TY  - JOUR
U1  - Zeitschriftenartikel, wissenschaftlich - begutachtet (reviewed)
A1  - Brandenstein, Melanie von
A1  - Bernhart, Stephan H.
A1  - Pansky, Andreas
A1  - Richter, Claudia
A1  - Kohl, Tobias
A1  - Deckert, Martina
A1  - Heidenreich, Axel
A1  - Stadler, Peter F.
A1  - Montesinos-Rongen, Manuel
A1  - Fries, Jochen W. U.
T1  - Beyond the 3'UTR binding-microRNA-induced protein truncation via DNA binding
JF  - Oncotarget
N2  - 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.
KW  - Vim3
KW  - Mxi-2
KW  - miR-498
KW  - miR-15
KW  - DNA interaction
UN  - https://nbn-resolving.org/urn:nbn:de:hbz:1044-opus-40296
SN  - 1949-2553
SS  - 1949-2553
U6  - https://doi.org/10.18632/oncotarget.26023
DO  - https://doi.org/10.18632/oncotarget.26023
PM  - 30214689
VL  - 9
IS  - 67
SP  - 32855
EP  - 32867
PB  - Impact Journals
ER  -