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MeSH Review

Genes, jun

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Disease relevance of Genes, jun


High impact information on Genes, jun

  • AP-1 consists of the products of the fos and jun oncogenes, which associate as dimers to bind TPA-responsive promoter elements (TRE) efficiently [6].
  • One consequence of MEF2C activation is increased c-jun gene transcription [7].
  • Because of the similarity between the recognition sites for GCN4 and AP-1, we examined the possibility that AP-1 could be the product of the c-jun proto-oncogene [8].
  • The protein products of the fos and jun proto-oncogenes form a heterodimeric complex that participates in a stable high affinity interaction with DNA elements containing AP-1 binding sites [9].
  • Transcriptional run-on assays revealed that treatment of serum-starved NKM-1 with 50 ng/ml G-CSF or M-CSF increased the transcription rate of the junB gene and the c-fos gene by 1.8-fold and 2.9-fold, respectively, but did not induce any transcript of the c-jun gene [10].

Chemical compound and disease context of Genes, jun


Biological context of Genes, jun


Anatomical context of Genes, jun

  • Protein kinase C regulates proliferation of mast cells and the expression of the mRNAs of fos and jun proto-oncogenes during activation by IgE-Ag or calcium ionophore A23187 [17].
  • Moreover, treatment of T cells with actinomycin D to block further transcription before their culture with PWM suggests that the increase in c-jun gene expression by PWM is also regulated at least in part by a posttranscriptional mechanism [18].
  • Using the factor-dependent myelogenous leukemia cell lines GF-D8 and Mo7, we show that TGF-beta interferes with stem cell factor (SCF)-induced proliferation by downmodulating c-jun gene expression [19].
  • These results show transient induction of immediate-early response genes in B cells and support a potential role for the c-jun gene product in regulation of IL-6 transcription and secretion [20].
  • In accordance with the results obtained by analysis of the mRNA, we found that estrogen increases 3- to 4-fold c-jun gene transcription in the uterus, at the same time it induces its mRNA accumulation [21].

Associations of Genes, jun with chemical compounds

  • We found that As3+, but not As5+, which is toxic but not carcinogenic, is a potent stimulator of AP-1 transcriptional activity and an efficient inducer of c-fos and c-jun gene expression [22].
  • The jun gene lacks preserved coding domains of tyrosine-specific protein kinases [23].
  • Both proteins were found to contain a peptide sequence reminiscent of a leucine-repeat motif ("leucine-zipper") that is also found in the myc, fos, and jun oncogenes [24].
  • The DNA binding activity of the c-jun proto-oncogene product is inhibited by oxidation of a specific cysteine residue (Cys-252) in the DNA binding domain [25].
  • Platelet-derived growth factor-beta receptor was not phosphorylated on Ang II stimulation, and Ang II-induced c-jun gene expression was not affected by tyrphostin AG1478 [26].

Gene context of Genes, jun

  • Furthermore, we observed significant time-dependent increases in the expression of the c-fos and c-jun proto-oncogenes after addition of IGF-I (n = 5 per group, P <.05) [27].
  • Differential regulation of fos and jun gene expression and AP-1 cis-element activity by endothelin isopeptides. Possible implications for mitogenic signaling by endothelin [28].
  • In addition, although the c-jun proto-oncogene product was detected in stimulated human T cells, two additional T cell-specific proteins (45 and 43 kDa) bind to the GM-CSF, IL-3, and IL-5 promoters and are functionally and immunologically distinct from c-jun or OAP40 (jun-D) [29].
  • Because HDAC inhibitors suppressed the induction of c-jun gene expression, resulting in reduced COX-2 transcription, it was important to determine whether other known AP-1 target genes were also modulated [30].
  • Tumor necrosis factor-alpha induces expression of monocyte chemoattractant JE via fos and jun genes in clonal osteoblastic MC3T3-E1 cells [31].

Analytical, diagnostic and therapeutic context of Genes, jun

  • Nonetheless, the ligation-mediated PCR technology was used here to demonstrate, at nucleotide resolution, that p53-/-p21+/+ DLD1 excises UVB-induced cyclobutane pyrimidine dimers from the c-jun proto-oncogene at a significantly lower rate than the isogenic p53-/-p21-/- derivative [32].
  • Western blotting analysis of c-Fos and c-Jun suggested that up-regulation of c-fos and c-jun gene expression does not directly contribute to the induction of AP-1 activation [33].
  • Northern blot analysis revealed that lack of BGP mRNA expression was associated with expression of both c-fos and c-jun proto-oncogenes in SOS [5].
  • Coronal hypothalamic sections and control ovarian tissues were incubated with 45-mer oligonucleotide probes complementary to porcine c-fos and c-jun genes using standard in situ hybridization histochemistry techniques [34].
  • DNA array analysis revealed that expression of genes such as the RhoG and D4-GDI genes was down-regulated in TEL-overexpressing cells, while that of the representative growth-related genes such as the c-myc, c-fos and c-jun genes was not remarkably changed [35].


  1. Transcriptional regulation of c-jun gene expression by arabinofuranosylcytosine in human myeloid leukemia cells. Kharbanda, S.M., Sherman, M.L., Kufe, D.W. J. Clin. Invest. (1990) [Pubmed]
  2. Phosphorylation of the adenovirus E1A-associated 300 kDa protein in response to retinoic acid and E1A during the differentiation of F9 cells. Kitabayashi, I., Eckner, R., Arany, Z., Chiu, R., Gachelin, G., Livingston, D.M., Yokoyama, K.K. EMBO J. (1995) [Pubmed]
  3. Induction of jun gene family members by transforming growth factor alpha but not 17 beta-estradiol in human breast cancer cells. Davidson, N.E., Prestigiacomo, L.J., Hahm, H.A. Cancer Res. (1993) [Pubmed]
  4. The c-jun proto-oncogene down-regulates the rat alpha-fetoprotein promoter in HepG2 hepatoma cells without binding to DNA. Bois-Joyeux, B., Denissenko, M., Thomassin, H., Guesdon, S., Ikonomova, R., Bernuau, D., Feldmann, G., Danan, J.L. J. Biol. Chem. (1995) [Pubmed]
  5. Correlation between lack of bone Gla protein mRNA expression in rat transplantable osteosarcomas and expression of both c-fos and c-jun proto-oncogenes. Honoki, K., Dohi, Y., Tabata, S., Mii, Y., Miyauchi, Y., Tsutsumi, M., Tsujiuchi, T., Morishita, T., Miura, S., Moriyama, T. Mol. Carcinog. (1993) [Pubmed]
  6. IP-1: a dominant inhibitor of Fos/Jun whose activity is modulated by phosphorylation. Auwerx, J., Sassone-Corsi, P. Cell (1991) [Pubmed]
  7. Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation. Han, J., Jiang, Y., Li, Z., Kravchenko, V.V., Ulevitch, R.J. Nature (1997) [Pubmed]
  8. Oncogene jun encodes a sequence-specific trans-activator similar to AP-1. Angel, P., Allegretto, E.A., Okino, S.T., Hattori, K., Boyle, W.J., Hunter, T., Karin, M. Nature (1988) [Pubmed]
  9. Parallel association of Fos and Jun leucine zippers juxtaposes DNA binding domains. Gentz, R., Rauscher, F.J., Abate, C., Curran, T. Science (1989) [Pubmed]
  10. Induction of junB expression, but not c-jun, by granulocyte colony-stimulating factor or macrophage colony-stimulating factor in the proliferative response of human myeloid leukemia cells. Adachi, K., Saito, H. J. Clin. Invest. (1992) [Pubmed]
  11. Doxorubicin-induced alterations of c-myc and c-jun gene expression in rat glioblastoma cells: role of c-jun in drug resistance and cell death. Pourquier, P., Montaudon, D., Huet, S., Larrue, A., Clary, A., Robert, J. Biochem. Pharmacol. (1998) [Pubmed]
  12. The effects of vitamin E succinate on the expression of c-jun gene and protein in human gastric cancer SGC-7901 cells. Zhao, Y., Wu, K., Xia, W., Shan, Y.J., Wu, L.J., Yu, W.P. World J. Gastroenterol. (2002) [Pubmed]
  13. Epidermal growth factor induction of the c-jun promoter by a Rac pathway. Clarke, N., Arenzana, N., Hai, T., Minden, A., Prywes, R. Mol. Cell. Biol. (1998) [Pubmed]
  14. Rapid and preferential activation of the c-jun gene during the mammalian UV response. Devary, Y., Gottlieb, R.A., Lau, L.F., Karin, M. Mol. Cell. Biol. (1991) [Pubmed]
  15. Neuroprotection by histone deacetylase-related protein. Morrison, B.E., Majdzadeh, N., Zhang, X., Lyles, A., Bassel-Duby, R., Olson, E.N., D'Mello, S.R. Mol. Cell. Biol. (2006) [Pubmed]
  16. Coordinate expression of c-fos and jun B is induced in the rat striatum by cocaine. Moratalla, R., Vickers, E.A., Robertson, H.A., Cochran, B.H., Graybiel, A.M. J. Neurosci. (1993) [Pubmed]
  17. Protein kinase C regulates proliferation of mast cells and the expression of the mRNAs of fos and jun proto-oncogenes during activation by IgE-Ag or calcium ionophore A23187. Baranes, D., Razin, E. Blood (1991) [Pubmed]
  18. Regulation of c-jun gene expression in human T lymphocytes. Chauhan, D., Kharbanda, S.M., Rubin, E., Barut, B.A., Mohrbacher, A., Kufe, D.W., Anderson, K.C. Blood (1993) [Pubmed]
  19. Transforming growth factor-beta relieves stem cell factor-induced proliferation of myelogenous leukemia cells through inhibition of binding of the transcription factor NF-jun. Sott, C., Dorner, B., Karawajew, L., Herrmann, F., Brach, M.A. Blood (1994) [Pubmed]
  20. Identification of upstream signals regulating interleukin-6 gene expression during in vitro treatment of human B cells with pokeweed mitogen. Chauhan, D., Kharbanda, S., Uchiyama, H., Urashima, M., Fragoso, R., Sen, J., Kufe, D.W., Anderson, K.C. Blood (1994) [Pubmed]
  21. Estrogen stimulates transcription of c-jun protooncogene. Weisz, A., Cicatiello, L., Persico, E., Scalona, M., Bresciani, F. Mol. Endocrinol. (1990) [Pubmed]
  22. The tumor promoter arsenite stimulates AP-1 activity by inhibiting a JNK phosphatase. Cavigelli, M., Li, W.W., Lin, A., Su, B., Yoshioka, K., Karin, M. EMBO J. (1996) [Pubmed]
  23. Avian sarcoma virus 17 carries the jun oncogene. Maki, Y., Bos, T.J., Davis, C., Starbuck, M., Vogt, P.K. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  24. Structure and expression of the murine retinoblastoma gene and characterization of its encoded protein. Bernards, R., Shackleford, G.M., Schackleford, G.M., Gerber, M.R., Horowitz, J.M., Friend, S.H., Schartl, M., Bogenmann, E., Rapaport, J.M., McGee, T., Dryja, T.P. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  25. Identification of residues in the human DNA repair enzyme HAP1 (Ref-1) that are essential for redox regulation of Jun DNA binding. Walker, L.J., Robson, C.N., Black, E., Gillespie, D., Hickson, I.D. Mol. Cell. Biol. (1993) [Pubmed]
  26. Angiotensin II type 1 receptor-induced extracellular signal-regulated protein kinase activation is mediated by Ca2+/calmodulin-dependent transactivation of epidermal growth factor receptor. Murasawa, S., Mori, Y., Nozawa, Y., Gotoh, N., Shibuya, M., Masaki, H., Maruyama, K., Tsutsumi, Y., Moriguchi, Y., Shibazaki, Y., Tanaka, Y., Iwasaka, T., Inada, M., Matsubara, H. Circ. Res. (1998) [Pubmed]
  27. Insulin-like growth factor I is a comitogen for hepatocyte growth factor in a rat model of hepatocellular carcinoma. Price, J.A., Kovach, S.J., Johnson, T., Koniaris, L.G., Cahill, P.A., Sitzmann, J.V., McKillop, I.H. Hepatology (2002) [Pubmed]
  28. Differential regulation of fos and jun gene expression and AP-1 cis-element activity by endothelin isopeptides. Possible implications for mitogenic signaling by endothelin. Simonson, M.S., Jones, J.M., Dunn, M.J. J. Biol. Chem. (1992) [Pubmed]
  29. Coordinate regulation of multiple human lymphokine genes by Oct-1 and potentially novel 45 and 43 kDa polypeptides. Kaushansky, K., Shoemaker, S.G., O'Rork, C.A., McCarty, J.M. J. Immunol. (1994) [Pubmed]
  30. Histone deacetylase inhibitors suppress the induction of c-Jun and its target genes including COX-2. Yamaguchi, K., Lantowski, A., Dannenberg, A.J., Subbaramaiah, K. J. Biol. Chem. (2005) [Pubmed]
  31. Tumor necrosis factor-alpha induces expression of monocyte chemoattractant JE via fos and jun genes in clonal osteoblastic MC3T3-E1 cells. Hanazawa, S., Takeshita, A., Amano, S., Semba, T., Nirazuka, T., Katoh, H., Kitano, S. J. Biol. Chem. (1993) [Pubmed]
  32. Ablation of p21waf1cip1 expression enhances the capacity of p53-deficient human tumor cells to repair UVB-induced DNA damage. Therrien, J.P., Loignon, M., Drouin, R., Drobetsky, E.A. Cancer Res. (2001) [Pubmed]
  33. Redox regulation of adenovirus-induced AP-1 activation by overexpression of manganese-containing superoxide dismutase. Zhang, H.J., Drake, V.J., Xu, L., Hu, J., Domann, F.E., Oberley, L.W., Kregel, K.C. J. Virol. (2002) [Pubmed]
  34. Prostaglandin F2alpha-induced nest-building behaviour is associated with increased hypothalamic c-fos and c-jun mRNA expression. Walton, S.L., Burne, T.H., Gilbert, C.L. J. Neuroendocrinol. (2002) [Pubmed]
  35. Effects of overexpression of the Ets family transcription factor TEL on cell growth and differentiation of K562 cells. Sakurai, T., Yamada, T., Kihara-Negishi, F., Teramoto, S., Sato, Y., Izawa, T., Oikawa, T. Int. J. Oncol. (2003) [Pubmed]
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