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Laboratory of Tumor Virus Biology, Bldg 41, Room C111, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
The bovine papillomavirus type 1 (BPV-1) long control region (LCR) contains at least three consensus binding sites for the transcription factor Sp1 at nucleotides (nt) 7800, 7833 and 7854. A high basal-level P89 expression vector consisting of an origin-deleted LCR fused to the chloramphenicol acetyltransferase (CAT) gene was utilized to determine the role of these Sp1 sites in the regulation of transcription from the BPV-1 P89 promoter. The three Sp1 sites were capable of binding Sp1 in vitro. Mutation of these sites in the background of the origin-deleted LCR-CAT or a wild-type LCR-CAT construct resulted in decreased basal expression from P89. In addition, mutation of the Sp1 sites in the wild-type background caused a reduction in E2-transactivation potential. These data illustrate the importance of these Sp1 sites in regulating both basal and E2-transactivated P89 expression.
* Author for correspondence. Present address: Pro-Virus Inc., 1530 E. Jefferson St, Rockville, MD 20852, USA. Fax +1 301 230 0158.
Present address: Cancer Biology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Received 6 June 1995;
accepted 5 October 1995.
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