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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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Detalles Bibliográficos
Autores principales:	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:	Online Artículo Texto
Lenguaje:	English
Publicado:	Oxford University Press 2017
Materias:	Genome Integrity, Repair and Replication
Acceso en línea:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5737864/ https://www.ncbi.nlm.nih.gov/pubmed/28977657 http://dx.doi.org/10.1093/nar/gkx715

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