REGULATION OF TRANSCRIPTION IN SV40 AND ADENOVIRUS

DNA肿瘤病毒的转化区。SV 40和JCV，以及 腺病毒调节病毒和细胞基因的转录。 的 这些研究的目的是探讨T/t 抗原和E1 A蛋白调节转录及其与 细胞转化 在腺病毒中， 含有蛋白质ATF和EIIF的结合位点，作为增强子， 可被EIA和SV 40 T/t抗原反式激活。 具体 ATF和EIIF结合位点的突变抑制EIIA 增强子200倍。插入突变的分析表明， 上游ATF和EIIF结合位点相对于 DNA螺旋上的下游EIIF结合位点是重要的。符合 先前的发现，使用凝胶位移分析，我们证明， 野生型腺病毒感染后EIIF的活性增加。在 相反，使用相同的凝胶移位条件，ATF的结合活性 会因病毒感染而减少因为ATF实际上是一个 相关转录因子，研究正在进行中， 差异调节应答腺病毒感染。

The transforming region of the DNA tumor viruses. SV40 and JCV, and adenovirus regulates transcription of viral and cellular genes. The purpose of these studies is to investigate the mechanism by which the T/t antigen(s) and E1A proteins modulate transcription and its relationship to cellular transformation. In adenovirus, The EIIA upstream sequences which contain the binding sites for proteins ATF and EIIF act as an enhancer and can be trans-activated by both EIA and SV40 T/t antigens. Specific mutation of either the ATF and EIIF binding sites inhibited the EIIA enhancer 200-fold. Analysis of insertion mutation suggests that the spatial alignment of the upstream ATF and EIIF binding sites with respect to the downstream EIIF binding site on the DNA helix is important. Consistent with previous findings, using gel shift analysis we demonstrate that the binding activity of EIIF is increased following wild-type adenovirus infection. In contrast, using identical gel shift conditions, the binding activity of ATF is decreased by viral infection . Since ATF is actually a family of closely related transcription factors, studies are in progress to look at differential regulation in response to adenovirus infection.