• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Oncogene >The transcription-repression domain of the adenovirus E1A oncoprotein targets p300 at the promoter
【24h】

The transcription-repression domain of the adenovirus E1A oncoprotein targets p300 at the promoter

机译：腺病毒E1A癌蛋白的转录抑制域在启动子处靶向p300

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Extensive mutational/functional analysis of the transcription-repression domain encoded in the N-terminal 80 amino acids of the adenovirus E1A 243R oncoprotein suggests a model for the molecular mechanism of E1A repression: E1A accesses transcriptional co-activators such as p300 on specific promoters and then interacts with TBP to disrupt the TBP–TATA complex. In support of this model, as reported here, a basal core promoter activated by tethering p300 is repressible by E1A at the promoter level as shown by chromatin immunoprecipitation (ChIP) analysis. Sequestration of p300 by E1A does not play a significant role, as indicated by dose-response measurements. Furthermore, when the core promoter is transcriptionally activated by tethering activation domains of several transcription factors that can recruit p300 (p65, MyoD, cMyb and TFE3), transcription is repressible by E1A. However, when the core promoter is activated by factors not known to recruit p300 (USF1 and USF2), transcription is resistant to E1A repression. Finally, tethering p300 to the non-repressible adenovirus major late promoter (MLP) renders it repressible by E1A. ChIP analysis shows that E1A occupies the repressed MLP. These findings provide support for the hypothesis that p300 can serve as a scaffold for the E1A repression domain to access specific cellular gene promoters involved in growth regulation.
机译：对腺病毒E1A 243R癌蛋白的N端80个氨基酸编码的转录抑制域进行广泛的突变/功能分析，为E1A抑制的分子机制提供了一个模型：E1A访问特定启动子上的转录共激活因子，例如p300和然后与TBP相互作用以破坏TBP-TATA复合物。为支持该模型，如本文报道的那样，通过染色质免疫沉淀（ChIP）分析显示，E1A可以通过栓塞p300激活的基础核心启动子抑制E1A。正如剂量反应测量所表明的，E1A对p300的螯合作用并不重要。此外，当核心启动子通过可募集p300的几种转录因子（p65，MyoD，cMyb和TFE3）的束缚激活域进行转录激活时，E1A可抑制转录。但是，当核心启动子被未知的募集p300的因子（USF1和USF2）激活时，转录对E1A阻遏具有抗性。最后，将p300与不可阻遏的腺病毒主要晚期启动子（MLP）绑定在一起使其可被E1A阻遏。 ChIP分析显示E1A占据了被抑制的MLP。这些发现为p300可以充当E1A抑制域的支架以访问参与生长调节的特定细胞基因启动子的假设提供了支持。

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