人类β干扰素基因病毒诱导中不同增强子结构域之间的协同作用。
Synergism between distinct enhanson domains in viral induction of the human beta interferon gene.
作者信息
Leblanc J F, Cohen L, Rodrigues M, Hiscott J
机构信息
Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.
出版信息
Mol Cell Biol. 1990 Aug;10(8):3987-93. doi: 10.1128/mcb.10.8.3987-3993.1990.
Abstract
This study demonstrates distinct virus-inducible enhanson properties for three regions of the human beta interferon (IFN-beta) promoter; maximum virus inducibility required syngerism among all three enhansons. Expression of the IRF-1 transcription factor differentially increased the expression of plasmids containing (AAGTGA)4 or PRDIII (-94 to -78) motifs but was inefficient in the induction of the intact IFN-beta promoter. The human T-cell lymphotropic virus type I Tax protein was a strong positive activator of PRDII (-64 to -55)-containing plasmids but was also unable to stimulate the IFN-beta promoter. Induction of the intact IFN-beta promoter linked to a reporter plasmid was achieved in lymphoid and epithelioid cellular backgrounds by a triple transfection with IRF-1 and Tax expression plasmids or a combination of IRF-1 and phorbol ester, indicating that at least two trans-activating events and the association of two proteins on the promoter template are required for IFN-beta activation.
摘要
本研究证明了人类β干扰素（IFN-β）启动子的三个区域具有不同的病毒诱导增强子特性；最大病毒诱导性需要所有三个增强子之间协同作用。IRF-1转录因子的表达差异性地增加了含有（AAGTGA）4或PRDIII（-94至-78）基序的质粒的表达，但在诱导完整的IFN-β启动子时效率不高。人类I型嗜T细胞病毒Tax蛋白是含PRDII（-64至-55）质粒的强阳性激活剂，但也无法刺激IFN-β启动子。通过用IRF-1和Tax表达质粒或IRF-1与佛波酯的组合进行三重转染，在淋巴样和上皮样细胞背景中实现了与报告质粒相连的完整IFN-β启动子的诱导，这表明IFN-β激活至少需要两个反式激活事件以及两种蛋白质在启动子模板上的结合。
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