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首页> 外文期刊>Molecular and Cellular Biology >Transcriptional activation of RNA polymerase III-dependent genes by the human T-cell leukemia virus type 1 tax protein.
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Transcriptional activation of RNA polymerase III-dependent genes by the human T-cell leukemia virus type 1 tax protein.

机译:人类T细胞白血病病毒1型税收蛋白对RNA聚合酶III依赖性基因的转录激活。

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摘要

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.
机译:人类T细胞白血病病毒编码的税收蛋白是RNA聚合酶II转录的许多病毒和细胞基因的有效激活剂。我们发现染色质和源自人类T细胞白血病病毒1型感染的人类T淋巴细胞的细胞提取物均支持比染色质或未感染T淋巴细胞的提取物更高水平的5S rRNA和tRNA基因转录。病毒蛋白Tax可能是导致较高水平的II类基因转录的原因,因为发现纯化的Tax加入到未感染的细胞提取物或重组系统中后会刺激两个基因。限制性成分转录测定法和DNA结合测定法均将III类基因转录因子TFIIIB鉴定为Tax活性的主要靶标。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通过加快转录起始复合物装配的速度和/或程度来刺激RNA聚合酶III依赖性基因的表达。

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