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.
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Mar 15 1993|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology