Liu Y Z, Latchman D S
Department of Molecular Pathology, University College London Medical School, U.K.
Biochem J. 1997 Feb 15;322 ( Pt 1)(Pt 1):155-8. doi: 10.1042/bj3220155.
Although the HIV-1 long terminal repeat (LTR) contains four potential binding sites for the octamer-binding protein, Oct-1, which is known to interact with the HIV-1 Tat protein, the effect of the Oct-1 factor on HIV LTR-driven gene expression has not previously been reported. We show here that both Oct-1, and to a lesser extent the related Oct-2 protein, can repress both the basal activity of the HIV-1 LTR and its transactivation by Tat. These effects are still observed with an HIV LTR construct containing only a single octamer-binding site located between the TATA box and the transcriptional start site. The stronger inhibitory effect of Oct-1 on both these promoters is dependent upon its C-terminal region which cannot be effectively replaced by the equivalent region of Oct-2. These effects are discussed in terms of the regulation of HIV LTR activity in different cell types and in response to T-cell activation.
尽管HIV-1长末端重复序列（LTR）含有4个八聚体结合蛋白Oct-1的潜在结合位点，已知Oct-1可与HIV-1反式激活因子（Tat）相互作用，但此前尚未报道Oct-1因子对HIV LTR驱动的基因表达的影响。我们在此表明，Oct-1以及在较小程度上相关的Oct-2蛋白，均可抑制HIV-1 LTR的基础活性及其被Tat反式激活的活性。对于仅在TATA框和转录起始位点之间含有单个八聚体结合位点的HIV LTR构建体，仍可观察到这些效应。Oct-1对这两种启动子的更强抑制作用取决于其C末端区域，该区域不能被Oct-2的等效区域有效替代。将根据不同细胞类型中HIV LTR活性的调节以及对T细胞激活的反应来讨论这些效应。
