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首页> 外文期刊>Nucleic Acids Research >A NUCLEAR MATRIX-SPECIFIC FACTOR THAT BINDS A SPECIFIC SEGMENT OF THE NEGATIVE REGULATORY ELEMENT (NRE) OF HIV-1 LTR AND INHIBITS NF-KAPPA-B ACTIVITY
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A NUCLEAR MATRIX-SPECIFIC FACTOR THAT BINDS A SPECIFIC SEGMENT OF THE NEGATIVE REGULATORY ELEMENT (NRE) OF HIV-1 LTR AND INHIBITS NF-KAPPA-B ACTIVITY

机译：结合特定矩阵的HIV-1 LTR负调节元素（NRE）和抑制NF-KAPPA-B活性的核矩阵因子

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摘要

The negative regulatory element (NRE) of human immunodeficiency virus type-1 (HIV-1) long terminal repeat (LTR) is a defined region that has been reported to downregulate LTR-directed HIV gene expression, However, information on the precise role of this region in regulating HIV gene transcription is lacking. We have investigated the possibility that these NRE sequences regulate HIV transcription by a mechanism mediated through a nuclear matrix-specific DNA-protein interaction. We find a nuclear matrix attachment region (MAR) present within the NRE of the HIV-1 LTR that recognizes a sequence-specific DNA-binding protein present in the nuclear matrix of HIV infected cells. Moreover, we also show that the purified DNA-binding nuclear matrix protein (NMP) specifically represses the DNA-binding activity of NF-kappa B. It is likely that the MAR and MAR-enriched specific DNA-binding NMP are brought into juxtaposition by the non-chromatin scaffolding of the nucleus, thus influencing NF-kappa B (and other nuclear proteins) DNA-binding activity through protein-protein and protein-DNA interactions. Our data suggest that one possible role of the NRE could be to act as a matrix attachment site in the nuclear matrix, thus, allowing interaction with a sequence-specific trans-acting factor. The negative effect on NF-kappa B activity due to this MAR-NMP-specific interaction provides a mechanism by which the NRE downregulates HIV gene expression.
机译：人类免疫缺陷病毒1型（HIV-1）长末端重复序列（LTR）的负调控元件（NRE）是一个已定义的区域，据报道它会下调LTR导向的HIV基因表达。缺乏调节HIV基因转录的区域。我们已经研究了这些NRE序列通过核基质特异性DNA-蛋白质相互作用介导的机制调节HIV转录的可能性。我们发现在HIV-1 LTR的NRE中存在一个核基质附着区（MAR），该区域识别存在于HIV感染细胞的核基质中的序列特异性DNA结合蛋白。此外，我们还表明，纯化的DNA结合核基质蛋白（NMP）特异性抑制NF-κB的DNA结合活性。MAR和MAR富集的特定DNA结合NMP可能通过并置而并置。核的非染色质支架，从而通过蛋白质-蛋白质和蛋白质-DNA相互作用影响NF-κB（和其他核蛋白质）的DNA结合活性。我们的数据表明，NRE的一种可能作用可能是充当核基质中的基质附着位点，从而允许与序列特异性反式作用因子相互作用。由于这种MAR-NMP特异性相互作用而对NF-κB活性的负面影响提供了一种机制，通过该机制NRE下调HIV基因表达。

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