Masuda M, Lee G, Yuasa T, Yoshikura H
Department of Bacteriology, Faculty of Medicine, University of Tokyo.
Microbiol Immunol. 1988;32(7):741-7. doi: 10.1111/j.1348-0421.1988.tb01435.x.
Transcriptional regulation of hepatitis B virus (HBV) surface antigen (HBs Ag) gene was studied in human hepatoma-derived cell lines. Treatment with dexamethasone (Dex; 1 microM) induced an increase in the smaller HBs-mRNA initiated within Pre-S region encoding S and Pre-S2 proteins, but not the larger HBs-mRNA initiated in the further upstream encoding Pre-S1 protein. The Bg1II-MstII fragment (map position 2425-3201) in the upstream of the S gene was used as a transcriptional promoter of chloramphenicol acetyltransferase (CAT) gene. The CAT activity brought about by this construct in the transient assay was elevated by 5-fold in the presence of Dex. Deletion analysis localized the sequence required for the full response to Dex within a 590-base pair fragment in the upstream of the transcriptional initiation site of the smaller HBs-mRNA. And this fragment contained the binding site for the nuclear factor I (NF-I), which might have some role in Dex-dependent transcriptional stimulation.
在人肝癌衍生细胞系中研究了乙型肝炎病毒（HBV）表面抗原（HBs Ag）基因的转录调控。用地塞米松（Dex；1微摩尔）处理可诱导在编码S和Pre-S2蛋白的前S区域内起始的较小HBs-mRNA增加，但不会诱导在更上游编码Pre-S1蛋白起始的较大HBs-mRNA增加。S基因上游的Bg1II-MstII片段（图谱位置2425-3201）用作氯霉素乙酰转移酶（CAT）基因的转录启动子。在瞬时分析中，该构建体在Dex存在下产生的CAT活性提高了5倍。缺失分析将对Dex的完全应答所需序列定位在较小HBs-mRNA转录起始位点上游的一个590碱基对片段内。并且该片段包含核因子I（NF-I）的结合位点，其可能在Dex依赖性转录刺激中起一定作用。
