Exposure to acute hypoxia induces a transient DNA damage response which includes Chk1 and TLK1
| Autor: | Zuzana Bencokova, Chris McGurk, Ester M. Hammond, Isabel M. Pires |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2016 |
| Předmět: |
DNA Replication
DNA Repair DNA damage DNA repair DNA Repair/drug effects Biology Protein Serine-Threonine Kinases cell Hypoxia/drug effects Models Biological environment and public health Signal Transduction/drug effects medicine Rad51 Recombinase/metabolism Protein Serine-Threonine Kinases/metabolism Phosphorylation Molecular Biology Oxygen/pharmacology checkpoint Kinase 1 Manchester Cancer Research Centre Extra View ResearchInstitutes_Networks_Beacons/mcrc DNA replication Phosphorylation/drug effects Cell Biology Hypoxia (medical) Cell cycle DNA Replication/drug effects Molecular biology Cell Hypoxia Cell biology Oxygen enzymes and coenzymes (carbohydrates) Apoptosis Checkpoint Kinase 1 Protein Kinases/metabolism Rad51 Recombinase Signal transduction medicine.symptom biological phenomena cell phenomena and immunity Protein Kinases Developmental Biology Signal Transduction DNA Damage |
| Zdroj: | Pires, I M, Bencokova, Z, McGurk, C & Hammond, E M 2010, ' Exposure to acute hypoxia induces a transient DNA damage response which includes Chk1 and TLK1 ', Cell cycle (Georgetown, Tex.), vol. 9, no. 13, pp. 2502-2507 . https://doi.org/10.4161/cc.9.13.12059 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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