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.
Copyright © 2013 Elsevier Inc. All rights reserved.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Antigens, Nuclear / physiology
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DNA Breaks, Double-Stranded*
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DNA End-Joining Repair / physiology*
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DNA Ligase ATP
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DNA Ligases / physiology
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DNA Repair Enzymes / physiology
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DNA-Activated Protein Kinase / physiology
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DNA-Binding Proteins / physiology
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Humans
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Ku Autoantigen
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Nuclear Proteins / physiology
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Phosphorylation / physiology
Substances
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Antigens, Nuclear
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DNA-Binding Proteins
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NHEJ1 protein, human
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Nuclear Proteins
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XRCC4 protein, human
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DNA-Activated Protein Kinase
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PRKDC protein, human
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Xrcc6 protein, human
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Ku Autoantigen
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DNA Ligases
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DNA Repair Enzymes
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DNA Ligase ATP