Suñé C, Garcia-Blanco M A
Departments of Pharmacology and Cancer Biology, Levine Science Research Center, Duke University Medical Center, Durham, North Carolina 27710, USA.
Mol Cell Biol. 1999 Jul;19(7):4719-28. doi: 10.1128/MCB.19.7.4719.
Tat protein strongly activates transcription from the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR) by enhancing the elongation efficiency of RNA polymerase II complexes. Tat-mediated transcriptional activation requires cellular cofactors and specific cis-acting elements within the HIV-1 promoter, among them a functional TATA box. Here, we have investigated the mechanism by which one of these cofactors, termed CA150, regulates HIV-1 transcription in vivo. We present a series of functional assays that demonstrate that the regulation of the HIV-1 LTR by CA150 has the same functional requirements as the activation by Tat. We found that CA150 affects elongation of transcription complexes assembled on the HIV-1 promoter in a TATA-box-dependent manner. We discuss the data in terms of the involvement of CA150 in the regulation of Tat-activated HIV-1 gene expression. In addition, we also provide evidence suggesting a role for CA150 in the regulation of cellular transcriptional processes.
Tat蛋白通过提高RNA聚合酶II复合物的延伸效率,强烈激活人类免疫缺陷病毒1型(HIV-1)长末端重复序列(LTR)的转录。Tat介导的转录激活需要细胞辅助因子以及HIV-1启动子内的特定顺式作用元件,其中包括一个功能性TATA框。在此,我们研究了其中一种名为CA150的辅助因子在体内调节HIV-1转录的机制。我们展示了一系列功能测定,证明CA150对HIV-1 LTR的调节与Tat激活具有相同的功能要求。我们发现CA150以TATA框依赖的方式影响在HIV-1启动子上组装的转录复合物的延伸。我们根据CA150参与Tat激活的HIV-1基因表达调节来讨论这些数据。此外,我们还提供了证据表明CA150在细胞转录过程的调节中发挥作用。