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Severe hypoxia has been demonstrated to induce a replication arrest which is associated with decreased levels of nucleotides. Chk1 is rapidly phosphorylated in response to severe hypoxia and in turn deactivates TLK1 through phosphorylation. Loss of Chk1 has been shown to sensitize cells to hypoxia/reoxygenation. After short (acute) exposure to hypoxia this is due to an increased rate of reoxygenation-induced replication restart and subsequent p53-dependent apoptosis. After longer (chronic) exposure to hypoxia S phase cells do not undergo reoxygenation-induced replication restart. Cells exposed to these levels of hypoxia however are sensitive to loss of Chk1. This suggests a new role for Chk1 in the cell cycle response to reoxygenation.

Original publication




Journal article


Cell Cycle

Publication Date





2502 - 2507


Cell Hypoxia, Checkpoint Kinase 1, DNA Damage, DNA Repair, DNA Replication, Models, Biological, Oxygen, Phosphorylation, Protein Kinases, Protein Serine-Threonine Kinases, Rad51 Recombinase, Signal Transduction