Regulation of Huntingtin Gene Expression by miRNA-137, -214, -148a, and Their Respective isomiRs
AbstractWith the advent of deep sequencing technology, a variety of miRNA length and sequence variants, termed isomiRNAs (isomiRs), have been discovered. However, the functional roles of these commonly detected isomiRs remain unknown. In this paper, we demonstrated that miRNAs regulate the expression of the HTT gene, whose mutation leads to Huntington’s disease (HD), a hereditary degenerative disorder. Specifically, we validated the interactions of canonical miRNAs, miR-137, miR-214, and miR-148a, with the HTT 3'UTR using a luciferase assay. Moreover, we applied synthetic miRNA mimics to examine whether a slight shifting of miRNA seed regions might alter the regulation of the HTT transcript. We also examined miR-137, miR-214, and miR-148a isomiRs and showed the activity of these isoforms on reporter constructs bearing appropriate sequences from the HTT 3'UTR. Hence, we demonstrated that certain 5'-end variants of miRNAs might be functional for the regulation of the same targets as canonical miRNAs. View Full-Text
- Supplementary File 1:
Supplementary Information (PDF, 415 KB)
Scifeed alert for new publicationsNever miss any articles matching your research from any publisher
- Get alerts for new papers matching your research
- Find out the new papers from selected authors
- Updated daily for 49'000+ journals and 6000+ publishers
- Define your Scifeed now
Kozlowska, E.; Krzyzosiak, W.J.; Koscianska, E. Regulation of Huntingtin Gene Expression by miRNA-137, -214, -148a, and Their Respective isomiRs. Int. J. Mol. Sci. 2013, 14, 16999-17016.
Kozlowska E, Krzyzosiak WJ, Koscianska E. Regulation of Huntingtin Gene Expression by miRNA-137, -214, -148a, and Their Respective isomiRs. International Journal of Molecular Sciences. 2013; 14(8):16999-17016.Chicago/Turabian Style
Kozlowska, Emilia; Krzyzosiak, Wlodzimierz J.; Koscianska, Edyta. 2013. "Regulation of Huntingtin Gene Expression by miRNA-137, -214, -148a, and Their Respective isomiRs." Int. J. Mol. Sci. 14, no. 8: 16999-17016.