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Exposure to acute hypoxia induces a transient DNA damage response which includes Chk1 and TLK1

Pires, Isabel M.; Bencokova, Zuzana; Hammond, Ester M.; McGurk, Chris

Authors

Zuzana Bencokova

Ester M. Hammond

Chris McGurk



Abstract

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 are however sensitive to loss of Chk1. This suggests a new role for Chk1 in the cell cycle response to reoxygenation. © 2010 Landes Bioscience.

Citation

Pires, I. M., Bencokova, Z., Hammond, E. M., & McGurk, C. (2010). Exposure to acute hypoxia induces a transient DNA damage response which includes Chk1 and TLK1. Cell cycle, 9(13), 2502-2507. https://doi.org/10.4161/cc.9.13.12059

Journal Article Type Review
Online Publication Date Jul 1, 2010
Publication Date 2010
Journal Cell Cycle
Print ISSN 1538-4101
Electronic ISSN 1551-4005
Publisher Taylor and Francis
Peer Reviewed Peer Reviewed
Volume 9
Issue 13
Pages 2502-2507
DOI https://doi.org/10.4161/cc.9.13.12059
Keywords Hypoxia; Reoxygenation; Replication restart; Chk1; TLK1
Public URL https://hull-repository.worktribe.com/output/417511
Publisher URL https://www.tandfonline.com/doi/full/10.4161/cc.9.13.12059