Polypyrimidine tract binding protein inhibits the function of HBV posttranscriptional regulatory element

程丽英; 万涛; 黄婷婷; 蔡雪飞; 张文露; 黄爱龙; 汤华

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Polypyrimidine tract binding protein inhibits the function of HBV posttranscriptional regulatory element

更新时间：2026-01-09

- Polypyrimidine tract binding protein inhibits the function of HBV posttranscriptional regulatory element
- Journal of Army Medical University Vol. 31, Issue 15, Pages: 1440-1442(2009)
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  CLC： R373.21;R394-33;R394.3
- Published：2009
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程丽英,万涛,黄婷婷,蔡雪飞,张文露,黄爱龙,汤华.多聚嘧啶序列结合蛋白抑制HBV转录后调节元件的功能[J].陆军军医大学学报(原第三军医大学学报),2009,31(15):1440-1442.

　CHENG Li-ying,WAN Tao,HUANG Ting-ting,CAI Xue-fei,ZHANG Wen-lu,HUANG Ai-long,TANG Hua.Polypyrimidine tract binding protein inhibits the function of HBV posttranscriptional regulatory element[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(15):1440-1442.
程丽英,万涛,黄婷婷,蔡雪飞,张文露,黄爱龙,汤华.多聚嘧啶序列结合蛋白抑制HBV转录后调节元件的功能[J].陆军军医大学学报(原第三军医大学学报),2009,31(15):1440-1442. DOI：

　CHENG Li-ying,WAN Tao,HUANG Ting-ting,CAI Xue-fei,ZHANG Wen-lu,HUANG Ai-long,TANG Hua.Polypyrimidine tract binding protein inhibits the function of HBV posttranscriptional regulatory element[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(15):1440-1442. DOI：

摘要

目的探讨多聚嘧啶序列结合蛋白(polypyrimidine tract binding protein，PTB)对乙型肝炎病毒转录后调节元件（HBV posttranscriptional regulatory element，HPRE）功能的影响。方法采用pDM138-HPRE CAT（chloramphenicol acetyl transferase）报告体系，通过质粒瞬时转染细胞的方式来探讨PTB对HPRE功能的影响。结果 CAT 活性检测表明：PTB的过表达使HPRE介导的CAT表达活性下降，并且呈剂量依赖性。当去除质粒上游剪接供体位点时，PTB仍然可以降低CAT的活性。结论 PTB抑制HPRE的功能，并且这种抑制作用不依赖于上游剪接供体位点。

Abstract

Objective To investigate the effects of polypyrimidine tract binding protein (PTB) on HBV posttranscriptional regulatory element (HPRE). Methods The chloramphenicol acetyl transferase (CAT) expression plasmid pDM138-HPRE system was used. Transient co-transfection was adopted to identify the roles of PTB in HPRE-regulated gene expression. Results Functional analysis indicated that PTB could inhibit HPRE function in pDM138-HPRE CAT assay system in a dose-dependent manner. PTB could also depress CAT activity when upstream splice donor site was deleted. Conclusion PTB can inhibit the function of HPRE

and this inhibition is independent on upstream splice donor site.

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