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人乳头瘤病毒 16 型的早期非编码区受细胞质多聚腺苷酸化因子的调节。

The early noncoding region of human papillomavirus type 16 is regulated by cytoplasmic polyadenylation factors.

机构信息

Department of Cellular and Molecular Medicine, Panum Institute, University of Copenhagen, DK-2200 Copenhagen N, Denmark.

出版信息

Virus Res. 2010 May;149(2):217-23. doi: 10.1016/j.virusres.2010.02.001. Epub 2010 Feb 8.

Abstract

All human papillomavirus type 16 (HPV-16) early mRNAs are polyadenylated at the poly(A) signal within the early 3' untranslated region (3'UTR). The 3'end of the early E5 open reading frame and the 3'UTR of HPV-16 is very AU-rich, with five regions similar to cytoplasmic polyadenylation elements (CPEs). We show here that a fragment of the early 3'end comprising four of the five CPE-like regions when inserted downstream of a reporter gene confers regulation of the gene expression. A key protein involved in cytoplasmic polyadenylation is CPEB. We show that the human CPEB1 can repress the activity of the reporter construct containing the HPV-16 early sequences. This repression can be counteracted by a human cytoplasmic poly(A) polymerase, hGLD-2 fused to CPEB1. The hGLD-2/CPEB1 fusion protein facilitates furthermore poly(A) elongation of early HPV transcripts.

摘要

所有人类乳头瘤病毒 16 型(HPV-16)早期 mRNA 都在早期 3'非翻译区(3'UTR)内的 poly(A)信号处多聚腺苷酸化。早期 E5 开放阅读框的 3'端和 HPV-16 的 3'UTR 富含 AU,有五个类似于细胞质多聚腺苷酸化元件(CPE)的区域。我们在这里表明,当包含五个 CPE 样区域中的四个的早期 3'端片段插入报告基因的下游时,该基因可以调节基因表达。参与细胞质多聚腺苷酸化的关键蛋白是 CPEB。我们表明,人 CPEB1 可以抑制含有 HPV-16 早期序列的报告构建体的活性。这种抑制可以被与人细胞质多聚(A)聚合酶 hGLD-2 融合的 CPEB1 逆转。hGLD-2/CPEB1 融合蛋白还促进了早期 HPV 转录物的 poly(A)延伸。

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