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乙型肝炎病毒X蛋白的反式激活作用依赖于AP-2及其他转录因子。

Transactivation by the hepatitis B virus X protein depends on AP-2 and other transcription factors.

作者信息

Seto E, Mitchell P J, Yen T S

机构信息

Department of Pathology, University of California School of Medicine, San Francisco 94143-0506.

出版信息

Nature. 1990 Mar 1;344(6261):72-4. doi: 10.1038/344072a0.

DOI:10.1038/344072a0
PMID:2154703
Abstract

The hepatitis B virus (HBV) X gene product (pX) could be important in disease pathogenesis because it is known to transactivate transcription from many viral and cellular gene promoters, including the HBV core gene promoter, the human immunodeficiency virus (HIV-1) long terminal repeat, and the c-myc promoter. We have previously shown that only a subset of the promoters that can be transactivated by pX is transactivated in any particular cell line, and have proposed that pX acts through multiple, cell type-specific transcription factors. We show here that pX acts through both AP-1 and AP-2 sites, and that pX has a transcription activation domain. We conclude that transactivation by pX depends on at least two distinct cellular DNA-binding transcription factors and we present a model for the action of pX.

摘要

乙型肝炎病毒(HBV)X基因产物(pX)在疾病发病机制中可能具有重要作用,因为已知它能反式激活许多病毒和细胞基因启动子的转录,包括HBV核心基因启动子、人类免疫缺陷病毒(HIV-1)长末端重复序列以及c-myc启动子。我们之前已经表明,在任何特定细胞系中,能被pX反式激活的启动子只是其中一部分,并且我们提出pX是通过多种细胞类型特异性转录因子发挥作用的。我们在此表明,pX通过AP-1和AP-2位点发挥作用,并且pX具有转录激活结构域。我们得出结论,pX的反式激活依赖于至少两种不同的细胞DNA结合转录因子,并且我们提出了一个pX作用的模型。

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Nature. 1990 Mar 1;344(6261):72-4. doi: 10.1038/344072a0.
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