Binninger D, Ferdinand F J, Rübsamen-Waigmann H
Chemotherapeutisches Forschungsinstitut Georg-Speyer-Haus, Frankfurt/Main, Federal Republic of Germany.
Arch Virol. 1989;107(3-4):291-9. doi: 10.1007/BF01317924.
Simian virus 40 (SV40) late region recombinant constructs containing the Rous sarcoma virus (RSV) src gene along with RSV enhancer stimulated expression but completely abolished SV40 DNA replication. Constructs, in which the heterologous enhancer sequences were omitted, did replicate normally in African green monkey kidney cells and, in the presence of helper virus, gave rise to infectious progeny. Inhibition of SV40 DNA replication follows a cis-acting mechanism and is most likely due to a conformational change of the SV40 chromatin structure.
含有劳斯肉瘤病毒(RSV)src基因以及RSV增强子的猿猴病毒40(SV40)晚期区域重组构建体刺激了表达,但完全消除了SV40 DNA复制。省略了异源增强子序列的构建体在非洲绿猴肾细胞中正常复制,并且在辅助病毒存在的情况下产生有感染性的后代。SV40 DNA复制的抑制遵循顺式作用机制,很可能是由于SV40染色质结构的构象变化。