REPRESSION OF HIV-1 TRANSCRIPTION BY A CELLULAR PROTEIN
REPRESSION OF HIV-1 TRANSCRIPTION BY A CELLULAR PROTEIN
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DOI：
10.1126/science.2006421
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发表时间：
1991-03-22
期刊：
影响因子：
56.9
通讯作者：
ROEDER, RG
中科院分区：
文献类型：
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作者：
KATO, H;HORIKOSHI, M;ROEDER, RG
细胞DNA结合蛋白LBP-1以浓度依赖的方式与人类免疫缺陷病毒1型(HIV-1)启动子转录起始点周围的两个位点顺序相互作用。虽然下游位点(位点I)的序列被发现促进转录，但纯化的LBP-1在体外通过与上游位点(位点II)结合而特异性地抑制转录，上游位点与TATA元件重叠。在LBP-1之前，人TATA结合因子(TFIID)与启动子的结合阻断了抑制，表明抑制是由于TFIID与TATA元件结合的抑制。此外，消除与第二位点结合的突变既防止了体外抑制，又增加了稳定转化细胞中HIV-1的转录。这些发现表明，一种细胞因子以细菌抑制物特有的方式调节HIV-1的转录，并且该因子可能在HIV-1潜伏期中起重要作用。
A cellular DNA binding protein, LBP-1, sequentially interacts in a concentration-dependent manner with two sites that surround the transcriptional initiation site of the human immunodeficiency virus type 1 (HIV-1) promoter. Although sequences in the downstream site (site I) were found to enhance transcription, purified LBP-1 specifically repressed transcription in vitro by binding to the upstream site (site II), which overlaps the TATA element. The binding of human TATA binding factor (TFIID) to the promoter before LBP-1 blocked repression, suggesting that repression resulted from an inhibition of TFIID binding to the TATA element. Furthermore, mutations that eliminated binding to site II both prevented repression in vitro and increased HIV-1 transcription in stably transformed cells. These findings suggest that a cellular factor regulates HIV-1 transcription in a manner that is characteristic of bacterial repressors and that this factor could be important in HIV-1 latency.