Abstract
Herpes simplex thymidine kinase (TK) promoter was shown to be repressed by the wild-type p53. Using a model system that the p53-binding site was linked to the thymidine kinase promoter, we demonstrated that single p53-specific binding site was sufficient to abolish the repression. On the contrary, the mutant p53 had the opposite effects on the HSV-TK promoter in BHK cells. The results suggest that the p53-binding site may act as an enhancer to regulate the gene expression in a novel way in vivo.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Binding Sites
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Cells, Cultured
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Cricetinae
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DNA
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Down-Regulation
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Gene Expression Regulation, Enzymologic*
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Molecular Sequence Data
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Mutation
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Promoter Regions, Genetic*
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Simplexvirus / enzymology
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Thymidine Kinase / genetics*
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Tumor Suppressor Protein p53
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DNA
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Thymidine Kinase
Associated data
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GENBANK/D25301
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GENBANK/D25302
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GENBANK/S57428
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GENBANK/S64630
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GENBANK/S64631
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GENBANK/S64632
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GENBANK/S64635
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GENBANK/S64636
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GENBANK/S64637
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GENBANK/X68692