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CCAAT元件在调控乙肝病毒表面蛋白表达中的关键作用。

Key role of a CCAAT element in regulating hepatitis B virus surface protein expression.

作者信息

Lu C C, Chen M, Ou J H, Yen T S

机构信息

Department of Pathology, University of California, San Francisco 94143.

出版信息

Virology. 1995 Feb 1;206(2):1155-8. doi: 10.1006/viro.1995.1042.

DOI:10.1006/viro.1995.1042
PMID:7856091
Abstract

Two separate promoters, the upstream preS1 and the downstream S promoters, give rise to transcripts encoding three forms of the hepatitis B virus surface protein. Overproduction of large surface protein because of increased preS1 transcripts leads to a block in secretion of all forms of the surface protein and of virion particles. We show here that a CCAAT element in the S promoter not only increases the amount of S transcripts, but also decreases the amount of preS1 transcripts by up to fivefold. Consequently, mutations in this element cause intracellular accumulation of surface proteins because of the secretory block. Therefore, this CCAAT element appears to be critical for maintaining the high ratio of S versus preS1 transcripts that is necessary for the viral life cycle.

摘要

两个独立的启动子,即上游的前S1启动子和下游的S启动子,产生编码三种形式乙肝病毒表面蛋白的转录本。由于前S1转录本增加导致大表面蛋白过量产生,进而阻碍了所有形式的表面蛋白和病毒粒子的分泌。我们在此表明,S启动子中的一个CCAAT元件不仅增加了S转录本的量,还将前S1转录本的量减少了多达五倍。因此,该元件中的突变由于分泌受阻导致表面蛋白在细胞内积累。所以,这个CCAAT元件对于维持病毒生命周期所必需的S转录本与前S1转录本的高比例似乎至关重要。

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