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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Detalhes bibliográficos
Publicado no:Nucleic Acids Res
Main Authors: 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
Formato: Artigo
Idioma:Inglês
Publicado em: Oxford University Press 2017
Assuntos:
Genome Integrity, Repair and Replication
Acesso em linha: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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