Abstract
THE hepatitis B virus (HBV) X gene product (pX) could be important in disease pathogenesis because it is known to transacti-vate transcription from many viral and cellular gene promoters1–8, including the HBV core gene promoter, the human immunodeficiency virus (HIV-1) long terminal repeat, and the c-myc promoter. We have previously shown that only a subset of the promoters that can be transactivated by pX is transactivated in any particular cell line, and have proposed that pX acts through multiple, cell type-specific transcription factors9. We show here that pX acts through both AP-1 and AP-2 sites, and that pX has a transcription activation domain. We conclude that transactiva-tion by pX depends on at least two distinct cellular DNA-binding transcription factors and we present a model for the action of pX.
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1. Twu, J. & Schloemer, R. H. J. Virol. 61, 3448–3453 (1987). 2. Spandau, D. F. & Lee, C. J. Virol. 62, 427–434 (1988). 3. Zahm, P, Hofschneider, P. H. & Koshy, R. Oncogene 3, 169–177 (1988). 4. Seto, E., Yen, T. S. B., Peterlin, B. M. & Ou, J. H. Proc. natn. Acad. Sci. U.S.A. 85,8286–8290 (1988). 5. Colgrove, R., Simon, G. & Ganem, D. J. Virol. 63, 4019–4026 (1989). 6. Siddiqui, "., Gaynor, R., Srinivasan, A., Mapoles, J. & Farr, R. W. Virology 169, 479–484 (1989). 7. Koike, K., Shirakata, Y., Kawada, M., Arii, M. & Kobayashi, M. Molec. Biol. Med. (in the press). 8. Twu, J. S., Rosen, C. A., Haseltine, W. A. & Robinson, W. S. J. Virol. 63, 2857–2860 (1989). 9. Seto, E., Zhou, D. X., Peterlin, B. M. & Yen, T. S. B. Virology 173, 764–766 (1989). 10. Zenke, M. et al. EMBO J. 5, 387–397 (1986). 11. Lee, W., Micheli, P. J. & Tjian, R. Cell 49, 741–752 (1987). 12. Sturm, R., Baumruker, T., Franza, B. R. Jr & Herr, W. Genes Dev. l, 1147–1160 (1987). 13. Jones, N. C., Rigby, P. W. J. & Ziff, E. B. Genes Dev. 2, 267–281 (1988). 14. Mitchell, P. J. & Tjian, R. Science 245, 371–378 (1989). 15. Mitchell, P. J., Wang, C. & Tjian, R. Cell 50, 847–861 (1987). 16. Williams, T., Admon, A., Lüscher, B. & Tjian, R. Genes Dev. 2, 1557–1569 (1988). 17. Perkins, K. K., Dailey, G. M. & Tjian, R. EMBO J. 7, 4265–4273 (1988). 18. Courey, A. J. & Tjian, R. Cell 55, 887–898 (1988). 19. Gill, G. & Ptashne, M. Nature 334, 721–724 (1988). 20. Lillie, J. W. & Green, M. R. Nature 338, 39–44 (1989). 21. Godowski, P. J., Picard, D. & Yamamoto, K. R. Science 241, 812–816 (1988). 22. Valenzuela, P., Quiroga, M., Zaldivar, J., Gray, P. & Rutter, W. J. in Animal Virus Genetics (eds Fields, B., Jaenisch, R. & Fox, C. F.) 57–70 (Academic, New York, 1980). 23. Gorman, C. in DNA Cloning, Vol. Il (ed. Glover, D. M.) 143–190 (IRL, Oxford, 1985). 24. Lüscher, B., Mitchell, P. J., Williams, T. & Tjian, R. Genes Dev. 3,1507–1517 (1989). 25. Imagawa, M., ChiÃ, R. & Karin, M. Cell 51, 251–260 (1987).
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Seto, E., Mitchell, P. & Benedict Yen, T. Transactivation by the hepatitis B virus X protein depends on AP-2 and other transcription factors. Nature 344, 72–74 (1990). https://doi.org/10.1038/344072a0
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DOI: https://doi.org/10.1038/344072a0
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