Hecht E M, Chesters P M, McCance D J
Department of Microbiology, U.M.D.S. Guy's Campus, London Bridge, U.K.
J Gen Virol. 1990 Aug;71 ( Pt 8):1823-8. doi: 10.1099/0022-1317-71-8-1823.
Plasmid DNA including the simian virus 40 (SV40) origin of replication undergoes uncontrolled, runaway replication in cos-1 cells owing to the intracellular production of SV40 large T antigen. Covalent linkage of such plasmids with human papillomavirus type 16 (HPV-16) DNA was found to prevent runaway replication. Replication control was found to be dependent on the presence of HPV-16 DNA sequences including the E1 open reading frame and part of the non-coding region.
由于细胞内产生猿猴病毒40(SV40)大T抗原,包含SV40复制起点的质粒DNA在cos - 1细胞中会发生不受控制的失控复制。人们发现,此类质粒与人乳头瘤病毒16型(HPV - 16)DNA的共价连接可防止失控复制。研究发现,复制控制取决于HPV - 16 DNA序列的存在,这些序列包括E1开放阅读框和部分非编码区。