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H2AX facilitates classical non-homologous end joining at the expense of limited nucleotide loss at repair junctions
Phosphorylated histone H2AX, termed ‘γH2AX’, mediates the chromatin response to DNA double strand breaks (DSBs) in mammalian cells. H2AX deficiency increases the numbers of unrepaired DSBs and translocations, which are partly associated with defects in non-homologous end joining (NHEJ) and contribut...
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| Veröffentlicht in: | Nucleic Acids Res |
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| Hauptverfasser: | , , , , , , , , , , , |
| Format: | Artigo |
| Sprache: | Inglês |
| Veröffentlicht: |
Oxford University Press
2017
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| Schlagworte: | |
| Online Zugang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5737864/ https://ncbi.nlm.nih.gov/pubmed/28977657 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/nar/gkx715 |
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