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普遍存在的转录因子Oct-1和肝脏特异性因子HNF-1都是激活乙肝病毒启动子转录所必需的。

The ubiquitous transcription factor Oct-1 and the liver-specific factor HNF-1 are both required to activate transcription of a hepatitis B virus promoter.

作者信息

Zhou D X, Yen T S

机构信息

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

出版信息

Mol Cell Biol. 1991 Mar;11(3):1353-9. doi: 10.1128/mcb.11.3.1353-1359.1991.

DOI:10.1128/mcb.11.3.1353-1359.1991
PMID:1996097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC369406/
Abstract

The liver-specific transcription factor HNF-1 activates transcription of several mammalian hepatocyte-specific genes. The hepatitis B virus preS1 promoter shows hepatocyte specificity, which has been ascribed to binding of HNF-1 to a cognate DNA sequence upstream of the TATA box. We show here that there is an adjacent site that binds the ubiquitous transcription factor Oct-1. Both the Oct-1 and HNF-1 sites are necessary for liver-specific transcription of the preS1 promoter, but neither site alone activates transcription. The Oct-1 site is also necessary for activation of the preS1 promoter in HeLa cells, expressing transfected HNF-1. Our results show that while Oct-1 is not restricted to hepatocytes, it nevertheless can play a critical role in the expression of a liver-specific gene.

摘要

肝脏特异性转录因子HNF-1可激活多种哺乳动物肝细胞特异性基因的转录。乙肝病毒前S1启动子具有肝细胞特异性，这归因于HNF-1与TATA框上游同源DNA序列的结合。我们在此表明存在一个相邻位点，可结合普遍存在的转录因子Oct-1。Oct-1和HNF-1位点对于前S1启动子的肝脏特异性转录都是必需的，但单独任何一个位点都不能激活转录。Oct-1位点对于在表达转染HNF-1的HeLa细胞中激活前S1启动子也是必需的。我们的结果表明，虽然Oct-1并不局限于肝细胞，但它仍可在肝脏特异性基因的表达中发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/6f89cf49e027/molcellb00166-0184-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/d38d7730a24b/molcellb00166-0181-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/e767a4948337/molcellb00166-0182-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/44c0a7499873/molcellb00166-0182-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/df2886ead8ab/molcellb00166-0183-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/6f89cf49e027/molcellb00166-0184-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/d38d7730a24b/molcellb00166-0181-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/e767a4948337/molcellb00166-0182-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/44c0a7499873/molcellb00166-0182-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/df2886ead8ab/molcellb00166-0183-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/369406/6f89cf49e027/molcellb00166-0184-a.jpg

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本文引用的文献

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用于研究乙型肝炎病毒复制周期、发病机制和药理学进展的模型的未来发展
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