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ATM and ATR are stress-response kinases which respond to a variety of insults including ionizing radiation, replication arrest, ultraviolet radiation and hypoxia/re-oxygenation. Hypoxia occupies a unique niche in the study of both ATR- and ATM-mediated checkpoint pathways. Hypoxia is a physiologically significant stress that occurs in virtually all solid tumors and differs from most other stresses in that it does not induce DNA damage. Previous studies have indicated that hypoxia provides a unique way to induce ATR in response to inhibition of DNA replication. During tumor expansion hypoxia is inevitably followed by periods of re-oxygenation which in vitro has been shown to induce significant levels of DNA damage and an ATM response. Therefore both ATR and ATM have a role to play in hypoxia/re-oxygenation.

Original publication




Journal article


DNA Repair (Amst)

Publication Date





1117 - 1122


Animals, Ataxia Telangiectasia Mutated Proteins, Cell Cycle Proteins, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Embryo, Mammalian, Fluorescent Dyes, Humans, Hypoxia, Microscopy, Fluorescence, Models, Biological, Models, Genetic, Oxygen, Protein Serine-Threonine Kinases, Signal Transduction, Time Factors, Tumor Suppressor Proteins