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Originally published In Press as doi:10.1074/jbc.M007120200 on September 29, 2000

J. Biol. Chem., Vol. 276, Issue 2, 867-874, January 12, 2001
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High and Low Levels of Cottontail Rabbit Papillomavirus E2 Protein Generate Opposite Effects on Gene Expression*

Takuma FujiiDagger §, Janet L. Brandsma, Xueyan PengDagger , Srinivasan SrimatkandadaDagger , Lei LiDagger , Allon CanaanDagger , and Albert B. DeisserothDagger ||

From the Dagger  Section of Medical Oncology, Department of Internal Medicine, and Genetic Therapy Program of the Yale Cancer Center and the  Department of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8032

The papillomavirus E2 protein plays an important role in viral transcriptional regulation and replication. We chose to study the cottontail rabbit papillomavirus (CRPV) E2 protein as a transcriptional regulator because of the availability of an animal model for papilloma formation, which may be relevant for human papillomavirus (HPV) infection and replication. We studied the effect of expression levels of E2 on the long control region, which contains transcriptional promoter and enhancer elements, and synthetic E2-dependent artificial promoters in which the E2 was the dominant factor in the transcriptional activation. These experiments indicated that high levels of E2 were inhibitory and low levels were stimulatory for transactivation. In addition, we showed that the complex formed between CRPV E2 and the cognate binding site was less stable than the complex formed between HPV E2 and the same cognate binding site. Furthermore, we showed that CRPV E2 binding to its transcriptional regulatory sequence was stabilized by other proteins such as E1, which produced increments in transcriptional activation of E2-dependent genes. The data may be used to define conditions in which the rabbit model can be used for the screening of drugs which are inhibitory to the HPV and CRPV replication and gene expression.


* This work was supported by grants (to A. D.) from the Hull Development Fund, the George and Barbara Bush Leukemia Research Fund, the Ensign Professorship of Medicine, and the Yale Cancer Center Development Fund for interim developmental support.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Present address: Dept. of Obstetrics and Gynecology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan.

|| To whom correspondence should be addressed. Tel.: 203-737-5608; Fax: 203-737-5698; E-mail: albert.deisseroth@yale.edu.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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