Enhanceosome formation over the beta interferon promoter underlies a remote-control mechanism mediated by YY1 and YY2

Enhanceosome formation over the beta interferon promoter underlies a remote-control mechanism mediated by YY1 and YY2
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DOI:
10.1128/mcb.25.22.10159-10170.2005
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发表时间:
2005-11-01
影响因子:
5.3
通讯作者:
Bode, J
Bode, J
中科院分区:
生物学2区
文献类型:
--
作者:
Klar, M;Bode, J

文献摘要

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人类和小鼠的β干扰素基因的表达受到病毒反应元件(VRE)的直接控制,该元件在转录起始点上游110个碱基终止。尽管根据病毒感染产生的信号在VRE上形成的增强体有丰富的信息,但早期的观察表明存在其他远上游调控元件,到目前为止还没有分子基础。在DNA结构计算分析的指导下,我们可以定位三个未知的转录因子结合区,分别位于-0.5、-2和-3kb。我们的研究描绘了因子YY1和YY2在-3kb和-2kb(也称为HS1和HS2)处的相互作用,这与新的因子YY2拮抗YYI的负面作用的观点是一致的。将描述人类和小鼠控制区之间的差异。
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 YYI. Differences between the human and murine control regions will be described.