ArticleCell cycle (Georgetown, Tex.)2010
Exposure to acute hypoxia induces a transient DNA damage response which includes Chk1 and TLK1.
Article in Cell cycle (Georgetown, Tex.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Characterising Cancer Cell Responses to Cyclic Hypoxia Using Mathematical Modelling.Bulletin of mathematical biology · 2024Article
- NADH elevation during chronic hypoxia leads to VHL-mediated HIF-1α degradation via SIRT1 inhibition.Cell & bioscience · 2023Article
- Claspin-Dependent and -Independent Chk1 Activation by a Panel of Biological Stresses.Biomolecules · 2023Article
- Overcoming the Impact of Hypoxia in Driving Radiotherapy Resistance in Head and Neck Squamous Cell Carcinoma.Cancers · 2022Review
- Novel Therapeutic Approaches with DNA Damage Response Inhibitors for Melanoma Treatment.Cells · 2022Review
- Replication catastrophe induced by cyclic hypoxia leads to increased APOBEC3B activity.Nucleic acids research · 2021Article
- Inside the hypoxic tumour: reprogramming of the DDR and radioresistance.Cell death discovery · 2020Review
- The effect of 1.5 T cardiac magnetic resonance on human circulating leucocytes.European heart journal · 2018Article
- Hypoxia-induced alterations of G2 checkpoint regulators.Molecular oncology · 2016Article
- Review
- Article
- Nanocurcumin Prevents Hypoxia Induced Stress in Primary Human Ventricular Cardiomyocytes by Maintaining Mitochondrial Homeostasis.PloS one · 2015Article
- Tumor hypoxia as a driving force in genetic instability.Genome integrity · 2013Article
- CH-01 is a hypoxia-activated prodrug that sensitizes cells to hypoxia/reoxygenation through inhibition of Chk1 and Aurora A.ACS chemical biology · 2013Article
- Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: how mutations can result in therapy resistance and how to overcome resistance.Oncotarget · 2012Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
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 however are sensitive to loss of Chk1. This suggests a new role for Chk1 in the cell cycle response to reoxygenation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.