Tanaka T, Nakamura T, Takagi H, Sato M
First Department of Anatomy, Osaka City University Medical School, Japan.
Biochem Biophys Res Commun. 1997 Oct 9;239(1):176-81. doi: 10.1006/bbrc.1997.7447.
The human immunodeficiency virus-1 (HIV-1) protein Tat, encoded by one of the HIV regulatory genes, tat, is reported to be essential for HIV gene expression and replication in infected cells. Observations suggest that several cellular factors cooperate with Tat in this process. Tat binding protein-1 (TBP-1) is reported to be one such cellular factor that specifically suppresses Tat-mediated transactivation of HIV replication in vitro. Here we have cloned a novel factor, TBP-1 interacting protein (TBPIP) from the mouse, which interacts with mouse TBP-1. TBPIP contains several kinase phosphorylation sites and co-localizes with TBP-1 in vivo. The fact that Tat activity is altered synergistically by the TBP-1 and an additional TBP-1 binding protein has not been reported before. We provide evidence that expression of TBPIP enhances the inhibitory action of TBP-1 on Tat-mediated transactivation in vitro. Our results suggest that TBPIP may have a key role in suppressing the Tat-mediated transactivation.
人类免疫缺陷病毒1型(HIV-1)的tat基因是HIV的调控基因之一,该基因编码的Tat蛋白据报道对HIV在受感染细胞中的基因表达和复制至关重要。有观察表明,在此过程中有几种细胞因子与Tat协同作用。据报道,Tat结合蛋白-1(TBP-1)就是这样一种细胞因子,它在体外能特异性抑制Tat介导的HIV复制反式激活。在此,我们从小鼠中克隆了一种新的因子,即TBP-1相互作用蛋白(TBPIP),它能与小鼠TBP-1相互作用。TBPIP含有多个激酶磷酸化位点,且在体内与TBP-1共定位。之前尚未报道过Tat活性会被TBP-1和另一种TBP-1结合蛋白协同改变。我们提供的证据表明,TBPIP的表达增强了TBP-1在体外对Tat介导的反式激活的抑制作用。我们的结果表明,TBPIP可能在抑制Tat介导的反式激活中起关键作用。