首页> 美国卫生研究院文献>Journal of Virology >Replication-dependent activation of the adenovirus major late promoter is mediated by the increased binding of a transcription factor to sequences in the first intron.
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Replication-dependent activation of the adenovirus major late promoter is mediated by the increased binding of a transcription factor to sequences in the first intron.

机译:腺病毒主要晚期启动子的复制依赖性激活是由转录因子与第一个内含子中序列的结合增加所介导的。

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摘要

During lytic infection, the adenovirus major late promoter (MLP) is primarily activated after the onset of viral DNA replication. Using a combination of DNA binding and in vitro transcription assays, we delineated a discrete MLP element spanning positions +80 to +106 which is essential for the replication-dependent activation of this promoter. We also identified a 40-kilodalton protein (the downstream element factor [DEF]) which binds to the +86-TTGTCAGTTT-+95 motif within this element. Whereas the DEF-binding activity is barely detectable in uninfected cells, it is readily visualized in adenovirus-infected cells, but only after the onset of viral DNA replication. Preventing the interaction of DEF with the MLP template impairs the in vitro transcriptional stimulation. We conclude that this replication-dependent activation of the MLP is, at least in part, mediated by induction of the specific binding of DEF to the MLP downstream element.
机译:在裂解感染过程中,病毒DNA复制开始后,腺病毒主要晚期启动子(MLP)会首先被激活。通过结合使用DNA结合和体外转录测定,我们描绘了一个跨度在+80至+106位置的离散MLP元件,这对于该启动子的复制依赖性激活至关重要。我们还鉴定了一个40公斤的蛋白质(下游元素因子[DEF]),该蛋白与该元素内的+ 86-TTGTCAGTTT- + 95基序结合。尽管在未感染的细胞中几乎无法检测到DEF结合活性,但在腺病毒感染的细胞中很容易观察到它,但仅在病毒DNA复制开始后才可见。阻止DEF与MLP模板的相互作用会损害体外转录刺激。我们得出结论,MLP的这种复制依赖性激活至少部分地通过诱导DEF与MLP下游元件的特异性结合而介导。

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