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Gene Review

JUN  -  jun proto-oncogene

Bos taurus

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Disease relevance of JUN

  • After four rounds of panning three phages (AP1, AP2 and AP3) were shown to have specific binding properties toward AP by enzyme-linked immunosorbent assay [1].
  • Rhein inhibits interleukin-1 beta-induced activation of MEK/ERK pathway and DNA binding of NF-kappa B and AP-1 in chondrocytes cultured in hypoxia: a potential mechanism for its disease-modifying effect in osteoarthritis [2].
  • We conclude that flow-adapted endothelial cells generate ROS with ischemia that results in activation of NF-kappaB and AP-1 and an increase of DNA synthesis [3].

High impact information on JUN

  • The binding of AP-1 clathrin adaptor particles to Golgi membranes requires ADP-ribosylation factor, a small GTP-binding protein [4].
  • Dominant-negative mutants of Cdc42 and Rho, as well as recombinant C3 exoenzyme, attenuated the shear stress activation of c-Jun NH2-terminal kinases (JNKs), suggesting that Cdc42 and Rho regulate the shear stress induction of AP-1/TRE activity through JNKs [5].
  • Neither the transcription factor AP-1 binding site nor the GATA-2-factor binding site, necessary for the basal level of transcription of ET-1 gene, is sufficient to confer shear-responsiveness to the reporter gene [6].
  • Here, we show that both lymphocyte proliferation and activation of the transcription factor AP-1 are mediated by Src-family protein tyrosine kinases (PTKs) in a parasite-dependent fashion [7].
  • Purified protein phosphatase types 1 (PP1) and 2A (PP2A) were microinjected into cell lines containing stably transfected lacZ marker genes under the control of an enhancer recognized by AP-1 [8].

Chemical compound and disease context of JUN

  • With ischemia, flow-adapted cells exhibited increases of 1.7-fold in nuclear NF-kappaB and 1.5-fold in nuclear AP-1; these changes were abolished by pretreatment with N-acetylcysteine or DPI [3].

Biological context of JUN


Anatomical context of JUN


Associations of JUN with chemical compounds

  • The involvement of serine/threonine protein phosphatases in signaling pathways which modulate the activity of the transcription factor AP-1 was examined [8].
  • The effect of paclitaxel on AP-1 promoter activity was studied by chloramphenicol acetyltransferase assays in IL-1-stimulated chondrocytes [16].
  • We found that besides depending on the phosphorylation state of a casein kinase II site, interaction of the furin tail with AP-1 and its mu1subunit is mediated by a tyrosine motif and to less extent by a leucine-isoleucine signal, whereas a monophenylalanine motif is only involved in binding to the intact AP-1 complex [13].
  • We found that Dex negatively regulates PRL-induced proliferation and AP-1 site activation [17].
  • Spermine-NO (1 microM) and L-arginine (400 microM) prevented the aminoguanidine-induced ablation of AP-1 activation in response to TNF [18].

Physical interactions of JUN


Other interactions of JUN


Analytical, diagnostic and therapeutic context of JUN

  • Microinjection of PP2A potentiated serum-stimulated beta-galactosidase expression from the AP-1-regulated promoter [8].
  • We have analyzed this interaction between the Golgi-restricted AP1 complex and the plasma membrane-restricted AP2 complex with the MPR46 tail in vitro by using a biosensor [14].
  • The DNA-binding activity of AP-1 was assessed using the electrophoretic mobility shift assay [18].
  • Total RNA and nuclear protein extractions were performed to study mRNA steady-state levels (real-time polymerase chain reaction) and AP-1/NF-kappaB DNA binding (Electrophoretic Mobility Shift Assays), respectively [22].
  • The MtrC AP1-specific antiserum strongly recognized the MtrC protein on Western blots and appeared to bind native MtrC protein in situ [23].


  1. Preparation of a whole genome phage library using fragmented Escherichia coli genome and its characterization of protein binding properties by surface plasmon resonance. Yano, K., Yoshino, T., Shionoya, M., Sawata, S.Y., Ikebukuro, K., Karube, I. Biosensors & bioelectronics. (2003) [Pubmed]
  2. Rhein inhibits interleukin-1 beta-induced activation of MEK/ERK pathway and DNA binding of NF-kappa B and AP-1 in chondrocytes cultured in hypoxia: a potential mechanism for its disease-modifying effect in osteoarthritis. Martin, G., Bogdanowicz, P., Domagala, F., Ficheux, H., Pujol, J.P. Inflammation (2003) [Pubmed]
  3. Simulated ischemia in flow-adapted endothelial cells leads to generation of reactive oxygen species and cell signaling. Wei, Z., Costa, K., Al-Mehdi, A.B., Dodia, C., Muzykantov, V., Fisher, A.B. Circ. Res. (1999) [Pubmed]
  4. The binding of AP-1 clathrin adaptor particles to Golgi membranes requires ADP-ribosylation factor, a small GTP-binding protein. Stamnes, M.A., Rothman, J.E. Cell (1993) [Pubmed]
  5. Distinct roles for the small GTPases Cdc42 and Rho in endothelial responses to shear stress. Li, S., Chen, B.P., Azuma, N., Hu, Y.L., Wu, S.Z., Sumpio, B.E., Shyy, J.Y., Chien, S. J. Clin. Invest. (1999) [Pubmed]
  6. Regulation of endothelin 1 gene by fluid shear stress is transcriptionally mediated and independent of protein kinase C and cAMP. Malek, A.M., Greene, A.L., Izumo, S. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  7. Constitutive exclusion of Csk from Hck-positive membrane microdomains permits Src kinase-dependent proliferation of Theileria-transformed B lymphocytes. Baumgartner, M., Angelisová, P., Setterblad, N., Mooney, N., Werling, D., Horejsí, V., Langsley, G. Blood (2003) [Pubmed]
  8. Protein phosphatase 2A potentiates activity of promoters containing AP-1-binding elements. Alberts, A.S., Deng, T., Lin, A., Meinkoth, J.L., Schönthal, A., Mumby, M.C., Karin, M., Feramisco, J.R. Mol. Cell. Biol. (1993) [Pubmed]
  9. Temporal response of liver signal transduction elements during in vivo endotoxin challenge in cattle: Effects of growth hormone treatment. Li, C.J., Kahl, S., Carbaugh, D., Elsasser, T.H. Domest. Anim. Endocrinol. (2007) [Pubmed]
  10. Regulation of expression of the CYP11A (P450scc) gene in bovine ovarian luteal cells by forskolin and phorbol esters. Begeot, M., Shetty, U., Kilgore, M., Waterman, M., Simpson, E. J. Biol. Chem. (1993) [Pubmed]
  11. Molecular genetic analysis of the regulatory and catalytic domains of protein kinase C. Kaibuchi, K., Fukumoto, Y., Oku, N., Takai, Y., Arai, K., Muramatsu, M. J. Biol. Chem. (1989) [Pubmed]
  12. Mediation of interleukin-1beta-induced transforming growth factor beta1 expression by activator protein 4 transcription factor in primary cultures of bovine articular chondrocytes: possible cooperation with activator protein 1. Andriamanalijaona, R., Felisaz, N., Kim, S.J., King-Jones, K., Lehmann, M., Pujol, J.P., Boumediene, K. Arthritis Rheum. (2003) [Pubmed]
  13. Sorting of furin at the trans-Golgi network. Interaction of the cytoplasmic tail sorting signals with AP-1 Golgi-specific assembly proteins. Teuchert, M., Schäfer, W., Berghöfer, S., Hoflack, B., Klenk, H.D., Garten, W. J. Biol. Chem. (1999) [Pubmed]
  14. The 46-kDa mannose 6-phosphate receptor contains multiple binding sites for clathrin adaptors. Höning, S., Sosa, M., Hille-Rehfeld, A., von Figura, K. J. Biol. Chem. (1997) [Pubmed]
  15. The proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1 stimulate neuropeptide gene transcription and secretion in adrenochromaffin cells via activation of extracellularly regulated kinase 1/2 and p38 protein kinases, and activator protein-1 transcription factors. Ait-Ali, D., Turquier, V., Grumolato, L., Yon, L., Jourdain, M., Alexandre, D., Eiden, L.E., Vaudry, H., Anouar, Y. Mol. Endocrinol. (2004) [Pubmed]
  16. Inhibition of activator protein 1 activity by paclitaxel suppresses interleukin-1-induced collagenase and stromelysin expression by bovine chondrocytes. Hui, A., Min, W.X., Tang, J., Cruz, T.F. Arthritis Rheum. (1998) [Pubmed]
  17. Prolactin (PRL)-PRL receptor system increases cell proliferation involving JNK (c-Jun amino terminal kinase) and AP-1 activation: inhibition by glucocorticoids. Olazabal, I., Muñoz, J., Ogueta, S., Obregón, E., García-Ruiz, J.P. Mol. Endocrinol. (2000) [Pubmed]
  18. Tumor necrosis factor-alpha-induced activating protein-1 activity is modulated by nitric oxide-mediated protein kinase G activation. Gertzberg, N., Clements, R., Jaspers, I., Ferro, T.J., Neumann, P., Flescher, E., Johnson, A. Am. J. Respir. Cell Mol. Biol. (2000) [Pubmed]
  19. Polymorphic AP-1 binding site in bovine CSN1S1 shows quantitative differences in protein binding associated with milk protein expression. Kuss, A.W., Gogol, J., Bartenschlager, H., Geldermann, H. J. Dairy Sci. (2005) [Pubmed]
  20. Pituitary adenylate cyclase-activating polypeptide stimulates secretoneurin release and secretogranin II gene transcription in bovine adrenochromaffin cells through multiple signaling pathways and increased binding of pre-existing activator protein-1-like transcription factors. Turquier, V., Yon, L., Grumolato, L., Alexandre, D., Fournier, A., Vaudry, H., Anouar, Y. Mol. Pharmacol. (2001) [Pubmed]
  21. Both inducible and constitutive activator protein-1-like transcription factors are used for transcriptional activation of the galanin gene by different first and second messenger pathways. Anouar, Y., Lee, H.W., Eiden, L.E. Mol. Pharmacol. (1999) [Pubmed]
  22. Comparative effects of IL-1beta and hydrogen peroxide (H2O2) on catabolic and anabolic gene expression in juvenile bovine chondrocytes. Martin, G., Andriamanalijaona, R., Mathy-Hartert, M., Henrotin, Y., Pujol, J.P. Osteoarthr. Cartil. (2005) [Pubmed]
  23. Generation of antiserum to specific epitopes. Marchion, D.C., Manning, D.S., Shafer, W.M., Judd, R.C. Mol. Biotechnol. (1996) [Pubmed]
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