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小鼠微小病毒P38启动子的有效反式激活需要NS1的上游结合。

Efficient transactivation of the minute virus of mice P38 promoter requires upstream binding of NS1.

作者信息

Lorson C, Burger L R, Mouw M, Pintel D J

机构信息

Department of Molecular Microbiology and Immunology, University of Missouri School of Medicine, Columbia 65212, USA.

出版信息

J Virol. 1996 Feb;70(2):834-42. doi: 10.1128/JVI.70.2.834-842.1996.

Abstract

The P38 promoter of the autonomous parvovirus minute virus of mice is strongly transactivated by the nonstructural protein NS1, a sequence-specific DNA-binding protein. In the context of the complete viral genome, the only unique cis-acting signals required for P38 transactivation by NS1 are the proximal Sp1 site and the TATA element. In the absence of additional upstream sequences, a dependence upon the NS1 binding site within the transactivation response region is observed. Addition of synthetic NS1 binding sites to transactivation response region deletion mutants can restore the ability of NS1 to transactivate P38, and NS1 transactivation has been directly correlated to its ability to bind upstream of the P38 promoter.

摘要

小鼠自主细小病毒的P38启动子被非结构蛋白NS1强烈反式激活,NS1是一种序列特异性DNA结合蛋白。在完整病毒基因组的背景下,NS1对P38进行反式激活所需的唯一独特顺式作用信号是近端Sp1位点和TATA元件。在没有其他上游序列的情况下,观察到对反式激活反应区域内NS1结合位点的依赖性。向反式激活反应区域缺失突变体中添加合成的NS1结合位点可以恢复NS1反式激活P38的能力,并且NS1反式激活与其在P38启动子上游结合的能力直接相关。

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