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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Genes, fos

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Disease relevance of Genes, fos

  • During cardiocyte hypertrophy evoked by endothelin-1, Phenylephrine, or PMA, the steady state level of BNP mRNA increased as rapidly as the "immediate-early" induction of the c-fos gene expression, and reached a maximal level within 1 h [1].
  • Well differentiated hepatoma cells (Fao) possess both the long and short forms of the leptin receptor and respond to leptin with a stimulation of c-fos gene expression [2].
  • Previous studies showed that T antigen could activate simple promoters containing the TATA elements from the hsp70 and c-fos gene promoters but failed to significantly activate similar promoters containing the TATA elements from the promoters of the SV40 early and adenovirus E2a genes [3].
  • Retinoic acid suppresses polyoma virus transformation by inhibiting transcription of the c-fos proto-oncogene [4].
  • Previous studies have reported that the c-fos gene via formation of activator protein-1 (AP-1) transcription factor contributes to adaptive responses to continuous hypoxia [5].

Psychiatry related information on Genes, fos

  • The c-FOS gene product, a putative transacting transcriptional regulator of the amyloid precursor protein (APP) gene, is a candidate locus for the familial Alzheimer's disease (FAD) mutation on chromosome 14 (FAD14) [6].
  • Upon activation of opiate receptors by morphine, the c-fos gene is activated and Fos protein may act as a signal transducer uniquely involved in the mechanism of opiate addiction at the level of gene regulation [7].

High impact information on Genes, fos

  • Through its SH2 domain, p91 directly interacts with the EGF receptor in a ligand-dependent manner. p91 is a necessary component of an EGF-induced DNA-binding factor that recognizes a previously identified regulatory element, SIE (c-sis-inducible element), in the c-fos gene promoter [8].
  • Transcription factor p91 interacts with the epidermal growth factor receptor and mediates activation of the c-fos gene promoter [8].
  • We report here that transport of the protein product of the c-fos proto-oncogene from the cytoplasm, where it is synthesized, into the nucleus, where it operates as part of the AP-1 transcription complex, is not spontaneous but depends on the continuous stimulation of cells by serum factors [9].
  • The functional association between DNA topoisomerase I and gene activity has been analyzed using the tightly regulated c-fos proto-oncogene, which undergoes rapid transitions between active and inactive states of transcription [10].
  • There is a dramatic increase in the FSE2 binding complex when Fos levels are induced with serum, benzodiazepine, and nerve growth factor or are expressed from a v-fos gene [11].

Chemical compound and disease context of Genes, fos


Biological context of Genes, fos


Anatomical context of Genes, fos


Associations of Genes, fos with chemical compounds


Gene context of Genes, fos

  • Although JAK1 is phosphorylated in response to EGF, it is not required for STAT activation or for induction of the c-fos gene [31].
  • Induction of c-fos gene expression and DNA synthesis were also abolished by the inhibition of EGF-R function [32].
  • Furthermore, we demonstrate that BMP2 inhibits PDGF-induced transcription of c-fos gene, a natural target of Elk-1 that normally forms a ternary complex that activates the serum response element of the c-fos gene [33].
  • While Epo is known to activate c-fos gene expression, the mechanism of AP-1 activation is unknown [34].
  • These data argue for a combined regulation of cpcA that includes a translational regulation like that of yeast GCN4 as well as a transcriptional regulation like that of the mammalian jun and fos genes [35].

Analytical, diagnostic and therapeutic context of Genes, fos


  1. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload. Nakagawa, O., Ogawa, Y., Itoh, H., Suga, S., Komatsu, Y., Kishimoto, I., Nishino, K., Yoshimasa, T., Nakao, K. J. Clin. Invest. (1995) [Pubmed]
  2. Selective interaction between leptin and insulin signaling pathways in a hepatic cell line. Szanto, I., Kahn, C.R. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  3. Simian virus 40 large T antigen stabilizes the TATA-binding protein-TFIIA complex on the TATA element. Damania, B., Lieberman, P., Alwine, J.C. Mol. Cell. Biol. (1998) [Pubmed]
  4. Retinoic acid suppresses polyoma virus transformation by inhibiting transcription of the c-fos proto-oncogene. Talmage, D.A., Listerud, M. Oncogene (1994) [Pubmed]
  5. Role of oxidative stress in intermittent hypoxia-induced immediate early gene activation in rat PC12 cells. Yuan, G., Adhikary, G., McCormick, A.A., Holcroft, J.J., Kumar, G.K., Prabhakar, N.R. J. Physiol. (Lond.) (2004) [Pubmed]
  6. Analysis of the c-FOS gene on chromosome 14 and the promoter of the amyloid precursor protein gene in familial Alzheimer's disease. Rogaev, E.I., Lukiw, W.J., Vaula, G., Haines, J.L., Rogaeva, E.A., Tsuda, T., Alexandrova, N., Liang, Y., Mortilla, M., Amaducci, L. Neurology (1993) [Pubmed]
  7. Morphine activation of c-fos expression in rat brain. Chang, S.L., Squinto, S.P., Harlan, R.E. Biochem. Biophys. Res. Commun. (1988) [Pubmed]
  8. Transcription factor p91 interacts with the epidermal growth factor receptor and mediates activation of the c-fos gene promoter. Fu, X.Y., Zhang, J.J. Cell (1993) [Pubmed]
  9. Nuclear localization of c-Fos, but not v-Fos proteins, is controlled by extracellular signals. Roux, P., Blanchard, J.M., Fernandez, A., Lamb, N., Jeanteur, P., Piechaczyk, M. Cell (1990) [Pubmed]
  10. Rapid induction of c-fos transcription reveals quantitative linkage of RNA polymerase II and DNA topoisomerase I enzyme activities. Stewart, A.F., Herrera, R.E., Nordheim, A. Cell (1990) [Pubmed]
  11. Common DNA binding site for Fos protein complexes and transcription factor AP-1. Rauscher, F.J., Sambucetti, L.C., Curran, T., Distel, R.J., Spiegelman, B.M. Cell (1988) [Pubmed]
  12. Angiotensin II induces c-fos expression in smooth muscle via transcriptional control. Naftilan, A.J., Pratt, R.E., Eldridge, C.S., Lin, H.L., Dzau, V.J. Hypertension (1989) [Pubmed]
  13. Influence of the proto-oncogene c-fos on cisplatin sensitivity. Moorehead, R.A., Singh, G. Biochem. Pharmacol. (2000) [Pubmed]
  14. Estrogen regulation of c-fos gene expression through phosphatidylinositol-3-kinase-dependent activation of serum response factor in MCF-7 breast cancer cells. Duan, R., Xie, W., Li, X., McDougal, A., Safe, S. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  15. Regulation of c-fos gene expression by lipopolysaccharide and cycloheximide in C6 rat glioma cells. Kim, Y.H., Choi, M.R., Song, D.K., Huh, S.O., Jang, C.G., Suh, H.W. Brain Res. (2000) [Pubmed]
  16. Evaluation of the cardiac isoform of alpha2-macroglobulin as a factor inducing cardiac hypertrophy. Rajamanickam, C., Jeejabai, R. Methods Mol. Med. (2005) [Pubmed]
  17. Casein kinase II enhances the DNA binding activity of serum response factor. Manak, J.R., de Bisschop, N., Kris, R.M., Prywes, R. Genes Dev. (1990) [Pubmed]
  18. DNA topoisomerase II cleaves at specific sites in the 5' flanking region of c-fos proto-oncogenes in vitro. Darby, M.K., Herrera, R.E., Vosberg, H.P., Nordheim, A. EMBO J. (1986) [Pubmed]
  19. Growth hormone stimulates c-fos gene expression by means of protein kinase C without increasing inositol lipid turnover. Doglio, A., Dani, C., Grimaldi, P., Ailhaud, G. Proc. Natl. Acad. Sci. U.S.A. (1989) [Pubmed]
  20. Activation of the human "beta 2-interferon/hepatocyte-stimulating factor/interleukin 6" promoter by cytokines, viruses, and second messenger agonists. Ray, A., Tatter, S.B., May, L.T., Sehgal, P.B. Proc. Natl. Acad. Sci. U.S.A. (1988) [Pubmed]
  21. Signal transduction pathways of angiotensin II--induced c-fos gene expression in cardiac myocytes in vitro. Roles of phospholipid-derived second messengers. Sadoshima, J., Izumo, S. Circ. Res. (1993) [Pubmed]
  22. Interleukin-3-dependent expression of the c-myc and c-fos proto-oncogenes in hemopoietic cell lines. Conscience, J.F., Verrier, B., Martin, G. EMBO J. (1986) [Pubmed]
  23. Extracellular ATP induces immediate-early gene expression but not cellular hypertrophy in neonatal cardiac myocytes. Zheng, J.S., Boluyt, M.O., O'Neill, L., Crow, M.T., Lakatta, E.G. Circ. Res. (1994) [Pubmed]
  24. Angiotensin II stimulates c-Jun NH2-terminal kinase in cultured cardiac myocytes of neonatal rats. Kudoh, S., Komuro, I., Mizuno, T., Yamazaki, T., Zou, Y., Shiojima, I., Takekoshi, N., Yazaki, Y. Circ. Res. (1997) [Pubmed]
  25. Altered cJUN expression: an early event in human lung carcinogenesis. Szabo, E., Riffe, M.E., Steinberg, S.M., Birrer, M.J., Linnoila, R.I. Cancer Res. (1996) [Pubmed]
  26. Systemic morphine suppresses noxious stimulus-evoked Fos protein-like immunoreactivity in the rat spinal cord. Presley, R.W., Menétrey, D., Levine, J.D., Basbaum, A.I. J. Neurosci. (1990) [Pubmed]
  27. Constitutive expression of c-fos antisense RNA blocks c-fos gene induction by interferon and by phorbol ester and reduces c-myc expression in F9 embryonal carcinoma cells. Levi, B.Z., Ozato, K. Genes Dev. (1988) [Pubmed]
  28. Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke. Wang, X.D., Liu, C., Bronson, R.T., Smith, D.E., Krinsky, N.I., Russell, M. J. Natl. Cancer Inst. (1999) [Pubmed]
  29. H2O2 and antioxidants have opposite effects on activation of NF-kappa B and AP-1 in intact cells: AP-1 as secondary antioxidant-responsive factor. Meyer, M., Schreck, R., Baeuerle, P.A. EMBO J. (1993) [Pubmed]
  30. A selective transcriptional induction system for mammalian cells based on Gal4-estrogen receptor fusion proteins. Braselmann, S., Graninger, P., Busslinger, M. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  31. Roles of JAKs in activation of STATs and stimulation of c-fos gene expression by epidermal growth factor. Leaman, D.W., Pisharody, S., Flickinger, T.W., Commane, M.A., Schlessinger, J., Kerr, I.M., Levy, D.E., Stark, G.R. Mol. Cell. Biol. (1996) [Pubmed]
  32. 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]
  33. Bone morphogenetic protein 2 inhibits platelet-derived growth factor-induced c-fos gene transcription and DNA synthesis in mesangial cells. Involvement of mitogen-activated protein kinase. Ghosh Choudhury, G., Kim, Y.S., Simon, M., Wozney, J., Harris, S., Ghosh-Choudhury, N., Abboud, H.E., Ghosh Choundhury, G., Ghosh-Choundhury, N. J. Biol. Chem. (1999) [Pubmed]
  34. Tyrosine residues within the intracellular domain of the erythropoietin receptor mediate activation of AP-1 transcription factors. Bergelson, S., Klingmüller, U., Socolovsky, M., Hsiao, J.G., Lodish, H.F. J. Biol. Chem. (1998) [Pubmed]
  35. Transcriptional autoregulation and inhibition of mRNA translation of amino acid regulator gene cpcA of filamentous fungus Aspergillus nidulans. Hoffmann, B., Valerius, O., Andermann, M., Braus, G.H. Mol. Biol. Cell (2001) [Pubmed]
  36. Monocytic cell type-specific transcriptional induction of collagenase. Pierce, R.A., Sandefur, S., Doyle, G.A., Welgus, H.G. J. Clin. Invest. (1996) [Pubmed]
  37. Functional dissection of p56lck, a protein tyrosine kinase which mediates interleukin-2-induced activation of the c-fos gene. Shibuya, H., Kohu, K., Yamada, K., Barsoumian, E.L., Perlmutter, R.M., Taniguchi, T. Mol. Cell. Biol. (1994) [Pubmed]
  38. Cascade induction of c-fos, c-myc, and heat shock 70K transcripts during regression of the rat ventral prostate gland. Buttyan, R., Zakeri, Z., Lockshin, R., Wolgemuth, D. Mol. Endocrinol. (1988) [Pubmed]
  39. Centrally administered adrenomedullin 2 activates hypothalamic oxytocin-secreting neurons, causing elevated plasma oxytocin level in rats. Hashimoto, H., Hyodo, S., Kawasaki, M., Mera, T., Chen, L., Soya, A., Saito, T., Fujihara, H., Higuchi, T., Takei, Y., Ueta, Y. Am. J. Physiol. Endocrinol. Metab. (2005) [Pubmed]
  40. The medullary dorsal reticular nucleus facilitates pain behaviour induced by formalin in the rat. Almeida, A., Størkson, R., Lima, D., Hole, K., Tjølsen, A. Eur. J. Neurosci. (1999) [Pubmed]
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