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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Bibliographische Detailangaben
Veröffentlicht in:Nucleic Acids Res
Hauptverfasser: Feng, Yi-Li, Xiang, Ji-Feng, Liu, Si-Cheng, Guo, Tao, Yan, Guo-Fang, Feng, Ye, Kong, Na, Li, Hao- Dan, Huang, Yang, Lin, Hui, Cai, Xiu-Jun, Xie, An-Yong
Format: Artigo
Sprache:Inglês
Veröffentlicht: Oxford University Press 2017
Schlagworte:
Genome Integrity, Repair and Replication
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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