c-Jun ist ein Bestandteil des Transkriptionsfaktors AP-1 und ein Protoonkogen.
Eigenschaften 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. Das Homolog des c-Jun () aus Retroviren wird als v-Jun () bezeichnet.
Interaktionen c-Jun interagiert mit verschiedenen Proteinen: TGIF1M. 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, . Ets Related GeneA. 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. Retinoblastom-ProteinJ. 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. CREBBPY. 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. ATF2C. 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.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. 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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.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.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.C. F. Meyer, X. Wang, C. Chang, D. Templeton, T. H. 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Band 278, Nummer 22, Mai 2003, S. 19682–19690, doi:10.1074/jbc.M212681200, PMID 12615916. PIN1G. 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, . FOSL1 SMAD3Y. 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.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.N. T. Liberati, M. B. Datto, J. P. 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In: Molecular and cellular biology. Band 19, Nummer 10, Oktober 1999, S. 7138–7146, PMID 10490649, . BCL6F. 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. Band 169, Nummer 4, August 2002, S. 1922–1929, PMID 12165517. BCL3S. 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. Receptor androgénicoN. 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. 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