NF45 and NF90 Bind HIV-1 RNA and Modulate HIV Gene Expression.
NF45 and NF90 Bind HIV-1 RNA and Modulate HIV Gene Expression.
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DOI：
10.3390/v8020047
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发表时间：
2016-02-16
期刊：
影响因子：
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通讯作者：
Belshan M
中科院分区：
文献类型：
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作者：
Li Y;Belshan M
先前在我们实验室进行的蛋白质组学筛选发现核因子45 （NF45）和核因子90 （NF90）是参与人类免疫缺陷病毒1型（HIV-1）复制的潜在细胞因子。两者都是调节基因表达的RNA结合蛋白；NF90已被证明可以调节细胞周期蛋白T1的表达，而细胞周期蛋白T1是tat依赖性病毒基因表达反式激活所必需的。本研究通过过表达研究NF45和NF90在HIV复制中的作用。任何一个因子的异位表达增强了HIV感染、基因表达和病毒产生。NF45和NF90 RNA结合域的缺失减弱了HIV感染和基因表达的增强。这两种蛋白质都被发现与HIV RNA相互作用。RNA衰变实验表明NF90而非NF45延长了HIV RNA的半衰期。总的来说，这些研究表明NF45和NF90都通过它们的RNA结合域增强了HIV感染。
A previous proteomic screen in our laboratory identified nuclear factor 45 (NF45) and nuclear factor 90 (NF90) as potential cellular factors involved in human immunodeficiency virus type 1 (HIV-1) replication. Both are RNA binding proteins that regulate gene expression; and NF90 has been shown to regulate the expression of cyclin T1 which is required for Tat-dependent trans-activation of viral gene expression. In this study the roles of NF45 and NF90 in HIV replication were investigated through overexpression studies. Ectopic expression of either factor potentiated HIV infection, gene expression, and virus production. Deletion of the RNA binding domains of NF45 and NF90 diminished the enhancement of HIV infection and gene expression. Both proteins were found to interact with the HIV RNA. RNA decay assays demonstrated that NF90, but not NF45, increased the half-life of the HIV RNA. Overall, these studies indicate that both NF45 and NF90 potentiate HIV infection through their RNA binding domains.