miR-148 targets human DNMT3b protein coding region.
By Anja M Duursma, M. Kedde, Mariette Schrier, Carlos le Sage, Reuven Agami. RNA: A publication of the RNA Society, 2008
612 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/3d98ead77eccd920196209d050e465ea99c1f67c
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In Cancer Research
- Olivier Voinnet
- Aster Legesse-Miller
- J. Lieberman
- M. Gorospe
- M. Hollstein
- A. Lal
- C. Harris
- A. Robles
In Molecular Biology
- Olivier Voinnet
- Aster Legesse-Miller
- J. Lieberman
- M. Gorospe
- M. Hollstein
- A. Lal
- C. Harris
- A. Robles
Citations in the corpus
- Genetic variation in microRNA networks: the implications for cancer research (2010, positive): “Therefore, the expression of miR-148 changes the relative abundance of DNMT3B splice variant”
- miR-24 inhibits cell proliferation by suppressing expression of E2F2, MYC and other cell cycle regulatory genes by binding to “seedless” 3′UTR microRNA recognition elements (2009, background): “Other recent studies also identified coding region MREs (Duursma et al., 2008; Tay et al., 2008).”
- A search for conserved sequences in coding regions reveals that the let-7 microRNA targets Dicer within its coding sequence (2008, background): “One recent report has shown downregulation via a coding region target directly (29).”
- Revisiting the principles of microRNA target recognition and mode of action (2009, background): “Accordingly, two recent studies in human cells have identified functional miRNA target sites in the ORFs of DNA methyltransferase 3b ( DNMT3B ) and of the cell-cycle inhibitor p16 INK4A (also known as CDKN2A”
- Desperately seeking microRNA targets (2010, methodology): “Commonly used algorithms place variable weight on: (i) complementarity to the miRNA seed region; (ii) evolutionary conservation of the MRE; (iii) free energy of the miRNA-mRNA heteroduplex; and (iv) mRNA sequence features outside the target sit”
- p53 polymorphisms: cancer implications (2009, background): “The recent finding that microRNAs (miRNAs) can inhibit translation by targeting the coding sequences of genes invites speculation that there are as yet undiscovered miRNAs that can target p53 in a similar fashion, which might explain how silent TP53 polymorphisms in the coding region of the gene c”
- AltAnalyze and DomainGraph: analyzing and visualizing exon expression data (2010, background): “Recently, it was found that alternative splicing can also regulate the inclusion of microRNA (miRNA) binding sites as an important means of controlling protein expression (9).”