β干扰素启动子上增强体的形成是由YY1和YY2介导的远程控制机制的基础。
Enhanceosome formation over the beta interferon promoter underlies a remote-control mechanism mediated by YY1 and YY2.
作者信息
Klar Martin, Bode Juergen
机构信息
German Research Center for Biotechnology (GBF), RDIF/Epigenetic Regulation, Mascheroder Weg 1, 38124 Braunschweig, Germany.
出版信息
Mol Cell Biol. 2005 Nov;25(22):10159-70. doi: 10.1128/MCB.25.22.10159-10170.2005.
Abstract
The expression of beta interferon genes from humans and mice is under the immediate control of a virus-responsive element (VRE) that terminates 110 bp upstream from the transcriptional start site. Whereas a wealth of information is available for the enhanceosome that is formed on the VRE upon the signals generated by viral infection, early observations indicating the existence of other far-upstream control elements have so far remained without a molecular fundament. Guided by a computational analysis of DNA structures, we could locate three as-yet-unknown transcription factor-binding regions at -0.5, -2, and -3 kb. Our present study delineates the interplay of factors YY1 and YY2 as it occurs at the sites at -3 kb and -2 kb (otherwise called HS1 and HS2), consistent with the idea that the novel factor YY2 antagonizes the negative actions exerted by YY1. Differences between the human and murine control regions will be described.
摘要
人类和小鼠β干扰素基因的表达直接受病毒反应元件（VRE）的控制，该元件位于转录起始位点上游110 bp处。尽管关于病毒感染产生的信号在VRE上形成的增强体已有大量信息，但早期表明存在其他远上游控制元件的观察结果至今仍缺乏分子基础。通过对DNA结构的计算分析，我们在-0.5、-2和-3 kb处定位到三个未知的转录因子结合区域。我们目前的研究描述了因子YY1和YY2在-3 kb和-2 kb位点（即HS1和HS2）的相互作用，这与新因子YY2拮抗YY1的负向作用的观点一致。还将描述人类和小鼠控制区域之间的差异。
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