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糖皮质激素受体识别乙型肝炎病毒DNA中的特定核苷酸序列,导致乙肝病毒增强子活性增加。

The glucocorticoid receptor recognizes a specific nucleotide sequence in hepatitis B virus DNA causing increased activity of the HBV enhancer.

作者信息

Tur-Kaspa R, Shaul Y, Moore D D, Burk R D, Okret S, Poellinger L, Shafritz D A

机构信息

Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, New York 10461.

出版信息

Virology. 1988 Dec;167(2):630-3.

PMID:3201757
Abstract

The hepatitis B virus (HBV) genome contains a specific DNA binding site for the glucocorticoid receptor. Using DNase I footprinting, this binding site was localized at HBV map positions 341-370 clockwise from the EcoRI site. The DNA sequence protected in the footprint contains two tandem copies of the GRE core hexanucleotide 5'-TGTTCCT-3'. Deletion analysis and reconstruction experiments in plasmid expression vectors demonstrated that this glucocorticoid receptor binding sequence serves as a signal for augmenting glucocorticoid-dependent activity of the HBV enhancer, which is located approximately 730 nucleotides downstream in the HBV genome. Even though it does not serve as an independent enhancer element, the HBV glucocorticoid receptor domain can therefore be categorized as a functional GRE.

摘要

乙肝病毒(HBV)基因组包含糖皮质激素受体的一个特定DNA结合位点。利用DNA酶I足迹法,该结合位点定位在从EcoRI位点顺时针方向的HBV图谱位置341 - 370处。足迹中受保护的DNA序列包含糖皮质激素反应元件(GRE)核心六核苷酸5'-TGTTCCT-3'的两个串联拷贝。在质粒表达载体中进行的缺失分析和重建实验表明,这个糖皮质激素受体结合序列作为增强HBV增强子糖皮质激素依赖性活性的信号,该增强子位于HBV基因组下游约730个核苷酸处。因此,尽管HBV糖皮质激素受体结构域不作为一个独立的增强子元件,但可归类为功能性GRE。

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