ReviewMutation research. Reviews in mutation research
The fork and the kinase: a DNA replication tale from a CHK1 perspective.
Review in Mutation research. Reviews in mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
44 citing papers in PubMed, 64 citations in OpenAlex.
- Targeting common denominators of DNA damage tolerance mechanisms as therapeutic strategy to cope with dynamic phenotypic changes in triple-negative breast cancer cells.Cell death discovery · 2026Article
- Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025Review
- Versatile enhancement of the killing potential of anti-cancer agents achieved by peptide mimetics of the PCNA interface towards specialized DNA polymerases.Cell death & disease · 2025Article
- Replication stress responses in human lymphocytes change sex-specifically during aging.Nucleic acids research · 2025Article
- Targeting DNA Damage Repair to Enhance Antitumor Immunity in Radiotherapy: Mechanisms and Opportunities.International journal of molecular sciences · 2025Review
- Assessing the antioxidant properties of Naringin and Rutin and investigating their oxidative DNA damage effects in breast cancer.Scientific reports · 2024Article
- CHK1-CDC25A-CDK1 regulate cell cycle progression and protect genome integrity in early mouse embryos.EMBO reports · 2023Article
- Review
- Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.Science advances · 2023Article
- Innate immune response restarts adaptive immune response in tumors.Frontiers in immunology · 2023Review
- Targeting the DNA Damage Response and DNA Repair Pathways to Enhance Radiosensitivity in Colorectal Cancer.Cancers · 2022Review
- Enhancing anti-tumour innate immunity by targeting the DNA damage response and pattern recognition receptors in combination with radiotherapy.Frontiers in oncology · 2022Review
- FANCD2 limits acetaldehyde-induced genomic instability during DNA replication in esophageal keratinocytes.Molecular oncology · 2021Article
- A Catalytically Independent Function of Human DNA Polymerase Kappa Controls the Stability and Abundance of Checkpoint Kinase 1.Molecular and cellular biology · 2021Article
- Structural Chromosome Instability: Types, Origins, Consequences, and Therapeutic Opportunities.Cancers · 2021Review
- Review
- GDC-0575, a CHK1 Inhibitor, Impairs the Development of Colitis and Colitis-Associated Cancer by Inhibiting CCR2OncoTargets and therapy · 2021Article
- Mus81-Eme1-dependent aberrant processing of DNA replication intermediates in mitosis impairs genome integrity.Science advances · 2020Article
- The CHK1 inhibitor MU380 significantly increases the sensitivity of human docetaxel-resistant prostate cancer cells to gemcitabine through the induction of mitotic catastrophe.Molecular oncology · 2020Article
- Active Replication Checkpoint Drives Genome Instability in Fission YeastMolecular and cellular biology · 2020Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Replication fork progression is being continuously hampered by exogenously introduced and naturally occurring DNA lesions and other physical obstacles. Checkpoint kinase 1 (Chk1) is activated at replication forks that encounter damaged DNA. Subsequently, Chk1 inhibits the initiation of new replication factories and stimulates the firing of dormant origins (those in the vicinity of stalled forks). Chk1 also avoids fork collapse into DSBs (double strand breaks) and promotes fork elongation. At the molecular level, the current model considers stalled forks as the site of Chk1 activation and the nucleoplasm as the location where Chk1 phosphorylates target proteins. This model certainly serves to explain how Chk1 modulates origin firing, but how Chk1 controls the fate of stalled forks is less clear. Interestingly, recent reports demonstrating that Chk1 phosphorylates chromatin-bound proteins and even holds kinase-independent functions might shed light on how Chk1 contributes to the elongation of damaged DNA. Indeed, such findings have unveiled a puzzling connection between Chk1 and DNA lesion bypass, which might be central to promoting fork elongation and checkpoint attenuation. In summary, Chk1 is a multifaceted and versatile signaling factor that acts at ongoing forks and replication origins to determine the extent and quality of the cellular response to replication stress.
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What OpenQuestion holds
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.