Novel TALEN-generated mCitrine-FANCD2 fusion reporter mouse model for in vivo research of DNA damage response
Jazyk angličtina Země Nizozemsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
32717583
DOI
10.1016/j.dnarep.2020.102936
PII: S1568-7864(20)30185-3
Knihovny.cz E-zdroje
- Klíčová slova
- DNA damage, Fanconi anemia, Mouse, TALEN, mCitrine,
- MeSH
- bakteriální proteiny MeSH
- luminescentní proteiny MeSH
- modely u zvířat * MeSH
- myši inbrední C57BL MeSH
- myši MeSH
- oprava DNA MeSH
- poškození DNA MeSH
- protein FANCD2 genetika MeSH
- rekombinantní fúzní proteiny * MeSH
- reportérové geny * MeSH
- TALENs MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- bakteriální proteiny MeSH
- citrine protein, bacteria MeSH Prohlížeč
- luminescentní proteiny MeSH
- protein FANCD2 MeSH
- rekombinantní fúzní proteiny * MeSH
- TALENs MeSH
Reporter gene mouse lines are routinely used for studies related to functional genomics, proteomics, cell biology or cell-based drug screenings, and represent a crucial platform for in vivo research. In the generation of knock-in reporter lines, new gene targeting methods provide several advantages over the standard transgenic techniques. First of all, specific targeting of the genome allows expression of the reporter gene under controlled conditions, whether in a specific locus in the genome or in a "safe harbor" locus. Historically, the ROSA26 locus is used for gene knock-in strategies by homologous recombination in mouse embryonic stem cells. The other preferred place for integration of the reporter transgene in the mouse genome is the endogenous promoter of a target gene. In this study, we employed TALENs to generate a reporter fusion protein expressed from its native promoter. For monitoring DNA damage response, we generated a mouse line expressing a mCitrine-tagged version of the FANCD2 protein, involved in DNA damage response and repair, and the Fanconi anemia (FA) pathway. This model could be a valuable tool for in vivo investigation of DNA damage.
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