Ectopic expression of RNF168 and 53BP1 increases mutagenic but not physiological non-homologous end joiningDali Zong(Karolinska Institutet), André Nussenzweig(National Institutes of Health)Nucleic Acids ResearchApril 27, 201510.1093/nar/gkv336Cited by 30SaveCiteExport RISWatch citationsRelated PapersChemosensitization by phenothiazines in human lung cancer cells: impaired resolution of γH2AX and increased oxidative stress elicit apoptosis associated with lysosomal expansion and intense vacuolation|Cell Death and Disease|2011|60Comprehensive mapping of cell fates in microsatellite unstable cancer cells supports dual targeting of WRN and ATR|Genes & Development|2023|20