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Author (up) Barzilai, A.; Yamamoto, K.-I. file  url
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  Title DNA damage responses to oxidative stress Type Journal Article
  Year 2004 Publication DNA Repair Abbreviated Journal DNA Repair (Amst)  
  Volume 3 Issue 8-9 Pages 1109-1115  
  Keywords Animals; Apoptosis; Cell Cycle; Cell Lineage; *DNA Damage; *DNA Repair; Humans; Hypoxia; Mitochondria/pathology; Oxidation-Reduction; *Oxidative Stress; Reactive Oxygen Species  
  Abstract The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.  
  Call Number Serial 1707  
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