Kristjuhan A, Maimets T
Institute of Molecular and Cell Biology, Estonian Biocentre, Tartu University, Estonia.
Eur J Biochem. 1995 Dec 15;234(3):827-31. doi: 10.1111/j.1432-1033.1995.827_a.x.
Tumor suppressor protein p53 binds to DNA in a sequence-specific manner and activates transcription from promoters near its binding site. It is also known to repress promoters lacking the p53-binding site. In this study, we demonstrate that p53 can act as a transcriptional activator or repressor in vivo using the same reporter with the DNA-binding site CON and these effects depend on the amount of p53 expressed. Both in Saos2 and Cos7 cells, lower concentrations of p53 lead to activation and higher concentrations lead to repression of the model promoter containing the consensus p53-binding site CON. The N-terminal part of p53 is necessary for the transcriptional activation. It is not needed, however, for the repression of the same promoter, indicating that different domains of p53 are involved in activation and repression.
肿瘤抑制蛋白p53以序列特异性方式与DNA结合，并激活其结合位点附近启动子的转录。已知它还能抑制缺乏p53结合位点的启动子。在本研究中，我们证明p53在体内可以使用具有DNA结合位点CON的相同报告基因作为转录激活剂或抑制剂，并且这些效应取决于p53的表达量。在Saos2和Cos7细胞中，较低浓度的p53导致激活，而较高浓度导致含有共有p53结合位点CON的模型启动子受到抑制。p53的N末端部分对于转录激活是必需的。然而，对于同一启动子的抑制则不需要它，这表明p53的不同结构域参与激活和抑制过程。
