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人类1型T细胞白血病病毒tax蛋白对RNA聚合酶III依赖性基因的转录激活作用。

Transcriptional activation of RNA polymerase III-dependent genes by the human T-cell leukemia virus type 1 tax protein.

作者信息

Gottesfeld J M, Johnson D L, Nyborg J K

机构信息

Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA.

出版信息

Mol Cell Biol. 1996 Apr;16(4):1777-85. doi: 10.1128/MCB.16.4.1777.

Abstract

The human T-cell leukemia virus-encoded tax protein is a potent activator of many viral and cellular genes transcribed by RNA polymerase II. We find that both chromatin and cell extracts derived from human T-cell leukemia virus type 1-infected human T lymphocytes support higher levels of 5S rRNA and tRNA gene transcription than chromatin or extracts from uninfected T lymphocytes. The viral protein Tax was likely responsible for this higher level of class II gene transcription, as purified Tax was found to stimulate both genes when added to the uninfected cell extract or in reconstituted systems. Both limiting-component transcription assays and DNA binding assays identified the class III gene transcription factor TFIIIB as the principle target of Tax activity. Surprisingly, we find that Tax increases the effective concentration of active TFIIIB molecules. These data suggest that Tax stimulates RNA polymerase III-dependent gene expression by accelerating the rate and/or extent of transcription initiation complex assembly.

摘要

人类T细胞白血病病毒编码的Tax蛋白是由RNA聚合酶II转录的许多病毒和细胞基因的有效激活剂。我们发现,来自1型人类T细胞白血病病毒感染的人类T淋巴细胞的染色质和细胞提取物比未感染的T淋巴细胞的染色质或提取物支持更高水平的5S rRNA和tRNA基因转录。病毒蛋白Tax可能是造成这种II类基因转录水平较高的原因,因为当添加到未感染的细胞提取物中或在重组系统中时,纯化的Tax被发现可刺激这两种基因。有限成分转录分析和DNA结合分析均确定III类基因转录因子TFIIIB是Tax活性的主要靶点。令人惊讶的是,我们发现Tax增加了活性TFIIIB分子的有效浓度。这些数据表明,Tax通过加速转录起始复合物组装的速率和/或程度来刺激RNA聚合酶III依赖性基因表达。

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