Repair of DNA double strand breaks by non-homologous end joining.
DNA double strand breaks (DSB) are the most serious form of DNA damage. If not repaired they can lead to cell death. If misrepaired DSBs contribute to chromosomal aberrations and genomic instability. Non-homologous end joining (NHEJ) is one of two major pathways for the repair of DSBs in human cells. Proteins known to be required for NHEJ include the DNA-dependent protein kinase (DNA-PK), XRCC4, DNA ligase IV, and Artemis. This review discusses how these and other accessory proteins may function in the repair of DSBs produced by ionizing radiation (IR) and by V(D)J recombination.
Lees-Miller
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SP
Cancer Biology Research Group, Department of Biochemistry and Molecular Biology, University of Calgary, 3330 Hospital Drive, NW, Calgary, Alta., Canada T2N 4N1. leesmill@ucalgary.ca
Meek
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D000818:Animals; D004249:DNA Damage; D004260:DNA Repair; D051747:DNA-Activated Protein Kinase; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology; D019143:Evolution, Molecular; D006801:Humans; D009687:Nuclear Proteins; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000502:physiology / Q000627:therapeutic use; D011995:Recombination, Genetic / Q000235:genetics / Q000502:physiology*
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D051747:DNA-Activated Protein Kinase; C497263:PRKDC protein, human; D017346:Protein Serine-Threonine Kinases