病毒感染在体内诱导协同激活的转录因子在IFN-β增强子上组装。
Virus infection induces the assembly of coordinately activated transcription factors on the IFN-beta enhancer in vivo.
作者信息
Wathelet M G, Lin C H, Parekh B S, Ronco L V, Howley P M, Maniatis T
机构信息
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
出版信息
Mol Cell. 1998 Mar;1(4):507-18. doi: 10.1016/s1097-2765(00)80051-9.
We have identified a virus-activated factor (VAF) that binds to a regulatory element shared by different virus-inducible genes. We provide evidence that VAF contains two members of the interferon regulatory factor (IRF) family of transcriptional activator proteins (IRF-3 and IRF-7), as well as the transcriptional coactivator proteins p300 and CBP. Remarkably, VAF, as well as recombinant IRF-3 and IRF-7 proteins, binds very weakly to the interferon-beta (IFN-beta) gene promoter in vitro. However, in virus-infected cells, both proteins are recruited to the endogenous IFN-beta promoter as part of a protein complex that includes ATF-2/c-Jun and NF-kappa B. These observations provide a unique example of the coordinate activation of multiple transcriptional activator proteins and their highly cooperative assembly into a transcriptional enhancer complex in vivo.
我们鉴定出一种病毒激活因子（VAF），它能与不同病毒诱导基因共有的调控元件结合。我们提供的证据表明，VAF包含转录激活蛋白干扰素调节因子（IRF）家族的两个成员（IRF-3和IRF-7），以及转录共激活蛋白p300和CBP。值得注意的是，VAF以及重组IRF-3和IRF-7蛋白在体外与干扰素-β（IFN-β）基因启动子的结合非常弱。然而，在病毒感染的细胞中，这两种蛋白作为包含ATF-2/c-Jun和NF-κB的蛋白复合物的一部分被募集到内源性IFN-β启动子上。这些观察结果提供了一个独特的例子，即多种转录激活蛋白在体内协同激活，并高度协作地组装成转录增强子复合物。
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