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人T细胞白血病病毒1型反义转录受病毒tax蛋白上调。

Upregulation of human T-cell leukemia virus type 1 antisense transcription by the viral tax protein.

作者信息

Landry Sébastien, Halin Marilène, Vargas Amandine, Lemasson Isabelle, Mesnard Jean-Michel, Barbeau Benoit

机构信息

Université du Québec à Montréal, Département des Sciences Biologiques, Centre de recherche BioMed, Montréal, Québec, Canada.

出版信息

J Virol. 2009 Feb;83(4):2048-54. doi: 10.1128/JVI.01264-08. Epub 2008 Dec 10.

DOI:10.1128/JVI.01264-08
PMID:19073733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2643783/
Abstract

Several studies have recently demonstrated the existence of human T-cell leukemia virus type 1 (HTLV-1) antisense transcripts, which allow the synthesis of the newly described HBZ protein. Although previous reports have been aimed at understanding the potential role of the HBZ protein in HTLV-1 pathogenesis, little is known as to how this viral gene is regulated. Here, using our K30-3'asLuc reporter construct, we show that the viral Tax protein upregulates antisense transcription through its action on the TRE sequences located in the 3' long terminal repeat. Generation of stable clones in 293T cells demonstrated that Tax-induced HBZ expression is importantly influenced by the integration site in the host genome. The cellular DNA context could thus affect the level of HBZ mRNA expression in infected cells.

摘要

最近的几项研究证实了1型人类T细胞白血病病毒(HTLV-1)反义转录本的存在,该转录本可合成新发现的HBZ蛋白。尽管此前的报道旨在了解HBZ蛋白在HTLV-1发病机制中的潜在作用,但对于该病毒基因是如何调控的却知之甚少。在此,我们使用K30-3'asLuc报告基因构建体表明,病毒Tax蛋白通过作用于位于3'长末端重复序列中的TRE序列上调反义转录。在293T细胞中产生稳定克隆表明,Tax诱导的HBZ表达受到宿主基因组整合位点的重要影响。因此,细胞DNA环境可能会影响受感染细胞中HBZ mRNA的表达水平。

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The coactivators CBP/p300 and the histone chaperone NAP1 promote transcription-independent nucleosome eviction at the HTLV-1 promoter.共激活因子CBP/p300和组蛋白伴侣NAP1促进人嗜T淋巴细胞病毒1型(HTLV-1)启动子处的转录非依赖性核小体排除。
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