Caputo A, Barbanti-Brodano G, Wang E, Ricciardi R P
Virology. 1986 Jul 30;152(2):459-65. doi: 10.1016/0042-6822(86)90148-0.
The early promoters of BKV and SV40 plasmids were transactivated in both BKV and SV40-transformed cells which failed to support replication of these plasmids. This suggests that the T-antigen of either virus can transactivate BKV and SV40 early promoters by either increasing the availability of cellular transcription factors or by directly interacting with specific sequences which comprise the transcriptional control region of the early promoters. We also observed that removal of 8-bp on the early side of T-antigen binding site I of BKV does not alter viral-plasmid replication.
BK病毒(BKV)和猿猴空泡病毒40(SV40)质粒的早期启动子在BKV和SV40转化的细胞中均被反式激活,而这些细胞无法支持这些质粒的复制。这表明,两种病毒的T抗原均可通过增加细胞转录因子的可用性或直接与构成早期启动子转录控制区的特定序列相互作用,来反式激活BKV和SV40的早期启动子。我们还观察到,去除BKV的T抗原结合位点I早期一侧的8个碱基对,不会改变病毒质粒的复制。