DNA damage and decisions: CtIP coordinates DNA repair and cell cycle checkpoints.
Maintenance of genome stability depends on efficient, accurate repair of DNA damage. DNA double-strand breaks (DSBs) are among the most lethal types of DNA damage, with the potential to cause mutation, chromosomal rearrangement, and genomic instability that could contribute to cancer. DSB damage can be repaired by various pathways including nonhomologous end-joining (NHEJ) and homologous recombination (HR). However, the cellular mechanisms that regulate the choice of repair pathway are not well understood. Recent studies suggest that the tumor suppressor protein CtIP controls the decision to repair DSB damage by HR. It does so by regulating the initiation of DSB end resection after integrating signals from the DNA damage checkpoint response and cell cycle cues.
You
Zhongsheng
Z
Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA. zyou@wustl.edu
Bailis
Julie M
JM
D000429:Alcohol Oxidoreductases / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000378:metabolism*; D002453:Cell Cycle; D053903:DNA Breaks, Double-Stranded; D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000378:metabolism; D006801:Humans; D009687:Nuclear Proteins / Q000378:metabolism*
D002352:Carrier Proteins; D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D000429:Alcohol Oxidoreductases; C096794:C-terminal binding protein
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