawa, T., Samuelson, W., Povia, D., Kennedy, T.P., Piantodosi, C.A. Am. J. Respir. Crit. Care Med. (1996) [Pubmed]
  18. Simvastatin suppresses tissue factor expression and increases fibrinolytic activity in tumor necrosis factor-alpha-activated human peritoneal mesothelial cells. Haslinger, B., Kleemann, R., Toet, K.H., Kooistra, T. Kidney Int. (2003) [Pubmed]
  19. The role of nuclear factor-kappa B in interleukin-8 expression by human adenoidal fibroblasts. Takaki, M., Ushikai, M., Deguchi, K., Nishimoto, K., Matsune, S., Kurono, Y. Laryngoscope (2003) [Pubmed]
  20. Functional polymorphism in NFKB1 promoter is related to the risks of oral squamous cell carcinoma occurring on older male areca (betel) chewers. Lin, S.C., Liu, C.J., Yeh, W.I., Lui, M.T., Chang, K.W., Chang, C.S. Cancer Lett. (2006) [Pubmed]
  21. Gene expression profiling identifies molecular subgroups among nodal peripheral T-cell lymphomas. Ballester, B., Ramuz, O., Gisselbrecht, C., Doucet, G., Loï, L., Loriod, B., Bertucci, F., Bouabdallah, R., Devilard, E., Carbuccia, N., Mozziconacci, M.J., Birnbaum, D., Brousset, P., Berger, F., Salles, G., Briére, J., Houlgatte, R., Gaulard, P., Xerri, L. Oncogene (2006) [Pubmed]
  22. Nuclear factor-kappaB dimer exchange promotes a p21(waf1/cip1) superinduction response in human T leukemic cells. Chang, P.Y., Miyamoto, S. Mol. Cancer Res. (2006) [Pubmed]
  23. Characterization of an immediate-early gene induced in adherent monocytes that encodes I kappa B-like activity. Haskill, S., Beg, A.A., Tompkins, S.M., Morris, J.S., Yurochko, A.D., Sampson-Johannes, A., Mondal, K., Ralph, P., Baldwin, A.S. Cell (1991) [Pubmed]
  24. Activation of NF-kappa B by nontypeable Hemophilus influenzae is mediated by toll-like receptor 2-TAK1-dependent NIK-IKK alpha /beta-I kappa B alpha and MKK3/6-p38 MAP kinase signaling pathways in epithelial cells. Shuto, T., Xu, H., Wang, B., Han, J., Kai, H., Gu, X.X., Murphy, T.F., Lim, D.J., Li, J.D. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  25. Transcriptional profiling of IKK2/NF-kappa B- and p38 MAP kinase-dependent gene expression in TNF-alpha-stimulated primary human endothelial cells. Viemann, D., Goebeler, M., Schmid, S., Klimmek, K., Sorg, C., Ludwig, S., Roth, J. Blood (2004) [Pubmed]
  26. TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex. Hsu, H., Huang, J., Shu, H.B., Baichwal, V., Goeddel, D.V. Immunity (1996) [Pubmed]
  27. Role of the MyD88 transduction signaling pathway in endothelial activation by antiphospholipid antibodies. Raschi, E., Testoni, C., Bosisio, D., Borghi, M.O., Koike, T., Mantovani, A., Meroni, P.L. Blood (2003) [Pubmed]
  28. Pyrrolidine dithiocarbamate inhibits the production of interleukin-6, interleukin-8, and granulocyte-macrophage colony-stimulating factor by human endothelial cells in response to inflammatory mediators: modulation of NF-kappa B and AP-1 transcription factors activity. Muñoz, C., Pascual-Salcedo, D., Castellanos, M.C., Alfranca, A., Aragonés, J., Vara, A., Redondo, J.M., de Landázuri, M.O. Blood (1996) [Pubmed]
  29. Ceramide is not a signal for tumor necrosis factor-induced gene expression but does cause programmed cell death in human vascular endothelial cells. Slowik, M.R., De Luca, L.G., Min, W., Pober, J.S. Circ. Res. (1996) [Pubmed]
  30. Characterization of mechanisms involved in transrepression of NF-kappa B by activated glucocorticoid receptors. Scheinman, R.I., Gualberto, A., Jewell, C.M., Cidlowski, J.A., Baldwin, A.S. Mol. Cell. Biol. (1995) [Pubmed]
  31. NF-kappaB activation represses tumor necrosis factor-alpha-induced autophagy. Djavaheri-Mergny, M., Amelotti, M., Mathieu, J., Besançon, F., Bauvy, C., Souquère, S., Pierron, G., Codogno, P. J. Biol. Chem. (2006) [Pubmed]
  32. Gossypin, a pentahydroxy glucosyl flavone, inhibits the transforming growth factor beta-activated kinase-1-mediated NF-kappaB activation pathway, leading to potentiation of apoptosis, suppression of invasion, and abrogation of osteoclastogenesis. Kunnumakkara, A.B., Nair, A.S., Ahn, K.S., Pandey, M.K., Yi, Z., Liu, M., Aggarwal, B.B. Blood (2007) [Pubmed]
  33. NF-kappaB suppression by the deubiquitinating enzyme Cezanne: a novel negative feedback loop in pro-inflammatory signaling. Enesa, K., Zakkar, M., Chaudhury, H., Luong, L.A., Rawlinson, L., Mason, J.C., Haskard, D.O., Dean, J.L., Evans, P.C. J. Biol. Chem. (2008) [Pubmed]
  34. Dynein light chain LC8 negatively regulates NF-kappaB through the redox-dependent interaction with IkappaBalpha. Jung, Y., Kim, H., Min, S.H., Rhee, S.G., Jeong, W. J. Biol. Chem. (2008) [Pubmed]
  35. Transcription factors NF-IL6 and NF-kappa B synergistically activate transcription of the inflammatory cytokines, interleukin 6 and interleukin 8. Matsusaka, T., Fujikawa, K., Nishio, Y., Mukaida, N., Matsushima, K., Kishimoto, T., Akira, S. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  36. NF-kappa B p100 (Lyt-10) is a component of H2TF1 and can function as an I kappa B-like molecule. Scheinman, R.I., Beg, A.A., Baldwin, A.S. Mol. Cell. Biol. (1993) [Pubmed]
  37. Cyclic AMP-independent ATF family members interact with NF-kappa B and function in the activation of the E-selectin promoter in response to cytokines. Kaszubska, W., Hooft van Huijsduijnen, R., Ghersa, P., DeRaemy-Schenk, A.M., Chen, B.P., Hai, T., DeLamarter, J.F., Whelan, J. Mol. Cell. Biol. (1993) [Pubmed]
  38. Production of interleukin 8 in adult T-cell leukemia cells: possible transactivation of the interleukin 8 gene by human T-cell leukemia virus type I tax. Mori, N., Murakami, S., Oda, S., Prager, D., Eto, S. Cancer Res. (1995) [Pubmed]
  39. Interaction of IgA with Fc alpha receptors of human mesangial cells activates transcription factor nuclear factor-kappa B and induces expression and synthesis of monocyte chemoattractant protein-1, IL-8, and IFN-inducible protein 10. Duque, N., Gómez-Guerrero, C., Egido, J. J. Immunol. (1997) [Pubmed]
  40. UXT is a novel and essential cofactor in the NF-kappaB transcriptional enhanceosome. Sun, S., Tang, Y., Lou, X., Zhu, L., Yang, K., Zhang, B., Shi, H., Wang, C. J. Cell Biol. (2007) [Pubmed]
  41. Up-regulation of vascular endothelial growth factor C in breast cancer cells by heregulin-beta 1. A critical role of p38/nuclear factor-kappa B signaling pathway. Tsai, P.W., Shiah, S.G., Lin, M.T., Wu, C.W., Kuo, M.L. J. Biol. Chem. (2003) [Pubmed]
  42. Tumor necrosis factor-alpha-induced interleukin-8 (IL-8) expression in endometriotic stromal cells, probably through nuclear factor-kappa B activation: gonadotropin-releasing hormone agonist treatment reduced IL-8 expression. Sakamoto, Y., Harada, T., Horie, S., Iba, Y., Taniguchi, F., Yoshida, S., Iwabe, T., Terakawa, N. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
  43. Ebp1 is a dsRNA-binding protein associated with ribosomes that modulates eIF2alpha phosphorylation. Squatrito, M., Mancino, M., Sala, L., Draetta, G.F. Biochem. Biophys. Res. Commun. (2006) [Pubmed]
  44. A proteasome inhibitor prevents activation of NF-kappa B and stabilizes a newly phosphorylated form of I kappa B-alpha that is still bound to NF-kappa B. Traenckner, E.B., Wilk, S., Baeuerle, P.A. EMBO J. (1994) [Pubmed]
  45. Induction of TNF receptor I-mediated apoptosis via two sequential signaling complexes. Micheau, O., Tschopp, J. Cell (2003) [Pubmed]
  46. Activation of endothelial-leukocyte adhesion molecule 1 (ELAM-1) gene transcription. Montgomery, K.F., Osborn, L., Hession, C., Tizard, R., Goff, D., Vassallo, C., Tarr, P.I., Bomsztyk, K., Lobb, R., Harlan, J.M. Proc. Natl. Acad. Sci. U.S.A. (1991) [Pubmed]
  47. CD40 induces human multiple myeloma cell migration via phosphatidylinositol 3-kinase/AKT/NF-kappa B signaling. Tai, Y.T., Podar, K., Mitsiades, N., Lin, B., Mitsiades, C., Gupta, D., Akiyama, M., Catley, L., Hideshima, T., Munshi, N.C., Treon, S.P., Anderson, K.C. Blood (2003) [Pubmed]
  48. Characterization of a functional NF-kappa B site in the human interleukin 1 beta promoter: evidence for a positive autoregulatory loop. Hiscott, J., Marois, J., Garoufalis, J., D'Addario, M., Roulston, A., Kwan, I., Pepin, N., Lacoste, J., Nguyen, H., Bensi, G. Mol. Cell. Biol. (1993) [Pubmed]
  49. Cells migrating to sites of tissue damage in response to the danger signal HMGB1 require NF-kappaB activation. Palumbo, R., Galvez, B.G., Pusterla, T., De Marchis, F., Cossu, G., Marcu, K.B., Bianchi, M.E. J. Cell Biol. (2007) [Pubmed]
  50. The AP-1 site at -150 bp, but not the NF-kappa B site, is likely to represent the major target of protein kinase C in the interleukin 2 promoter. Jain, J., Valge-Archer, V.E., Sinskey, A.J., Rao, A. J. Exp. Med. (1992) [Pubmed]
  51. Tumor necrosis factor receptor-associated factor 6 (TRAF6) stimulates extracellular signal-regulated kinase (ERK) activity in CD40 signaling along a ras-independent pathway. Kashiwada, M., Shirakata, Y., Inoue, J.I., Nakano, H., Okazaki, K., Okumura, K., Yamamoto, T., Nagaoka, H., Takemori, T. J. Exp. Med. (1998) [Pubmed]
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  53. Ribosomal protein S3: a KH domain subunit in NF-kappaB complexes that mediates selective gene regulation. Wan, F., Anderson, D.E., Barnitz, R.A., Snow, A., Bidere, N., Zheng, L., Hegde, V., Lam, L.T., Staudt, L.M., Levens, D., Deutsch, W.A., Lenardo, M.J. Cell (2007) [Pubmed]
  54. Complex regulation of human inducible nitric oxide synthase gene transcription by Stat 1 and NF-kappa B. Ganster, R.W., Taylor, B.S., Shao, L., Geller, D.A. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  55. Differential STAT3, STAT5, and NF-kappaB activation in human hematopoietic progenitors by endogenous interleukin-15: implications in the expression of functional molecules. Giron-Michel, J., Caignard, A., Fogli, M., Brouty-Boyé, D., Briard, D., van Dijk, M., Meazza, R., Ferrini, S., Lebousse-Kerdilès, C., Clay, D., Bompais, H., Chouaib, S., Péault, B., Azzarone, B. Blood (2003) [Pubmed]
  56. Expression of cytokine genes, cytokine receptor genes, and transcription factors in cultured Hodgkin and Reed-Sternberg cells. Gruss, H.J., Brach, M.A., Drexler, H.G., Bonifer, R., Mertelsmann, R.H., Herrmann, F. Cancer Res. (1992) [Pubmed]
  57. Sublytic concentrations of the membrane attack complex of complement induce endothelial interleukin-8 and monocyte chemoattractant protein-1 through nuclear factor-kappa B activation. Kilgore, K.S., Schmid, E., Shanley, T.P., Flory, C.M., Maheswari, V., Tramontini, N.L., Cohen, H., Ward, P.A., Friedl, H.P., Warren, J.S. Am. J. Pathol. (1997) [Pubmed]
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