Guo W T, Bell K D, Ou J H
Department of Microbiology, University of Southern California, Los Angeles 90033-1054.
J Virol. 1991 Dec;65(12):6686-92. doi: 10.1128/JVI.65.12.6686-6692.1991.
The hepatitis B virus EnhI enhancer element overlaps the promoter of the X gene. By performing methylation interference experiments, four protein factor binding sites clustered in a 120-bp region were found to control the EnhI enhancer and X promoter activities. Deletion mapping experiments indicated that the two upstream protein factor binding sites constituted a basal enhancer module. This module, likely bound by a liver-specific factor and a ubiquitous factor, could activate the herpes simplex virus thymidine kinase gene promoter by 5- or 10-fold, depending on the orientation, in Huh7 cells, a liver-derived cell line, but not in other cell types tested. The two downstream protein factor binding sites interact with the upstream basal enhancer module in an orientation- and distance-dependent manner to increase the enhancer activity by another 10-fold. In addition, at least one of the two downstream protein factor binding sites is also essential for the X promoter activity.
乙型肝炎病毒增强子I（EnhI）增强子元件与X基因的启动子重叠。通过进行甲基化干扰实验，发现在一个120碱基对区域内聚集的四个蛋白质因子结合位点控制着EnhI增强子和X启动子的活性。缺失图谱实验表明，两个上游蛋白质因子结合位点构成了一个基础增强子模块。该模块可能由肝脏特异性因子和普遍存在的因子结合，根据方向不同，可使单纯疱疹病毒胸苷激酶基因启动子在源自肝脏的细胞系Huh7细胞中激活5倍或10倍，但在其他测试的细胞类型中则不然。两个下游蛋白质因子结合位点以方向和距离依赖的方式与上游基础增强子模块相互作用，使增强子活性再增加10倍。此外，两个下游蛋白质因子结合位点中至少有一个对X启动子活性也是必不可少的。
