Yanagawa S, Tanaka H, Ishimoto A
Department of Viral Oncology, Kyoto University, Japan.
J Virol. 1991 Jan;65(1):526-31. doi: 10.1128/JVI.65.1.526-531.1991.
We analyzed the long terminal repeat (LTR) of mouse mammary tumor virus for sequences that influence its promoter activity by using the chloramphenicol acetyltransferase assay. A series of LTR deletion mutants and recombinants between LTR and simian virus 40 regulatory sequences were used for these studies. Through transfection experiments in three different human cell lines (T47D, MCF-7, and HeLa), we identified a novel mammary cell line-specific enhancer element on a 98-bp BanII fragment (from position -1075 to -978 upstream of the start site of transcription) which interacts with the hormone-responsive element of LTR. We also identified nuclear factors that specifically interacted with this BanII fragment in the nuclear extract from the mammary tumor cell line, T47D, but not from the HeLa cell line.
我们通过氯霉素乙酰转移酶测定法分析了小鼠乳腺肿瘤病毒的长末端重复序列（LTR），以寻找影响其启动子活性的序列。一系列LTR缺失突变体以及LTR与猿猴病毒40调控序列之间的重组体被用于这些研究。通过在三种不同的人类细胞系（T47D、MCF-7和HeLa）中进行转染实验，我们在一个98 bp的BanII片段（转录起始位点上游-1075至-978位）上鉴定出一种新型的乳腺细胞系特异性增强子元件，该元件与LTR的激素反应元件相互作用。我们还在乳腺肿瘤细胞系T47D而非HeLa细胞系的核提取物中鉴定出了与该BanII片段特异性相互作用的核因子。
