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鸡YB-2是一种Y盒蛋白,是禽成纤维细胞中劳斯肉瘤病毒长末端重复序列驱动转录的有效激活剂。

Chicken YB-2, a Y-box protein, is a potent activator of Rous sarcoma virus long terminal repeat-driven transcription in avian fibroblasts.

作者信息

Swamynathan S K, Nambiar A, Guntaka R V

机构信息

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

出版信息

J Virol. 1997 Apr;71(4):2873-80. doi: 10.1128/JVI.71.4.2873-2880.1997.

Abstract

We have previously reported on the cloning and characterization of chk-YB-2, a novel member of the Y-box family of proteins, that binds to the sequence 5'-GTACCACC-3' present on the noncoding strand of the Rous sarcoma virus (RSV) long terminal repeat (LTR) in a single-strand-specific manner. Here, we demonstrate that deletion or mutation of this motif not only eliminates chk-YB-2 binding in vitro but also down-regulates RSV LTR-driven transcription in avian cells. Selective abrogation of chk-YB-2 expression by using antisense oligonucleotides decreased RSV LTR-driven transcription in a promoter-specific manner. This inhibition was not observed when a reporter construct with a deletion in the chk-YB-2 binding site was used. Depletion of cellular chk-YB-2 by transfecting the cells with excess of its recognition sequence oligonucleotides also resulted in reduced transcription from the RSV LTR. Taken together, these results suggest that chk-YB-2 acts as an activator of LTR-promoted transcription in avian cells and that this activation is mediated primarily through the sequence 5'-GTACCACC-3'.

摘要

我们之前报道过chk-YB-2的克隆和特性分析,它是Y-box蛋白家族的一个新成员,能以单链特异性方式与劳斯肉瘤病毒(RSV)长末端重复序列(LTR)非编码链上的5'-GTACCACC-3'序列结合。在此,我们证明该基序的缺失或突变不仅消除了chk-YB-2在体外的结合,还下调了禽细胞中RSV LTR驱动的转录。通过使用反义寡核苷酸选择性消除chk-YB-2的表达,以启动子特异性方式降低了RSV LTR驱动的转录。当使用在chk-YB-2结合位点有缺失的报告构建体时,未观察到这种抑制作用。用过量的其识别序列寡核苷酸转染细胞来耗尽细胞中的chk-YB-2,也导致RSV LTR的转录减少。综上所述,这些结果表明chk-YB-2在禽细胞中作为LTR促进转录的激活因子,并且这种激活主要通过5'-GTACCACC-3'序列介导。

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