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人类免疫缺陷病毒的反式激活通过一种双峰机制发生。

Trans-activation of human immunodeficiency virus occurs via a bimodal mechanism.

作者信息

Cullen B R

出版信息

Cell. 1986 Sep 26;46(7):973-82. doi: 10.1016/0092-8674(86)90696-3.

Abstract

A novel, highly quantitative transient expression assay based on the human interleukin-2 (IL-2) gene was used to examine the trans-activation of the Human Immunodeficiency Virus (HIV/HTLV-III/LAV/ARV) long terminal repeat (LTR) in a range of eukaryotic cell lines. In the absence of the trans-activating viral gene product, tat-III, IL-2 transcripts specific for the HIV LTR were present in low abundance in transfected cells and showed a low translational efficiency, when compared with IL-2 mRNAs transcribed from other viral promoters. Coexpression of tat-III resulted in a marked increase in the steady state level of IL-2 mRNAs transcribed from the HIV LTR, and these mRNAs also demonstrated a specific enhancement of their translational efficiency. These results suggest a bimodal mechanism of action for tat-III in the trans-activation of HIV-specific gene expression.

摘要

一种基于人类白细胞介素-2(IL-2)基因的新型、高度定量的瞬时表达测定法,被用于检测一系列真核细胞系中人类免疫缺陷病毒(HIV/HTLV-III/LAV/ARV)长末端重复序列(LTR)的反式激活。在不存在反式激活病毒基因产物tat-III的情况下,HIV LTR特异性的IL-2转录本在转染细胞中含量较低,与从其他病毒启动子转录的IL-2 mRNA相比,其翻译效率也较低。tat-III的共表达导致从HIV LTR转录的IL-2 mRNA的稳态水平显著增加,并且这些mRNA的翻译效率也有特异性增强。这些结果表明tat-III在HIV特异性基因表达的反式激活中存在双模式作用机制。

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