ArticleMolecular and cellular biology2005
Chk1-dependent S-M checkpoint delay in vertebrate cells is linked to maintenance of viable replication structures.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 87 citations in OpenAlex.
- Nucleosomes represent a crucial target for the intra-S phase checkpoint in response to replication stress.Science advances · 2025Article
- Exploration of the carcinogenetic and immune role of CHK1 in human cancer.Journal of Cancer · 2024Article
- CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos.EMBO reports · 2023Article
- Chk1 and the Host Cell DNA Damage Response as a Potential Antiviral Target in BK Polyomavirus Infection.Viruses · 2021Article
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- Chk1-mediated phosphorylation of Cdh1 promotes the SCFCell death & disease · 2020Article
- Dicer prevents genome instability in response to replication stress.Oncotarget · 2019Article
- Nanoformulation of a Novel Pyrano[2,3-c] Pyrazole Heterocyclic Compound AMDPC Exhibits Anti-Cancer Activity via Blocking the Cell Cycle through aMolecules (Basel, Switzerland) · 2019Article
- A minimal threshold of FANCJ helicase activity is required for its response to replication stress or double-strand break repair.Nucleic acids research · 2018Article
- Ral A, via activating the mitotic checkpoint, sensitizes cells lacking a functional Nf1 to apoptosis in the absence of protein kinase C.Oncotarget · 2016Article
- Extensive RPA2 hyperphosphorylation promotes apoptosis in response to DNA replication stress in CHK1 inhibited cells.Nucleic acids research · 2015Article
- BRCA1 Is Required for Maintenance of Phospho-Chk1 and G2/M Arrest during DNA Cross-Link Repair in DT40 Cells.Molecular and cellular biology · 2015Article
- KA1-targeted regulatory domain mutations activate Chk1 in the absence of DNA damage.Scientific reports · 2015Article
- Phosphorylation of Minichromosome Maintenance 3 (MCM3) by Checkpoint Kinase 1 (Chk1) Negatively Regulates DNA Replication and Checkpoint Activation.The Journal of biological chemistry · 2015Article
- Suppression of CHK1 by ETS Family Members Promotes DNA Damage Response Bypass and Tumorigenesis.Cancer discovery · 2015Article
- Checkpoint-dependent and independent roles of the Werner syndrome protein in preserving genome integrity in response to mild replication stress.Nucleic acids research · 2014Article
- DNA replication stress in CHK1-depleted tumour cells triggers premature (S-phase) mitosis through inappropriate activation of Aurora kinase B.Cell death & disease · 2014Article
- A functional approach reveals a genetic and physical interaction between ribonucleotide reductase and CHK1 in mammalian cells.PloS one · 2014Article
- Increasing cisplatin sensitivity by schedule-dependent inhibition of AKT and Chk1.Cancer biology & therapy · 2014Article
- Redundancy of mammalian Y family DNA polymerases in cellular responses to genomic DNA lesions induced by ultraviolet light.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated mitotic delay during replication arrest (the S-M checkpoint) in DT40 B-lymphoma cells deficient in the Chk1 or Chk2 kinase. We show here that cells lacking Chk1, but not those lacking Chk2, enter mitosis with incompletely replicated DNA when DNA synthesis is blocked, but only after an initial delay. This initial delay persists when S-M checkpoint failure is induced in Chk2-/- cells with the Chk1 inhibitor UCN-01, indicating that it does not depend on Chk1 or Chk2 activity. Surprisingly, dephosphorylation of tyrosine 15 did not accompany Cdc2 activation during premature entry to mitosis in Chk1-/- cells, although mitotic phosphorylation of cyclin B2 did occur. Previous studies have shown that Chk1 is required to stabilize stalled replication forks during replication arrest, and strikingly, premature mitosis occurs only in Chk1-deficient cells which have lost the capacity to synthesize DNA as a result of progressive replication fork inactivation. These results suggest that Chk1 maintains the S-M checkpoint indirectly by preserving the viability of replication structures and that it is the continued presence of such structures, rather than the activation of Chk1 per se, which delays mitosis until DNA replication is complete.
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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.