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人乳头瘤病毒16型E7蛋白可补充5型腺病毒E1A氨基末端依赖性的5型腺病毒早期基因反式激活作用,并增加ATF和Oct-1的DNA结合活性。

The human papillomavirus type 16 E7 protein complements adenovirus type 5 E1A amino-terminus-dependent transactivation of adenovirus type 5 early genes and increases ATF and Oct-1 DNA binding activity.

作者信息

Wong H K, Ziff E B

机构信息

Department of Biochemistry, Howard Hughes Medical Institute, Kaplan Cancer Center, New York University School of Medicine, New York 10016, USA.

出版信息

J Virol. 1996 Jan;70(1):332-40. doi: 10.1128/JVI.70.1.332-340.1996.

Abstract

We have previously shown that conserved region 1 (CR1) of the adenovirus type 5 (Ad5) E1A protein synergizes with CR3 in the transactivation of Ad5 early genes (H.K. Wong and E. B. Ziff, J. Virol. 68:4910-4920, 1994). CR1 lies within the E1A amino terminus and binds host regulatory proteins such as the RB protein, p107, p130, and p300. Since simian virus 40 (SV40) large T antigen and human papillomavirus type 16 (HPV16) E7 protein also bind host regulatory factors, we investigated whether these viral proteins can complement E1A mutants which are defective in early gene activation. We show that the HPV16 E7 protein but not SV40 T antigen can complement mutations in the Ad5 E1A CR1 in the transactivation of viral early promoters. The inability of SV40 T antigen to complement suggests that RB binding on its own is not sufficient for early promoter transactivation by the E1A amino terminus. Nuclear runoff assays show that complementation by HPV16 E7 restores the ability of the E1A mutants to stimulate early gene expression at the level of transcription. Furthermore, nuclear extracts from the E7-transformed cells show increased binding activity of ATF and Oct-1, factors that can recognize the elements of Ad5 early genes, consistent with gene activation by E1A and E7 at the transcriptional level.

摘要

我们之前已经表明,腺病毒5型(Ad5)E1A蛋白的保守区域1(CR1)与CR3协同作用,可反式激活Ad5早期基因(H.K. Wong和E.B. Ziff,《病毒学杂志》68:4910 - 4920,1994年)。CR1位于E1A氨基末端,可结合宿主调节蛋白,如RB蛋白、p107、p130和p300。由于猴病毒40(SV40)大T抗原和人乳头瘤病毒16型(HPV16)E7蛋白也结合宿主调节因子,我们研究了这些病毒蛋白是否能互补在早期基因激活方面存在缺陷的E1A突变体。我们发现,HPV16 E7蛋白而非SV40 T抗原能够在病毒早期启动子的反式激活中互补Ad5 E1A CR1中的突变。SV40 T抗原无法互补表明,仅RB结合不足以使E1A氨基末端反式激活早期启动子。核转录分析表明,HPV16 E7的互补作用恢复了E1A突变体在转录水平刺激早期基因表达的能力。此外,来自E7转化细胞的核提取物显示,ATF和Oct - 1的结合活性增加,这两种因子能够识别Ad5早期基因的元件,这与E1A和E7在转录水平的基因激活作用一致。

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