c-Jun

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JUN
JUN
nach PDB 1A02
Andere Namen
  • Jun Proto-Oncogene
  • V-Jun Avian Sarcoma Virus 17 Oncogene Homolog
  • P39
  • Jun Activation Domain Binding Protein

Vorhandene Strukturdaten: 1A02, 1FOS, 1JNM, 1JUN, 1S9K, 1T2K

Eigenschaften des menschlichen Proteins
Masse/Länge Primärstruktur 331 Aminosäuren, 35676 Da
Bezeichner
Externe IDs
Vorkommen
Homologie-Familie Hovergen
Orthologe
Mensch Hausmaus
Entrez 3725 16476
UniProt P05412 P05627
PubMed-Suche 3725 16476

c-Jun ist ein Bestandteil des Transkriptionsfaktors AP-1 und ein Protoonkogen.[1]

Eigenschaften[Bearbeiten | Quelltext bearbeiten]

c-Jun ist am Zellzyklus und der Apoptose beteiligt. Mutationen im Gen von c-Jun treten bei verschiedenen Tumoren auf. c-Jun war der erste beschriebene onkogene Transkriptionsfaktor.[2] Das Homolog des c-Jun (englisch cellular Jun) aus Retroviren wird als v-Jun (englisch viral Jun) bezeichnet.[3]

Interaktionen[Bearbeiten | Quelltext bearbeiten]

c-Jun interagiert mit verschiedenen Proteinen:

Einzelnachweise[Bearbeiten | Quelltext bearbeiten]

  1. ↑ Chiu R, Boyle WJ, Meek J, Smeal T, Hunter T, Karin M: The c-Fos protein interacts with c-Jun/AP-1 to stimulate transcription of AP-1 responsive genes. In: Cell. 54. Jahrgang, Nr. 4, August 1988, S. 541–52, doi:10.1016/0092-8674(88)90076-1, PMID 3135940.
  2. ↑ Vogt PK: Fortuitous convergences: the beginnings of JUN. In: Nature Reviews Cancer. 2. Jahrgang, Nr. 6, Juni 2002, S. 465–9, doi:10.1038/nrc818, PMID 12189388.
  3. ↑ Wisdom R, Johnson RS, Moore C: c-Jun regulates cell cycle progression and apoptosis by distinct mechanisms. In: The EMBO Journal. 18. Jahrgang, Nr. 1, Januar 1999, S. 188–97, doi:10.1093/emboj/18.1.188, PMID 9878062, PMC 1171114 (freier Volltext).
  4. ↑ M. Pessah, C. Prunier, J. Marais, N. Ferrand, A. Mazars, F. Lallemand, J. M. Gauthier, A. Atfi: c-Jun interacts with the corepressor TG-interacting factor (TGIF) to suppress Smad2 transcriptional activity. In: Proceedings of the National Academy of Sciences. Band 98, Nummer 11, Mai 2001, S. 6198–6203, doi:10.1073/pnas.101579798, PMID 11371641, PMC 33445 (freier Volltext).
  5. ↑ A. Verger, E. Buisine, S. Carrère, R. Wintjens, A. Flourens, J. Coll, D. Stéhelin, M. Duterque-Coquillaud: Identification of amino acid residues in the ETS transcription factor Erg that mediate Erg-Jun/Fos-DNA ternary complex formation. In: The Journal of biological chemistry. Band 276, Nummer 20, Mai 2001, S. 17181–17189, doi:10.1074/jbc.M010208200, PMID 11278640.
  6. ↑ J. Nishitani, T. Nishinaka, C. H. Cheng, W. Rong, K. K. Yokoyama, R. Chiu: Recruitment of the retinoblastoma protein to c-Jun enhances transcription activity mediated through the AP-1 binding site. In: The Journal of biological chemistry. Band 274, Nummer 9, Februar 1999, S. 5454–5461, PMID 10026157.
  7. ↑ Y. Sano, F. Tokitou, P. Dai, T. Maekawa, T. Yamamoto, S. Ishii: CBP alleviates the intramolecular inhibition of ATF-2 function. In: The Journal of biological chemistry. Band 273, Nummer 44, Oktober 1998, S. 29098–29105, PMID 9786917.
  8. ↑ C. L. Newell, A. B. Deisseroth, G. Lopez-Berestein: Interaction of nuclear proteins with an AP-1/CRE-like promoter sequence in the human TNF-alpha gene. In: Journal of leukocyte biology. Band 56, Nummer 1, Juli 1994, S. 27–35, PMID 8027667.
  9. ↑ C. J. Kara, H. C. Liou, L. B. Ivashkiv, L. H. Glimcher: A cDNA for a human cyclic AMP response element-binding protein which is distinct from CREB and expressed preferentially in brain. In: Molecular and cellular biology. Band 10, Nummer 4, April 1990, S. 1347–1357, PMID 2320002, PMC 362236 (freier Volltext).
  10. ↑ a b T. Hai, T. Curran: Cross-family dimerization of transcription factors Fos/Jun and ATF/CREB alters DNA binding specificity. In: Proceedings of the National Academy of Sciences. Band 88, Nummer 9, Mai 1991, S. 3720–3724, PMID 1827203, PMC 51524 (freier Volltext).
  11. ↑ H. Zhong, J. Zhu, H. Zhang, L. Ding, Y. Sun, C. Huang, Q. Ye: COBRA1 inhibits AP-1 transcriptional activity in transfected cells. In: Biochemical and biophysical research communications. Band 325, Nummer 2, Dezember 2004, S. 568–573, doi:10.1016/j.bbrc.2004.10.079, PMID 15530430.
  12. ↑ Y. F. Hu, R. Li: JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction. In: Genes & development. Band 16, Nummer 12, Juni 2002, S. 1509–1517, doi:10.1101/gad.995502, PMID 12080089, PMC 186344 (freier Volltext).
  13. ↑ T. Ito, M. Yamauchi, M. Nishina, N. Yamamichi, T. Mizutani, M. Ui, M. Murakami, H. Iba: Identification of SWI.SNF complex subunit BAF60a as a determinant of the transactivation potential of Fos/Jun dimers. In: The Journal of biological chemistry. Band 276, Nummer 4, Januar 2001, S. 2852–2857, doi:10.1074/jbc.M009633200, PMID 11053448.
  14. ↑ a b P. Pognonec, K. E. Boulukos, C. Aperlo, M. Fujimoto, H. Ariga, A. Nomoto, H. Kato: Cross-family interaction between the bHLHZip USF and bZip Fra1 proteins results in down-regulation of AP1 activity. In: Oncogene. Band 14, Nummer 17, Mai 1997, S. 2091–2098, doi:10.1038/sj.onc.1201046, PMID 9160889.
  15. ↑ J. N. Glover, S. C. Harrison: Crystal structure of the heterodimeric bZIP transcription factor c-Fos-c-Jun bound to DNA. In: Nature. Band 373, Nummer 6511, Januar 1995, S. 257–261, doi:10.1038/373257a0, PMID 7816143.
  16. ↑ a b X. Yang, Y. Chen, D. Gabuzda: ERK MAP kinase links cytokine signals to activation of latent HIV-1 infection by stimulating a cooperative interaction of AP-1 and NF-kappaB. In: The Journal of biological chemistry. Band 274, Nummer 39, September 1999, S. 27981–27988, PMID 10488148.
  17. ↑ N. Nomura, Y. L. Zu, T. Maekawa, S. Tabata, T. Akiyama, S. Ishii: Isolation and characterization of a novel member of the gene family encoding the cAMP response element-binding protein CRE-BP1. In: The Journal of biological chemistry. Band 268, Nummer 6, Februar 1993, S. 4259–4266, PMID 8440710.
  18. ↑ T. Finkel, J. Duc, E. R. Fearon, C. V. Dang, G. F. Tomaselli: Detection and modulation in vivo of helix-loop-helix protein-protein interactions. In: The Journal of biological chemistry. Band 268, Nummer 1, Januar 1993, S. 5–8, PMID 8380166.
  19. ↑ a b c R. Venugopal, A. K. Jaiswal: Nrf2 and Nrf1 in association with Jun proteins regulate antioxidant response element-mediated expression and coordinated induction of genes encoding detoxifying enzymes. In: Oncogene. Band 17, Nummer 24, Dezember 1998, S. 3145–3156, doi:10.1038/sj.onc.1202237, PMID 9872330.
  20. ↑ J. Westermarck, C. Weiss, R. Saffrich, J. Kast, A. M. Musti, M. Wessely, W. Ansorge, B. Séraphin, M. Wilm, B. C. Valdez, D. Bohmann: The DEXD/H-box RNA helicase RHII/Gu is a co-factor for c-Jun-activated transcription. In: The EMBO journal. Band 21, Nummer 3, Februar 2002, S. 451–460, PMID 11823437, PMC 125820 (freier Volltext).
  21. ↑ a b C. C. Franklin, A. V. McCulloch, A. S. Kraft: In vitro association between the Jun protein family and the general transcription factors, TBP and TFIIB. In: The Biochemical journal. Band 305 ( Pt 3), Februar 1995, S. 967–974, PMID 7848298, PMC 1136352 (freier Volltext).
  22. ↑ T. Ishitani, G. Takaesu, J. Ninomiya-Tsuji, H. Shibuya, R. B. Gaynor, K. Matsumoto: Role of the TAB2-related protein TAB3 in IL-1 and TNF signaling. In: The EMBO journal. Band 22, Nummer 23, Dezember 2003, S. 6277–6288, doi:10.1093/emboj/cdg605, PMID 14633987, PMC 291846 (freier Volltext).
  23. ↑ H. Nishitoh, M. Saitoh, Y. Mochida, K. Takeda, H. Nakano, M. Rothe, K. Miyazono, H. Ichijo: ASK1 is essential for JNK/SAPK activation by TRAF2. In: Molecular cell. Band 2, Nummer 3, September 1998, S. 389–395, PMID 9774977.
  24. ↑ B. Dérijard, M. Hibi, I. H. Wu, T. Barrett, B. Su, T. Deng, M. Karin, R. J. Davis: JNK1: a protein kinase stimulated by UV light and Ha-Ras that binds and phosphorylates the c-Jun activation domain. In: Cell. Band 76, Nummer 6, März 1994, S. 1025–1037, PMID 8137421.
  25. ↑ O. Yazgan, C. M. Pfarr: Regulation of two JunD isoforms by Jun N-terminal kinases. In: The Journal of biological chemistry. Band 277, Nummer 33, August 2002, S. 29710–29718, doi:10.1074/jbc.M204552200, PMID 12052834.
  26. ↑ K. Tada, T. Okazaki, S. Sakon, T. Kobarai, K. Kurosawa, S. Yamaoka, H. Hashimoto, T. W. Mak, H. Yagita, K. Okumura, W. C. Yeh, H. Nakano: Critical roles of TRAF2 and TRAF5 in tumor necrosis factor-induced NF-kappa B activation and protection from cell death. In: The Journal of biological chemistry. Band 276, Nummer 39, September 2001, S. 36530–36534, doi:10.1074/jbc.M104837200, PMID 11479302.
  27. ↑ C. F. Meyer, X. Wang, C. Chang, D. Templeton, T. H. Tan: Interaction between c-Rel and the mitogen-activated protein kinase kinase kinase 1 signaling cascade in mediating kappaB enhancer activation. In: The Journal of biological chemistry. Band 271, Nummer 15, April 1996, S. 8971–8976, PMID 8621542.
  28. ↑ E. Cano, C. A. Hazzalin, E. Kardalinou, R. S. Buckle, L. C. Mahadevan: Neither ERK nor JNK/SAPK MAP kinase subtypes are essential for histone H3/HMG-14 phosphorylation or c-fos and c-jun induction. In: Journal of cell science. Band 108 ( Pt 11), November 1995, S. 3599–3609, PMID 8586671.
  29. ↑ C. Tournier, A. J. Whitmarsh, J. Cavanagh, T. Barrett, R. J. Davis: Mitogen-activated protein kinase kinase 7 is an activator of the c-Jun NH2-terminal kinase. In: Proceedings of the National Academy of Sciences. Band 94, Nummer 14, Juli 1997, S. 7337–7342, PMID 9207092, PMC 23822 (freier Volltext).
  30. ↑ S. K. Lee, J. H. Kim, Y. C. Lee, J. Cheong, J. W. Lee: Silencing mediator of retinoic acid and thyroid hormone receptors, as a novel transcriptional corepressor molecule of activating protein-1, nuclear factor-kappaB, and serum response factor. In: The Journal of biological chemistry. Band 275, Nummer 17, April 2000, S. 12470–12474, PMID 10777532.
  31. ↑ S. K. Lee, J. H. Kim, Y. C. Lee, J. Cheong, J. W. Lee: Silencing mediator of retinoic acid and thyroid hormone receptors, as a novel transcriptional corepressor molecule of activating protein-1, nuclear factor-kappaB, and serum response factor. In: The Journal of biological chemistry. Band 275, Nummer 17, April 2000, S. 12470–12474, PMID 10777532.
  32. ↑ E. Bianchi, S. Denti, R. Catena, G. Rossetti, S. Polo, S. Gasparian, S. Putignano, L. Rogge, R. Pardi: Characterization of human constitutive photomorphogenesis protein 1, a RING finger ubiquitin ligase that interacts with Jun transcription factors and modulates their transcriptional activity. In: The Journal of biological chemistry. Band 278, Nummer 22, Mai 2003, S. 19682–19690, doi:10.1074/jbc.M212681200, PMID 12615916.
  33. ↑ G. M. Wulf, A. Ryo, G. G. Wulf, S. W. Lee, T. Niu, V. Petkova, K. P. Lu: Pin1 is overexpressed in breast cancer and cooperates with Ras signaling in increasing the transcriptional activity of c-Jun towards cyclin D1. In: The EMBO journal. Band 20, Nummer 13, Juli 2001, S. 3459–3472, doi:10.1093/emboj/20.13.3459, PMID 11432833, PMC 125530 (freier Volltext).
  34. ↑ Y. Zhang, X. H. Feng, R. Derynck: Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription. In: Nature. Band 394, Nummer 6696, August 1998, S. 909–913, doi:10.1038/29814, PMID 9732876.
  35. ↑ F. Verrecchia, M. Pessah, A. Atfi, A. Mauviel: Tumor necrosis factor-alpha inhibits transforming growth factor-beta /Smad signaling in human dermal fibroblasts via AP-1 activation. In: The Journal of biological chemistry. Band 275, Nummer 39, September 2000, S. 30226–30231, doi:10.1074/jbc.M005310200, PMID 10903323.
  36. ↑ N. T. Liberati, M. B. Datto, J. P. Frederick, X. Shen, C. Wong, E. M. Rougier-Chapman, X. F. Wang: Smads bind directly to the Jun family of AP-1 transcription factors. In: Proceedings of the National Academy of Sciences. Band 96, Nummer 9, April 1999, S. 4844–4849, PMID 10220381, PMC 21779 (freier Volltext).
  37. ↑ D. J. Jung, H. S. Sung, Y. W. Goo, H. M. Lee, O. K. Park, S. Y. Jung, J. Lim, H. J. Kim, S. K. Lee, T. S. Kim, J. W. Lee, Y. C. Lee: Novel transcription coactivator complex containing activating signal cointegrator 1. In: Molecular and cellular biology. Band 22, Nummer 14, Juli 2002, S. 5203–5211, PMID 12077347, PMC 139772 (freier Volltext).
  38. ↑ a b Y. Yamaguchi, T. Wada, F. Suzuki, T. Takagi, J. Hasegawa, H. Handa: Casein kinase II interacts with the bZIP domains of several transcription factors. In: Nucleic acids research. Band 26, Nummer 16, August 1998, S. 3854–3861, PMID 9685505, PMC 147779 (freier Volltext).
  39. ↑ a b X. Zhang, M. H. Wrzeszczynska, C. M. Horvath, J. E. Darnell: Interacting regions in Stat3 and c-Jun that participate in cooperative transcriptional activation. In: Molecular and cellular biology. Band 19, Nummer 10, Oktober 1999, S. 7138–7146, PMID 10490649, PMC 84707 (freier Volltext).
  40. ↑ F. H. Vasanwala, S. Kusam, L. M. Toney, A. L. Dent: Repression of AP-1 function: a mechanism for the regulation of Blimp-1 expression and B lymphocyte differentiation by the B cell lymphoma-6 protooncogene. In: Journal of Immunology (Baltimore, Md. : 1950). Band 169, Nummer 4, August 2002, S. 1922–1929, PMID 12165517.
  41. ↑ S. Y. Na, J. E. Choi, H. J. Kim, B. H. Jhun, Y. C. Lee, J. W. Lee: Bcl3, an IkappaB protein, stimulates activating protein-1 transactivation and cellular proliferation. In: The Journal of biological chemistry. Band 274, Nummer 40, Oktober 1999, S. 28491–28496, PMID 10497212.
  42. ↑ N. Sato, M. D. Sadar, N. Bruchovsky, F. Saatcioglu, P. S. Rennie, S. Sato, P. H. Lange, M. E. Gleave: Androgenic induction of prostate-specific antigen gene is repressed by protein-protein interaction between the androgen receptor and AP-1/c-Jun in the human prostate cancer cell line LNCaP. In: The Journal of biological chemistry. Band 272, Nummer 28, Juli 1997, S. 17485–17494, PMID 9211894.
  43. ↑ J. P. Basuyaux, E. Ferreira, D. Stéhelin, G. Butticè: The Ets transcription factors interact with each other and with the c-Fos/c-Jun complex via distinct protein domains in a DNA-dependent and -independent manner. In: The Journal of biological chemistry. Band 272, Nummer 42, Oktober 1997, S. 26188–26195, PMID 9334186.
  44. ↑ A. G. Pearson, C. W. Gray, J. F. Pearson, J. M. Greenwood, M. J. During, M. Dragunow: ATF3 enhances c-Jun-mediated neurite sprouting. In: Brain research. Molecular brain research. Band 120, Nummer 1, Dezember 2003, S. 38–45, PMID 14667575.
  45. ↑ B. P. Chen, C. D. Wolfgang, T. Hai: Analysis of ATF3, a transcription factor induced by physiological stresses and modulated by gadd153/Chop10. In: Molecular and cellular biology. Band 16, Nummer 3, März 1996, S. 1157–1168, PMID 8622660, PMC 231098 (freier Volltext).
  46. ↑ A. Moreau, W. V. Yotov, F. H. Glorieux, R. St-Arnaud: Bone-specific expression of the alpha chain of the nascent polypeptide-associated complex, a coactivator potentiating c-Jun-mediated transcription. In: Molecular and cellular biology. Band 18, Nummer 3, März 1998, S. 1312–1321, PMID 9488446, PMC 108844 (freier Volltext).
  47. ↑ F. X. Claret, M. Hibi, S. Dhut, T. Toda, M. Karin: A new group of conserved coactivators that increase the specificity of AP-1 transcription factors. In: Nature. Band 383, Nummer 6599, Oktober 1996, S. 453–457, doi:10.1038/383453a0, PMID 8837781.
  48. ↑ M. Ubeda, M. Vallejo, J. F. Habener: CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 complex proteins. In: Molecular and cellular biology. Band 19, Nummer 11, November 1999, S. 7589–7599, PMID 10523647, PMC 84780 (freier Volltext).
  49. ↑ D. J. Jung, S. Y. Na, D. S. Na, J. W. Lee: Molecular cloning and characterization of CAPER, a novel coactivator of activating protein-1 and estrogen receptors. In: The Journal of biological chemistry. Band 277, Nummer 2, Januar 2002, S. 1229–1234, doi:10.1074/jbc.M110417200, PMID 11704680.
  50. ↑ S. K. Lee, S. L. Anzick, J. E. Choi, L. Bubendorf, X. Y. Guan, Y. K. Jung, O. P. Kallioniemi, J. Kononen, J. M. Trent, D. Azorsa, B. H. Jhun, J. H. Cheong, Y. C. Lee, P. S. Meltzer, J. W. Lee: A nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivo. In: The Journal of biological chemistry. Band 274, Nummer 48, November 1999, S. 34283–34293, PMID 10567404.
  51. ↑ S. K. Lee, S. Y. Na, S. Y. Jung, J. E. Choi, B. H. Jhun, J. Cheong, P. S. Meltzer, Y. C. Lee, J. W. Lee: Activating protein-1, nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ASC-2. In: Molecular endocrinology (Baltimore, Md.). Band 14, Nummer 6, Juni 2000, S. 915–925, doi:10.1210/mend.14.6.0471, PMID 10847592.
  52. ↑ S. K. Lee, H. J. Kim, S. Y. Na, T. S. Kim, H. S. Choi, S. Y. Im, J. W. Lee: Steroid receptor coactivator-1 coactivates activating protein-1-mediated transactivations through interaction with the c-Jun and c-Fos subunits. In: The Journal of biological chemistry. Band 273, Nummer 27, Juli 1998, S. 16651–16654, PMID 9642216.
  53. ↑ E. Bengal, L. Ransone, R. Scharfmann, V. J. Dwarki, S. J. Tapscott, H. Weintraub, I. M. Verma: Functional antagonism between c-Jun and MyoD proteins: a direct physical association. In: Cell. Band 68, Nummer 3, Februar 1992, S. 507–519, PMID 1310896.
  54. ↑ a b J. Hess, D. Porte, C. Munz, P. Angel: AP-1 and Cbfa/runt physically interact and regulate parathyroid hormone-dependent MMP13 expression in osteoblasts through a new osteoblast-specific element 2/AP-1 composite element. In: The Journal of biological chemistry. Band 276, Nummer 23, Juni 2001, S. 20029–20038, doi:10.1074/jbc.M010601200, PMID 11274169.
  55. ↑ a b R. C. D'Alonzo, N. Selvamurugan, G. Karsenty, N. C. Partridge: Physical interaction of the activator protein-1 factors c-Fos and c-Jun with Cbfa1 for collagenase-3 promoter activation. In: The Journal of biological chemistry. Band 277, Nummer 1, Januar 2002, S. 816–822, doi:10.1074/jbc.M107082200, PMID 11641401.
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