Gartel A L, Najmabadi F, Goufman E, Tyner A L
University of Illinois College of Medicine, Department of Genetics, M/C 669, 900 South Ashland Avenue, Chicago, IL 60607, USA.
Oncogene. 2000 Feb 17;19(7):961-4. doi: 10.1038/sj.onc.1203411.
We recently reported that E2F1 could transactivate the p21 promoter via cis-acting elements between -119 to +16 bp of the p21 gene. Here we show that activated V12-H-Ras can induce the p21 promoter through the same region of the p21 promoter by a p53-independent mechanism in NIH3T3 cells. In contrast, activated Ras was not able to induce the p21 promoter in E2F1-/- fibroblasts, suggesting that E2F1 is required for induction of the p21 promoter by activated Ras. Cotransfection of increasing concentrations of dominant negative E2F1 alone, or with dominant negative DP1 into NIH3T3 cells suppressed induction of the p21 promoter by activated Ras. These data suggest that p53-independent induction of the p21 promoter by activated Ras is mediated at least in part by E2F1. Oncogene (2000) 19, 961 - 964.
我们最近报道，E2F1可通过p21基因-119至+16 bp之间的顺式作用元件反式激活p21启动子。在此我们表明，激活的V12-H-Ras可通过p21启动子的同一区域，在NIH3T3细胞中通过一种不依赖p53的机制诱导p21启动子。相反，激活的Ras在E2F1基因敲除的成纤维细胞中无法诱导p21启动子，这表明E2F1是激活的Ras诱导p21启动子所必需的。单独转染浓度递增的显性负性E2F1，或与显性负性DP1一起转染到NIH3T3细胞中，可抑制激活的Ras对p21启动子的诱导。这些数据表明，激活的Ras对p21启动子的不依赖p53的诱导至少部分是由E2F1介导的。《癌基因》（2000年）第19卷，961 - 964页 。
