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Hypoxia/reoxygenation is a physiological stress that activates the DNA damage pathway. Significantly, this pathway is initiated during hypoxia, in the absence of detectable DNA damage. Our most recent study determined that during hypoxia, Chk 2 is phosphorylated in an ATM-dependent manner. In addition to this finding, we found that components of the MRN complex were not required for Chk 2 phosphorylation during hypoxia/reoxygenation. Once activated, Chk 2 initiates a signaling cascade, which induces a cell cycle arrest in the G2 phase. Loss of the Chk 2-mediated arrest correlated with an increase in sensitivity to hypoxia/reoxygenation. In contrast, loss of a p53-mediated reoxygenation-induced G1 arrest does not correlate with increased sensitivity to hypoxia/reoxygenation.

Original publication




Journal article


Cell Cycle

Publication Date





1304 - 1307


Ataxia Telangiectasia Mutated Proteins, Cell Cycle Proteins, Cell Hypoxia, DNA-Binding Proteins, Humans, Oxygen, Phosphorylation, Protein Serine-Threonine Kinases, Signal Transduction, Tumor Suppressor Protein p53, Tumor Suppressor Proteins