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Beyond the 3'UTR binding-microRNA-induced protein truncation via DNA binding

  • Here, we present a miR mechanism which is active in the nucleus and is essential for the production of intron included, C-terminal truncated and biologically active proteins, like e.g. Vim3. We exemplified this mechanism by miRs, miR-15a and miR-498, which are overexpressed in clear cell renal carcinoma or oncocytoma. Both miRs directly interact with DNA in an intronic region, leading to transcriptional stop, and therefore repress the full length version of the pre-mRNA, resulting in intron included truncated proteins (Mxi-2 and Vim3). A computational survey shows that this miR:DNA interactions mechanism may be generally involved in regulating the human transcriptome, with putative interaction sites in intronic regions for over 1000 genes. In this work, an entirely new mechanism is revealed how miRs can repress full length protein translation, resulting in C-terminal truncated proteins.

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Document Type:Article
Author:Melanie von Brandenstein, Stephan H. Bernhart, Andreas Pansky, Claudia Richter, Tobias Kohl, Martina Deckert, Axel Heidenreich, Peter F. Stadler, Manuel Montesinos-Rongen, Jochen W. U. Fries
Parent Title (English):Oncotarget
First Page:32855
Last Page:32867
Publisher:Impact Journals
Publishing Institution:Hochschule Bonn-Rhein-Sieg
Date of first publication:2018/08/28
Copyright:von Brandenstein et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0)
Keyword:DNA interaction; Mxi-2; Vim3; miR-15; miR-498
Departments, institutes and facilities:Fachbereich Angewandte Naturwissenschaften
Dewey Decimal Classification (DDC):5 Naturwissenschaften und Mathematik / 57 Biowissenschaften; Biologie / 570 Biowissenschaften; Biologie
Entry in this database:2018/09/19
Licence (German):License LogoCreative Commons - CC BY - Namensnennung 3.0