Efficient inhibition of miR-155 function in vivo by peptide nucleic acids.
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Authors
Fabani, Martin M
Abreu-Goodger, Cei
Williams, Donna
Torres, Adrian G
Gait, Michael J
Publication Date
2010-07Journal Title
Nucleic Acids Res
ISSN
0305-1048
Publisher
Oxford University Press (OUP)
Volume
38
Issue
13
Pages
4466-4475
Language
eng
Type
Article
This Version
VoR
Physical Medium
Print-Electronic
Metadata
Show full item recordCitation
Fabani, M. M., Abreu-Goodger, C., Williams, D., Lyons, P., Torres, A. G., Smith, K., Enright, A., et al. (2010). Efficient inhibition of miR-155 function in vivo by peptide nucleic acids.. Nucleic Acids Res, 38 (13), 4466-4475. https://doi.org/10.1093/nar/gkq160
Abstract
MicroRNAs (miRNAs) play an important role in diverse physiological processes and are potential therapeutic agents. Synthetic oligonucleotides (ONs) of different chemistries have proven successful for blocking miRNA expression. However, their specificity and efficiency have not been fully evaluated. Here, we show that peptide nucleic acids (PNAs) efficiently block a key inducible miRNA expressed in the haematopoietic system, miR-155, in cultured B cells as well as in mice. Remarkably, miR-155 inhibition by PNA in primary B cells was achieved in the absence of any transfection agent. In mice, the high efficiency of the treatment was demonstrated by a strong overlap in global gene expression between B cells isolated from anti-miR-155 PNA-treated and miR-155-deficient mice. Interestingly, PNA also induced additional changes in gene expression. Our analysis provides a useful platform to aid the design of efficient and specific anti-miRNA ONs for in vivo use.
Keywords
B-Lymphocytes, Cells, Cultured, Animals, Mice, Inbred C57BL, Mice, Knockout, Mice, MicroRNAs, Peptide Nucleic Acids, RNA, Messenger, Gene Expression Profiling, Gene Expression Regulation, Binding Sites, Microwaves
Identifiers
External DOI: https://doi.org/10.1093/nar/gkq160
This record's URL: https://www.repository.cam.ac.uk/handle/1810/269336
Rights
Attribution-NonCommercial 4.0 International, Attribution-NonCommercial 4.0 International
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