title: Detection and repair of ionizing radiation-induced DNA double strand breaks: new developments in nonhomologous end joining.
abstract: DNA damage can occur as a result of endogenous metabolic reactions and replication stress or from exogenous sources such as radiation therapy and chemotherapy. DNA double strand breaks are the most cytotoxic form of DNA damage, and defects in their repair can result in genome instability, a hallmark of cancer. The major pathway for the repair of ionizing radiation-induced DSBs in human cells is nonhomologous end joining. Here we review recent advances on the mechanism of nonhomologous end joining, as well as new findings on its component proteins and regulation.
authors: Departments of Biochemistry and Molecular Biology and Oncology, and Southern Alberta Cancer Research Institute, University of Calgary, Calgary, Canada.
authors: Chen
authors: C
authors: Wang
authors: Susan P
authors: SP
authors: Lees-Miller
mesh_terms: D034961:Antigens, Nuclear / Q000502:physiology; D053903:DNA Breaks, Double-Stranded; D059766:DNA End-Joining Repair / Q000502:physiology*; D000072481:DNA Ligase ATP; D011088:DNA Ligases / Q000502:physiology; D045643:DNA Repair Enzymes / Q000502:physiology; D051747:DNA-Activated Protein Kinase / Q000502:physiology; D004268:DNA-Binding Proteins / Q000502:physiology; D006801:Humans; D000072200:Ku Autoantigen; D009687:Nuclear Proteins / Q000502:physiology; D010766:Phosphorylation / Q000502:physiology
chemical_list: D034961:Antigens, Nuclear; D004268:DNA-Binding Proteins; C508551:NHEJ1 protein, human; D009687:Nuclear Proteins; C101467:XRCC4 protein, human; D051747:DNA-Activated Protein Kinase; C497263:PRKDC protein, human; C000606509:Xrcc6 protein, human; D000072200:Ku Autoantigen; D011088:DNA Ligases; D045643:DNA Repair Enzymes; D000072481:DNA Ligase ATP