Checking in on hypoxia/reoxygenation

Rachel A. Freiberg, Adam J. Krieg, Amato J. Giaccia, Ester M. Hammond

Research output: Contribution to journalReview article

20 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)1304-1307
Number of pages4
JournalCell Cycle
Volume5
Issue number12
DOIs
StatePublished - Jun 15 2006

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Keywords

  • ATM
  • Chk 2
  • Hypoxia
  • Reoxygenation

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

Cite this

Freiberg, R. A., Krieg, A. J., Giaccia, A. J., & Hammond, E. M. (2006). Checking in on hypoxia/reoxygenation. Cell Cycle, 5(12), 1304-1307. https://doi.org/10.4161/cc.5.12.2811