ArticleThe EMBO journal2003
Chk1-deficient tumour cells are viable but exhibit multiple checkpoint and survival defects.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
117 citing papers in PubMed, 240 citations in OpenAlex.
- Randomized phase II trial of cytosine arabinoside with and without the CHK1 inhibitor MK-8776 in relapsed and refractory acute myeloid leukemia.Leukemia research · 2017Trial
- β-tubulin phosphorylation by Chk1 is required for normal spindle formation during cell division.Communications biology · 2026Article
- CD40 drives tumor growth in non-small cell lung cancer via non-canonical immune-independent mechanisms.Cancer letters · 2026Article
- Article
- CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos.EMBO reports · 2023Article
- Histone H3 serine-57 is a CHK1 substrate whose phosphorylation affects DNA repair.Nature communications · 2023Article
- DNA damage checkpoint execution and the rules of its disengagement.Frontiers in cell and developmental biology · 2022Review
- Cell cycle control in cancer.Nature reviews. Molecular cell biology · 2022Review
- Critical role of SMG7 in activation of the ATR-CHK1 axis in response to genotoxic stress.Scientific reports · 2021Article
- Review
- Checkpoint kinase 1 is essential for fetal and adult hematopoiesis.EMBO reports · 2019Article
- Loss of p53 suppresses replication-stress-induced DNA breakage in G1/S checkpoint deficient cells.eLife · 2018Article
- CMPD1 inhibited human gastric cancer cell proliferation by inducing apoptosis and G2/M cell cycle arrest.Biological research · 2018Article
- Chk1 and 14-3-3 proteins inhibit atypical E2Fs to prevent a permanent cell cycle arrest.The EMBO journal · 2018Article
- AKT overactivation can suppress DNA repair via p70S6 kinase-dependent downregulation of MRE11.Oncogene · 2018Article
- The impact of replication stress on replication dynamics and DNA damage in vertebrate cells.Nature reviews. Genetics · 2017Review
- Deciphering alternative splicing and nonsense-mediated decay modulate expression in primary lymphoid tissues of birds infected with avian pathogenic E. coli (APEC).BMC genetics · 2017Article
- The G2 checkpoint inhibitor CBP-93872 increases the sensitivity of colorectal and pancreatic cancer cells to chemotherapy.PloS one · 2017Article
- Opposing effects of pericentrin and microcephalin on the pericentriolar material regulate CHK1 activation in the DNA damage response.Oncogene · 2016Article
- Extensive RPA2 hyperphosphorylation promotes apoptosis in response to DNA replication stress in CHK1 inhibited cells.Nucleic acids research · 2015Article
57 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The conserved protein kinase Chk1 is believed to play an important role in checkpoint responses to aberrant DNA structures; however, genetic analysis of Chk1 functions in metazoans is complicated by lethality of Chk1-deficient embryonic cells. We have used gene targeting to eliminate Chk1 function in somatic DT40 B-lymphoma cells. We find that Chk1-deficient DT40 cells are viable, but fail to arrest in G(2)/M in response to and are hypersensitive to killing by ionizing radiation. Chk1-deficient cells also fail to maintain viable replication forks or suppress futile origin firing when DNA polymerase is inhibited, leading to incomplete genome duplication and diminished cell survival after release from replication arrest. In contrast to embryonic cells, however, Chk1 is not required to delay mitosis when DNA synthesis is inhibited. Thus, Chk1 is dispensable for normal cell division in somatic DT40 cells but is essential for DNA damage-induced G(2)/M arrest and a subset of replication checkpoint responses. Furthermore, Chk1-dependent processes promote tumour cell survival after perturbations of DNA structure or metabolism.
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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.