...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell cycle >The dual specificity phosphatase Cdc25C is a direct target for transcriptional repression by the tumor suppressor p53.
【24h】

The dual specificity phosphatase Cdc25C is a direct target for transcriptional repression by the tumor suppressor p53.

机译：双重特异性磷酸酶Cdc25C是肿瘤抑制因子p53抑制转录的直接靶标。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The cdc25C gene has been shown to be a novel target for transcriptional downregulation by p53. Two independent mechanisms contribute to the p53-dependent repression of the cdc25C gene. First, an element in the cdc25C promoter consisting of a binding site for p53 plus an adjacent 8 base pairs confers p53-dependent repression. Mutation of either the p53 binding site or the adjacent 8 bp sequence abolishes this effect. The element conferring p53-dependent repression also contains a binding site for the transcription factor Sp1 and a mutant p53 protein that retains the ability to interact with the p53-binding site is defective in mediating repression. Second, a minimal promoter lacking the p53 binding site but containing a previously characterized CDE/CHR element is also repressed by p53. This repression is abrogated when a 5 bp mutation is introduced in the CHR sequence. These results support a model for p53 downregulating cdc25C expression, in part, by direct binding to a promoter element that is likely to require cooperation with an additional cellular factor.
机译：已经证明cdc25C基因是p53转录下调的新靶标。有两种独立的机制有助于cdc25C基因的p53依赖性抑制。首先，cdc25C启动子中的一个元素由p53的结合位点加上一个相邻的8个碱基对组成，赋予p53依赖性阻抑作用。 p53结合位点或相邻8 bp序列的突变消除了这种影响。赋予p53依赖性阻抑的元件还包含转录因子Sp1的结合位点，而保留与p53结合位点相互作用的能力的突变p53蛋白在介导阻遏方面存在缺陷。其次，缺少p53结合位点但含有先前表征的CDE / CHR元件的最小启动子也被p53抑制。当在CHR序列中引入5 bp突变时，这种抑制作用就消失了。这些结果部分通过直接结合可能需要与其他细胞因子协同作用的启动子元件来支持p53下调cdc25C表达的模型。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号