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CRISPR-Induced Expression of N-Terminally Truncated Dicer in Mouse Cells
R. Malik, P. Svoboda
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Free Medical Journals
od 2010
PubMed Central
od 2010
Europe PubMed Central
od 2010
ProQuest Central
od 2010-03-01
Open Access Digital Library
od 2010-01-01
Open Access Digital Library
od 2010-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2010
PubMed
33918028
DOI
10.3390/genes12040540
Knihovny.cz E-zdroje
- MeSH
- buňky 3T3 MeSH
- DEAD-box RNA-helikasy antagonisté a inhibitory genetika MeSH
- embryonální kmenové buňky cytologie metabolismus MeSH
- malá interferující RNA genetika MeSH
- myši MeSH
- promotorové oblasti (genetika) * MeSH
- ribonukleasa III antagonisté a inhibitory genetika MeSH
- RNA interference MeSH
- sekvence CRISPR * MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
RNA interference (RNAi) designates sequence-specific mRNA degradation mediated by small RNAs generated from long double-stranded RNA (dsRNA) by RNase III Dicer. RNAi appears inactive in mammalian cells except for mouse oocytes, where high RNAi activity exists because of an N-terminally truncated Dicer isoform, denoted DicerO. DicerO processes dsRNA into small RNAs more efficiently than the full-length Dicer expressed in somatic cells. DicerO is expressed from an oocyte-specific promoter of retrotransposon origin, which is silenced in other cell types. In this work, we evaluated CRISPR-based strategies for epigenetic targeting of the endogenous Dicer gene to restore DicerO expression and, consequently, RNAi. We show that reactivation of DicerO expression can be achieved in mouse embryonic stem cells, but it is not sufficient to establish a robust canonical RNAi response.
Citace poskytuje Crossref.org
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