Tsai H L, Kou G H, Chen S C, Wu C W, Lin Y S
Institute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
J Biol Chem. 1996 Feb 16;271(7):3534-40.
The IE2 gene of human cytomegalovirus has been implicated in the development of coronary restenosis, and the gene product appears to inhibit p53-dependent transactivation. Here we describe an analysis of the IE2-p53 interaction. Repression of p53 function by IE2 requires two separable domains of IE2. The N terminus of IE2 interacts with p53. IE2 has little effect on the ability of p53 to bind specific DNA sequences. Reduction of the transactivation activity of p53 is caused by a transcriptional repression function contributed by the C-terminal domain of IE2. These findings suggest that IE2 may function as a transcriptional repressor, which is recruited to p53's target genes by interacting with p53.
人巨细胞病毒的IE2基因与冠状动脉再狭窄的发生有关，该基因产物似乎能抑制p53依赖的反式激活作用。在此，我们描述了对IE2与p53相互作用的分析。IE2对p53功能的抑制需要IE2的两个可分离结构域。IE2的N末端与p53相互作用。IE2对p53结合特定DNA序列的能力影响很小。p53反式激活活性的降低是由IE2 C末端结构域的转录抑制功能引起的。这些发现表明，IE2可能作为一种转录抑制因子，通过与p53相互作用被招募到p53的靶基因上。
