O'Connor D J, Lam E W, Griffin S, Zhong S, Leighton L C, Burbidge S A, Lu X
Ludwig Institute for Cancer Research, St Mary's Hospital Medical School, London, UK.
EMBO J. 1995 Dec 15;14(24):6184-92. doi: 10.1002/j.1460-2075.1995.tb00309.x.
One way in which wild-type p53 is able to regulate cell cycle progression is thought to be via the induction of its downstream target gene Waf1/CIP1, thus indirectly regulating the transcriptional activity of E2F. The E2F transcription factors are known to be key effectors of the cell cycle. We report here that there is a physical and functional interaction between p53 and two of the components of the E2F transcription factors, E2F1 and DP1. The expression of wild-type p53 can inhibit the transcriptional activity of E2F, and the expression of both E2F1 and DP1 can also downregulate p53-dependent transcription. The transcriptional activity of p53 is known to be inhibited by the direct binding of mdm2, but we demonstrate here that both E2F1 and DP1 can inhibit p53 transcriptional activity independently of mdm2. Detailed studies of protein-protein interactions have provided evidence that E2F1 and its co-operating factor DP1 can complex with p53 both in vitro and in vivo.
野生型p53调节细胞周期进程的一种方式被认为是通过诱导其下游靶基因Waf1/CIP1,从而间接调节E2F的转录活性。已知E2F转录因子是细胞周期的关键效应因子。我们在此报告,p53与E2F转录因子的两个组分E2F1和DP1之间存在物理和功能相互作用。野生型p53的表达可抑制E2F的转录活性,E2F1和DP1的表达也可下调p53依赖性转录。已知p53的转录活性会被mdm2的直接结合所抑制,但我们在此证明,E2F1和DP1均可独立于mdm2抑制p53的转录活性。蛋白质-蛋白质相互作用的详细研究提供了证据,表明E2F1及其协同因子DP1在体外和体内均可与p53形成复合物。