Gene repression by coactivator repulsion.
Gene repression by coactivator repulsion.
复制标题
通过共激活剂排斥来抑制基因。
DOI：
10.1016/s1097-2765(05)00081-x
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发表时间：
2000
期刊：
影响因子：
16
通讯作者：
Thanos,D
中科院分区：
文献类型：
--
作者：
Senger,K;Merika,M;Agalioti,T;Yie,J;Escalante,CR;Chen,G;Aggarwal,AK;Thanos,D
我们发现IRF-2癌蛋白通过一种新机制抑制病毒诱导的IFN-β基因转录。病毒感染诱导IRF-2募集到一些内源性IFN-β增强子，作为增强体的一部分。携带IRF-2的增强体不能激活转录，因为IRF-2中存在一个结构域，该结构域阻止了CBP-Pol II全酶复合物的增强体依赖性募集。因此，IRF-2与增强体的结合限制了IFN-β启动子指导转录的数量。值得注意的是，IRF-2基因的缺失通过增加能够诱导IFN-β基因转录的细胞数量来增加IFN-β的表达，以应对病毒感染。
We show that the IRF-2 oncoprotein represses virus-induced IFN-β gene transcription via a novel mechanism. Virus infection induces recruitment of IRF-2 to some of the endogenous IFN-β enhancers as part of the enhanceosome. Enhanceosomes bearing IRF-2 cannot activate transcription, due to the presence of a domain in IRF-2 that prevents enhanceosome-dependent recruitment of the CBP-Pol II holoenzyme complex. As a consequence, IRF-2 incorporation into enhanceosomes restricts the number of IFN-β promoters directing transcription. Remarkably, deletion of the IRF-2 gene increases IFN-β expression by expanding the number of cells capable of inducing IFN-β gene transcription in response to virus infection.