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The HIV-1 Tat protein enhances megakaryocytic commitment of K562 cells by facilitating CREB transcription factor coactivation by CBP.HIV-1反式激活蛋白通过促进CBP对CREB转录因子的共激活作用,增强K562细胞向巨核细胞的定向分化。
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灵长类逆转录病毒与人类RNA干扰机制的相互作用分析。

Analysis of the interaction of primate retroviruses with the human RNA interference machinery.

作者信息

Lin Jennifer, Cullen Bryan R

机构信息

Center for Virology, Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.

出版信息

J Virol. 2007 Nov;81(22):12218-26. doi: 10.1128/JVI.01390-07. Epub 2007 Sep 12.

DOI:10.1128/JVI.01390-07
PMID:17855543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2169020/
Abstract

The question of whether retroviruses, including human immunodeficiency virus type 1 (HIV-1), interact with the cellular RNA interference machinery has been controversial. Here, we present data showing that neither HIV-1 nor human T-cell leukemia virus type 1 (HTLV-1) expresses significant levels of either small interfering RNAs or microRNAs in persistently infected T cells. We also demonstrate that the retroviral nuclear transcription factors HIV-1 Tat and HTLV-1 Tax, as well as the Tas transactivator encoded by primate foamy virus, fail to inhibit RNA interference in human cells. Moreover, the stable expression of physiological levels of HIV-1 Tat did not globally inhibit microRNA production or expression in infected human cells. Together, these data argue that HIV-1 and HTLV-1 neither induce the production of viral small interfering RNAs or microRNAs nor repress the cellular RNA interference machinery in infected cells.

摘要

包括1型人类免疫缺陷病毒(HIV-1)在内的逆转录病毒是否与细胞RNA干扰机制相互作用这一问题一直存在争议。在此,我们展示的数据表明,无论是HIV-1还是1型人类T细胞白血病病毒(HTLV-1),在持续感染的T细胞中都不会表达显著水平的小干扰RNA或微小RNA。我们还证明,逆转录病毒核转录因子HIV-1 Tat和HTLV-1 Tax,以及灵长类泡沫病毒编码的Tas反式激活因子,均无法在人类细胞中抑制RNA干扰。此外,生理水平的HIV-1 Tat的稳定表达并不会在受感染的人类细胞中全面抑制微小RNA的产生或表达。总之,这些数据表明,HIV-1和HTLV-1在受感染细胞中既不会诱导病毒小干扰RNA或微小RNA的产生,也不会抑制细胞RNA干扰机制。