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Gene Review

Jra  -  Jun-related antigen

Drosophila melanogaster

Synonyms: AP-1, AP1, CG2275, D-Jun, D-jun, ...
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Disease relevance of Jra

  • Furthermore, overexpression of c-Jun and c-Fos results in fourfold activation of the promoter in PCC-4 embryonal carcinoma cells [1].
  • Overexpression of the c-Jun proto-oncogene in MCF7 breast cancer cells results in a variety of phenotype changes related to malignant progression including increased motility and invasion [2].
  • Perturbation of the cell death mechanisms leads to various disorders, including neurodegenerative diseases, immunodeficiency diseases, and tumors. c-Jun N-terminal kinase (JNK) has crucial roles in the regulation of cell death in response to many stimuli [3].
  • Downmodulation of transcription factor activity through interaction with a cellular factor has been observed in several other systems, including the regulation of transcription factor E2F by retinoblastoma protein, and in studies of c-Jun [4].
  • Mutant Db11 was used for the isolation of two phages, phi J and phi K, which grew on Db10, Db11 and Db12, but not on three reference strains of S. marcescens [5].

High impact information on Jra

  • Observations from genetic epistasis and RNA quantification experiments indicate that AP-1 acts upstream of CREB, regulates levels of CREB messenger RNA, and functions at the top of the hierarchy of transcription factors known to regulate long-term plasticity [6].
  • Excess brk expression activates the c-Jun amino-terminal kinase pathway, which in turn triggers apoptosis in these cells [7].
  • The c-Jun amino-terminal kinases (JNKs) of the mitogen-activated protein kinase superfamily are involved in apoptotic signalling in various cultured cells [8].
  • Common and distinct roles of DFos and DJun during Drosophila development [9].
  • The Drosophila homolog of c-Jun regulates epithelial cell shape changes during the process of dorsal closure in mid-embryogenesis [9].

Biological context of Jra

  • Drosophila Jun is shown to be involved in different signal transduction pathways and developmental decisions [10].
  • The Drosophila Jun-N-terminal kinase is required for cell morphogenesis but not for DJun-dependent cell fate specification in the eye [11].
  • These results indicate that dFRA is a developmentally regulated transcription factor and suggest that its potential interplay with dJRA plays an important role in cell-type-specific transcription during Drosophila embryonic development [12].
  • Interestingly, in vertebrates, transforming growth factor-beta and c-Jun regulate collagenase gene expression during wound healing, a process that also involves the closing of an epithelial sheath [13].
  • We have characterized mutations in the Drosophila homolog of the mammalian proto-oncogene c-Jun gene (Djun) [14].

Anatomical context of Jra


Associations of Jra with chemical compounds

  • The predicted amino acid sequences reveal that both proteins contain a bipartite DNA-binding domain consisting of a leucine repeat and an adjacent basic region, which are characteristic of members of the AP-1 family [12].
  • Via a direct interaction with the basic region of Drosophila Jun (D-Jun), MBF1 prevents an oxidative modification (S-cystenyl cystenylation) of the critical cysteine and stimulates AP-1 binding to DNA [18].
  • Molecular cloning and characterization of human JNKK2, a novel Jun NH2-terminal kinase-specific kinase [19].
  • Downregulation of lipopolysaccharide response in Drosophila by negative crosstalk between the AP1 and NF-kappaB signaling modules [20].
  • Drosophila embryonic dorsal closure (DC) requires both integrin function and c-Jun amino-terminal kinase (JNK) signaling for opposed epithelial sheets to migrate, meet, and suture [21].

Physical interactions of Jra

  • In addition, a chimeric promoter consisting of six tandem high affinity Sp1-binding sites fused with the CAT gene was transactivated by overexpressed c-Jun in HepG2 cells [22].

Regulatory relationships of Jra


Other interactions of Jra


Analytical, diagnostic and therapeutic context of Jra


  1. SP3 and AP-1 mediate transcriptional activation of the lamin A proximal promoter. Muralikrishna, B., Parnaik, V.K. Eur. J. Biochem. (2001) [Pubmed]
  2. Transcriptional upregulation of SPARC, in response to c-Jun overexpression, contributes to increased motility and invasion of MCF7 breast cancer cells. Briggs, J., Chamboredon, S., Castellazzi, M., Kerry, J.A., Bos, T.J. Oncogene (2002) [Pubmed]
  3. Regulatory roles of JNK in programmed cell death. Kanda, H., Miura, M. J. Biochem. (2004) [Pubmed]
  4. Transcriptional activity of the zinc finger protein NGFI-A is influenced by its interaction with a cellular factor. Russo, M.W., Matheny, C., Milbrandt, J. Mol. Cell. Biol. (1993) [Pubmed]
  5. Insect pathogenic properties of Serratia marcescens: phage-resistant mutants with a decreased resistance to Cecropia immunity and a decreased virulence to Drosophila. Flyg, C., Kenne, K., Boman, H.G. J. Gen. Microbiol. (1980) [Pubmed]
  6. AP-1 functions upstream of CREB to control synaptic plasticity in Drosophila. Sanyal, S., Sandstrom, D.J., Hoeffer, C.A., Ramaswami, M. Nature (2002) [Pubmed]
  7. Cells compete for decapentaplegic survival factor to prevent apoptosis in Drosophila wing development. Moreno, E., Basler, K., Morata, G. Nature (2002) [Pubmed]
  8. Distortion of proximodistal information causes JNK-dependent apoptosis in Drosophila wing. Adachi-Yamada, T., Fujimura-Kamada, K., Nishida, Y., Matsumoto, K. Nature (1999) [Pubmed]
  9. Common and distinct roles of DFos and DJun during Drosophila development. Riesgo-Escovar, J.R., Hafen, E. Science (1997) [Pubmed]
  10. Jun in Drosophila development: redundant and nonredundant functions and regulation by two MAPK signal transduction pathways. Kockel, L., Zeitlinger, J., Staszewski, L.M., Mlodzik, M., Bohmann, D. Genes Dev. (1997) [Pubmed]
  11. The Drosophila Jun-N-terminal kinase is required for cell morphogenesis but not for DJun-dependent cell fate specification in the eye. Riesgo-Escovar, J.R., Jenni, M., Fritz, A., Hafen, E. Genes Dev. (1996) [Pubmed]
  12. The Drosophila Fos-related AP-1 protein is a developmentally regulated transcription factor. Perkins, K.K., Admon, A., Patel, N., Tjian, R. Genes Dev. (1990) [Pubmed]
  13. Drosophila Jun kinase regulates expression of decapentaplegic via the ETS-domain protein Aop and the AP-1 transcription factor DJun during dorsal closure. Riesgo-Escovar, J.R., Hafen, E. Genes Dev. (1997) [Pubmed]
  14. Drosophila Jun relays the Jun amino-terminal kinase signal transduction pathway to the Decapentaplegic signal transduction pathway in regulating epithelial cell sheet movement. Hou, X.S., Goldstein, E.S., Perrimon, N. Genes Dev. (1997) [Pubmed]
  15. Response of Djun and Dfos mRNA abundance to signal transduction pathways in cultured cells of Drosophila melanogaster. Xia, X., Goldstein, E.S. Mol. Biol. Rep. (1999) [Pubmed]
  16. Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity. Sanyal, S., Narayanan, R., Consoulas, C., Ramaswami, M. BMC neuroscience [electronic resource]. (2003) [Pubmed]
  17. Synaptic and genomic responses to JNK and AP-1 signaling in Drosophila neurons. Etter, P.D., Narayanan, R., Navratilova, Z., Patel, C., Bohmann, D., Jasper, H., Ramaswami, M. BMC neuroscience [electronic resource]. (2005) [Pubmed]
  18. Coactivator MBF1 preserves the redox-dependent AP-1 activity during oxidative stress in Drosophila. Jindra, M., Gaziova, I., Uhlirova, M., Okabe, M., Hiromi, Y., Hirose, S. EMBO J. (2004) [Pubmed]
  19. Molecular cloning and characterization of human JNKK2, a novel Jun NH2-terminal kinase-specific kinase. Wu, Z., Wu, J., Jacinto, E., Karin, M. Mol. Cell. Biol. (1997) [Pubmed]
  20. Downregulation of lipopolysaccharide response in Drosophila by negative crosstalk between the AP1 and NF-kappaB signaling modules. Kim, T., Yoon, J., Cho, H., Lee, W.B., Kim, J., Song, Y.H., Kim, S.N., Yoon, J.H., Kim-Ha, J., Kim, Y.J. Nat. Immunol. (2005) [Pubmed]
  21. The integrin effector PINCH regulates JNK activity and epithelial migration in concert with Ras suppressor 1. Kadrmas, J.L., Smith, M.A., Clark, K.A., Pronovost, S.M., Muster, N., Yates, J.R., Beckerle, M.C. J. Cell Biol. (2004) [Pubmed]
  22. c-Jun transactivates the promoter of the human p21(WAF1/Cip1) gene by acting as a superactivator of the ubiquitous transcription factor Sp1. Kardassis, D., Papakosta, P., Pardali, K., Moustakas, A. J. Biol. Chem. (1999) [Pubmed]
  23. Extrusion of cells with inappropriate Dpp signaling from Drosophila wing disc epithelia. Shen, J., Dahmann, C. Science (2005) [Pubmed]
  24. Glycogen synthase kinase-3: functions in oncogenesis and development. Plyte, S.E., Hughes, K., Nikolakaki, E., Pulverer, B.J., Woodgett, J.R. Biochim. Biophys. Acta (1992) [Pubmed]
  25. CKA, a novel multidomain protein, regulates the JUN N-terminal kinase signal transduction pathway in Drosophila. Chen, H.W., Marinissen, M.J., Oh, S.W., Chen, X., Melnick, M., Perrimon, N., Gutkind, J.S., Hou, S.X. Mol. Cell. Biol. (2002) [Pubmed]
  26. Genetic interactions between Drosophila melanogaster menin and Jun/Fos. Cerrato, A., Parisi, M., Anna, S.S., Missirlis, F., Guru, S., Agarwal, S., Sturgill, D., Talbot, T., Spiegel, A., Collins, F., Chandrasekharappa, S., Marx, S., Oliver, B. Dev. Biol. (2006) [Pubmed]
  27. AP-1--Introductory remarks. Wagner, E.F. Oncogene (2001) [Pubmed]
  28. Drosophila homolog of the mammalian jun oncogene is expressed during embryonic development and activates transcription in mammalian cells. Zhang, K., Chaillet, J.R., Perkins, L.A., Halazonetis, T.D., Perrimon, N. Proc. Natl. Acad. Sci. U.S.A. (1990) [Pubmed]
  29. An AP-1 binding site in the upstream region of Deb-A is part of a developmentally regulated negative element. Wang, G.L., Goldstein, E.S. Biochim. Biophys. Acta (1993) [Pubmed]
  30. Decreased survival of mosquito cells after stable transfection with a Drosophila ecdysteroid response element: possible involvement of a 40 kDa DNA binding protein. Jayachandran, G., Fallon, A.M. J. Insect Sci. (2002) [Pubmed]
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