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AGO介导的翻译抑制(及激活)。

Argonaute-mediated translational repression (and activation).

作者信息

Iwasaki Shintaro, Tomari Yukihide

机构信息

Institute of Molecular and Cellular Biosciences and Department of Medical Genome Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.

出版信息

Fly (Austin). 2009 Jul-Sep;3(3):204-6. Epub 2009 Jul 14.

Abstract

MicroRNAs (miRNAs) downregulate the expression of their target genes by inducing translational repression and/or mRNA decay. Under specific conditions, miRNAs can even activate translation of their target mRNAs. These processes occur via miRNA-protein complexes, or RNA-induced silencing complexes (RISCs), which contain Argonaute (Ago) subfamily protein as a core component. However, detailed mechanisms of miRNA-mediated translational regulation remain unclear. We recently reported that, in Drosophila, both of the two Ago proteins, Ago1 and Ago2, can repress translation of the target mRNAs, but by remarkably different mechanisms. Furthermore, we here show that Ago2, but not Ago1, can activate translation of the target mRNAs when they lack the poly(A) tail, suggesting that the length of poly(A) tail is an important determinant for the consequences of Ago2 function. This review focuses on how miRNAs regulate translation in light of these new findings.

摘要

微小RNA(miRNA)通过诱导翻译抑制和/或mRNA降解来下调其靶基因的表达。在特定条件下,miRNA甚至可以激活其靶mRNA的翻译。这些过程通过miRNA-蛋白质复合物或RNA诱导沉默复合物(RISC)发生,其中包含Argonaute(Ago)亚家族蛋白作为核心成分。然而,miRNA介导的翻译调控的详细机制仍不清楚。我们最近报道,在果蝇中,两种Ago蛋白Ago1和Ago2都可以抑制靶mRNA的翻译,但机制明显不同。此外,我们在此表明,当靶mRNA缺乏聚腺苷酸(poly(A))尾时,Ago2而非Ago1可以激活其翻译,这表明poly(A)尾的长度是Ago2功能结果的重要决定因素。本综述根据这些新发现重点探讨miRNA如何调控翻译。

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