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首页> 外文期刊>Molecular and Cellular Biology >NF-κB-Repressing Factor Inhibits Elongation of Human Immunodeficiency Virus Type 1 Transcription by DRB Sensitivity-Inducing Factor
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NF-κB-Repressing Factor Inhibits Elongation of Human Immunodeficiency Virus Type 1 Transcription by DRB Sensitivity-Inducing Factor

机译：NF-κB阻遏因子抑制人类免疫缺陷病毒1型转录的DRB敏感性诱导因子的延长。

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Human immunodeficiency virus type 1 (HIV-1) is able to establish a latent infection during which the integrated provirus remains transcriptionally silent. In response to specific stimuli, the HIV-1 long terminal repeat (LTR) is highly activated, enhancing both transcriptional initiation and elongation. Here, we have identified a specific binding sequence of the nuclear NF-κB-repressing factor (NRF) within the HIV-1 LTR. The aim of this work was to define the role of NRF in regulating the LTR. Our data show that the endogenous NRF is required for transcriptional activation of the HIV-1 LTR in stimulated cells. In unstimulated cells, however, NRF inhibits HIV-1 LTR activity at the level of transcription elongation. Binding of NRF to the LTR in unstimulated cells prevents recruitment of elongation factor DRB sensitivity-inducing factor and formation of processive elongation complexes by hyperphosphorylated RNA polymerase II. Our data suggest that NRF interrupts the regulatory coupling of LTR binding factors and transcription elongation events. This inhibitory mechanism might contribute to transcriptional quiescence of integrated HIV-1 provirus.
机译：1型人类免疫缺陷病毒（HIV-1）能够建立潜伏感染，在此期间整合的原病毒仍保持转录沉默。响应特定刺激，HIV-1长末端重复序列（LTR）被高度激活，从而增强转录起始和延伸。在这里，我们已经确定了HIV-1 LTR中核NF-κB阻遏因子（NRF）的特异性结合序列。这项工作的目的是确定NRF在调节LTR中的作用。我们的数据表明内源性NRF是受刺激细胞中HIV-1 LTR转录激活所必需的。然而，在未刺激的细胞中，NRF在转录延伸水平抑制HIV-1 LTR活性。 NRF与未刺激细胞中LTR的结合可防止过度磷酸化RNA聚合酶II募集延伸因子DRB敏感性诱导因子和形成持续性延伸复合物。我们的数据表明NRF中断LTR结合因子和转录延伸事件的调节耦合。这种抑制机制可能有助于整合的HIV-1前病毒的转录静止。

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