Release of the p53-induced repression on thymidine kinase promoter by single p53-binding sequence.
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.
Department of Biochemistry, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
J N
JN
Yuan
B H
BH
Liu
H
H
Lee
Y T
YT
Shaw
S T
ST
Chiou
W C
WC
Chang
M D
MD
Lai
D000818:Animals; D001483:Base Sequence; D001665:Binding Sites; D002478:Cells, Cultured; D006224:Cricetinae; D004247:DNA; D015536:Down-Regulation; D015971:Gene Expression Regulation, Enzymologic; D008969:Molecular Sequence Data; D009154:Mutation; D011401:Promoter Regions, Genetic; D018139:Simplexvirus / Q000201:enzymology; D013937:Thymidine Kinase / Q000235:genetics*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D016159:Tumor Suppressor Protein p53; D004247:DNA; D013937:Thymidine Kinase