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The hepatitis B virus post-transcriptional regulatory element contains two conserved RNA stem-loops which are required for function.

机译:乙型肝炎病毒转录后调控元件包含两个保守的RNA茎环,这是功能所必需的。

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摘要

Human Hepatitis B Virus (HBV) RNAs contain a cis -acting sequence, the post-transcriptional regulatory element (HPRE), which facilitates the cytoplasmic localization of intronless transcripts. Our previous studies have shown that the HPRE is composed of at least two independent sub-elements, HPREalpha and HPREbeta, which co-activate a reporter for RNA export in a greater than additive manner. Utilizing deletion, mutation and co-variational analyses, we have identified three regions important for full HPRE activity. The three separate regions of the HPRE function can function independently in a dose-dependent manner when multimerized. Two of these regions contain stem loops, HSLalpha and HSLbeta1, which are necessary for full HPRE function. These structures are conserved throughout the mammalian Hepadnaviruses. Disruption of either stem-loop structure by mutagenesis decreases HPRE function while compensatory mutations restore activity. The location of the stem-loops in the genome reveal that they are present in all of the HBV transcripts. HSLalpha and HSLbeta1 are likely to contain the binding sites for the cellular factor(s) which mediates HPRE function.
机译:人乙型肝炎病毒(HBV)RNA包含顺式作用序列,即转录后调控元件(HPRE),可促进无内含子转录本的细胞质定位。我们以前的研究表明,HPRE由至少两个独立的子元素HPREalpha和HPREbeta组成,它们以大于加成的方式共同激活RNA输出的报告基因。利用删除,突变和协变分析,我们已经确定了三个对于完整HPRE活动很重要的区域。当进行多聚时,HPRE功能的三个独立区域可以以剂量依赖的方式独立发挥作用。这些区域中的两个包含茎环HSLalpha和HSLbeta1,这是完整HPRE功能所必需的。这些结构在整个哺乳动物嗜肝DNA病毒中都是保守的。诱变破坏任一茎环结构会降低HPRE功能,而补偿性突变会恢复活性。茎环在基因组中的位置表明它们存在于所有HBV转录物中。 HSLalpha和HSLbeta1可能包含介导HPRE功能的细胞因子的结合位点。

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