Maekawa T, Sudo T, Kurimoto M, Ishii S
Laboratory of Molecular Genetics, RIKEN, Ibaraki, Japan.
Nucleic Acids Res. 1991 Sep 11;19(17):4689-94. doi: 10.1093/nar/19.17.4689.
The transcription factor HIV-TF1, which binds to a region about 60 bp upstream from the enhancer of the human immunodeficiency virus-1 (HIV-1), was purified from human B cells. HIV-TF1 had a molecular weight of 39,000. Binding of HIV-TF1 to the HIV long terminal repeat (LTR) activated transcription from the HIV promoter in vitro. The HIV-TF1-binding site in HIV LTR was similar to the site recognized by upstream stimulatory factor (USF) in the adenovirus major late promoter. DNA-binding properties of HIV-TF1 suggested that HIV-TF1 might be identical or related to USF. Interestingly, treatment of purified HIV-TF1 by phosphatase greatly reduced its DNA-binding activity, suggesting that phosphorylation of HIV-TF1 was essential for DNA binding. The disruption of HIV-TF1-binding site induced a 60% decrease in the level of transcription from the HIV promoter in vivo. These results suggest that HIV-TF1 is involved in transcriptional regulation of HIV-1.
转录因子HIV-TF1是从人B细胞中纯化出来的,它能与人免疫缺陷病毒1型(HIV-1)增强子上游约60个碱基对的区域结合。HIV-TF1的分子量为39,000。HIV-TF1与HIV长末端重复序列(LTR)的结合在体外激活了HIV启动子的转录。HIV LTR中HIV-TF1的结合位点类似于腺病毒主要晚期启动子中上游刺激因子(USF)识别的位点。HIV-TF1的DNA结合特性表明HIV-TF1可能与USF相同或相关。有趣的是,用磷酸酶处理纯化的HIV-TF1会大大降低其DNA结合活性,这表明HIV-TF1的磷酸化对于DNA结合至关重要。HIV-TF1结合位点的破坏导致体内HIV启动子转录水平下降60%。这些结果表明HIV-TF1参与了HIV-1的转录调控。