Leblanc J F, Hiscott J
Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.
Virology. 1992 Feb;186(2):760-3. doi: 10.1016/0042-6822(92)90043-o.
The trans-activation potential of herpes simplex virus (HSV) VP16, either alone or in combination with interferon regulatory factor 1 (IRF-1), was examined using hybrid promoters containing different regulatory elements from the interferon-beta promoter. Coexpression of HSV VP16 and IRF-1 differentially activated the AAGTGA hexamer construct Th(2), the AAAGGA hexamer Thm(2) construct, and the natural IFN-beta promoter. Surprisingly, high concentrations of IRF-1 inhibited expression of the PRDII containing reporter P2(1)/CAT. These results indicate that trans-activation by HSV VP16, acting through distinct cellular transcription factors, may be involved in stimulation of IFN-beta regulatory domains.
利用含有来自干扰素β启动子不同调控元件的杂合启动子，对单纯疱疹病毒（HSV）VP16单独或与干扰素调节因子1（IRF-1）联合的反式激活潜能进行了检测。HSV VP16与IRF-1的共表达差异性地激活了AAGTGA六聚体构建体Th(2)、AAAGGA六聚体Thm(2)构建体以及天然干扰素β启动子。令人惊讶的是，高浓度的IRF-1抑制了含PRDII的报告基因P2(1)/CAT的表达。这些结果表明，HSV VP16通过不同的细胞转录因子发挥作用的反式激活可能参与了对干扰素β调控域的刺激。
