Heterochromatinization associated with cell differentiation as a model to study DNA double strand break induction and repair in the context of higher-order chromatin structure
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
23454236
DOI
10.1016/j.apradiso.2013.01.029
PII: S0969-8043(13)00038-9
Knihovny.cz E-zdroje
- Klíčová slova
- Chromatin sensitivity to DSB induction, DNA double strand break (DSB) repair, Heterochromatin, Higher-order chromatin structure, Immature and terminally differentiated granulocytes, γH2AX/53BP1 repair foci,
- MeSH
- buněčná diferenciace * MeSH
- chromatin chemie MeSH
- hybridizace in situ fluorescenční MeSH
- konformace proteinů MeSH
- kultivované buňky MeSH
- lidé MeSH
- oprava DNA * MeSH
- poškození DNA * MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- chromatin MeSH
Cell differentiation is associated with extensive gene silencing, heterochromatinization and potentially decreasing need for repairing DNA double-strand breaks (DSBs). Differentiation stages of blood cells thus represent an excellent model to study DSB induction, repair and misrepair in the context of changing higher-order chromatin structure. We show that immature granulocytes form γH2AX and 53BP1 foci, contrary to the mature cells; however, these foci colocalize only rarely and DSB repair is inefficient. Moreover, specific chromatin structure of granulocytes probably influences DSB induction.
Citace poskytuje Crossref.org
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