Kim C H, Heath C, Bertuch A, Hansen U
Proc Natl Acad Sci U S A. 1987 Sep;84(17):6025-9. doi: 10.1073/pnas.84.17.6025.
We have identified a cellular transcription factor from uninfected HeLa cells that stimulates the simian virus 40 (SV40) late mode of transcription and specifically binds the SV40 21-base-pair repeat promoter element. In particular, the late SV40 transcription factor (LSF) stimulates transcription at initiation sites L325 and L264 of the SV40 late promoter, which are the major transcription sites utilized after DNA replication during the SV40 lytic cycle. In addition, LSF appears to stimulate transcription to a lesser extent from the late-early initiation site of the early promoter. LSF binds specifically to the 21-base-pair repeats of the SV40 promoters, forming specific protein-DNA complexes, which migrate more rapidly through nondenaturing polyacrylamide gels than that formed by the previously identified transcription factor Sp1. Thus, LSF is distinguishable from Sp1 in both its transcriptional and DNA-binding properties. These findings suggest a potential role of LSF in the early to late transcriptional switch during a SV40 lytic infection.
我们已从未感染的HeLa细胞中鉴定出一种细胞转录因子,它能刺激猿猴病毒40(SV40)的晚期转录模式,并特异性结合SV40的21个碱基对重复启动子元件。具体而言,晚期SV40转录因子(LSF)能刺激SV40晚期启动子的起始位点L325和L264处的转录,这两个位点是SV40裂解周期中DNA复制后主要利用的转录位点。此外,LSF似乎在较小程度上刺激早期启动子的晚期-早期起始位点的转录。LSF特异性结合SV40启动子的21个碱基对重复序列,形成特异性蛋白质-DNA复合物,该复合物在非变性聚丙烯酰胺凝胶中迁移的速度比先前鉴定的转录因子Sp1形成的复合物更快。因此,LSF在转录和DNA结合特性方面都与Sp1不同。这些发现表明LSF在SV40裂解感染过程中早期到晚期的转录转换中可能发挥作用。