ArticleNature2001
The DNA replication checkpoint response stabilizes stalled replication forks.
Article in Nature, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 423 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.
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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
423 citing papers in PubMed, 737 citations in OpenAlex.
- Chromosomal instability in cancer: sources, consequences and new therapeutic opportunities.Signal transduction and targeted therapy · 2026Review
- Oncogenic p53 induces mitotic errors in lung cancer cells by recopying DNA replication forks conferring targetable proliferation advantage.Cell death and differentiation · 2026Article
- Topological stress regulates replication fork dynamics in unperturbed S phase.Nature communications · 2026Article
- Stn1 supports Mec1 function in protecting stalled replication forks from degradation.PLoS genetics · 2025Article
- DNA2 and MSH2 cooperatively repair stabilized G4 and allow efficient telomere replication.Nature communications · 2025Article
- S-phase checkpoint protects from aberrant replication fork processing and degradation.Nucleic acids research · 2025Article
- The DNA replication checkpoint prevents PCNA/RFC depletion to protect forks from HLTF-induced collapse in human cells.Molecular cell · 2025Article
- The DNA replication checkpoint limits Okazaki fragment accumulation to protect and restart stalled forks.Molecular cell · 2025Article
- Breast cancer gene-1 (BRCA1) potentiates maladaptive repair after kidney injury.The Journal of experimental medicine · 2025Article
- DNA2 and MSH2 activity collectively mediate chemically stabilized G4 for efficient telomere replication.bioRxiv : the preprint server for biology · 2025Article
- Replication stress promotes cellular transformation in Drosophila epithelium.Cell death discovery · 2025Article
- Ubiquitin protease Ubp1 cooperates with Ubp10 and Ubp12 to revert lysine-164 PCNA ubiquitylation at replication forks.Nucleic acids research · 2025Article
- Replication-IDentifier links epigenetic and metabolic pathways to the replication stress response.Nature communications · 2025Article
- Revised mechanism of hydroxyurea-induced cell cycle arrest and an improved alternative.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- S-phase checkpoint prevents leading strand degradation from strand-associated nicks at stalled replication forks.Nucleic acids research · 2024Article
- Dysfunction of Gpl1-Gih35-Wdr83 Complex inInternational journal of molecular sciences · 2024Article
- ATR limits Rad18-mediated PCNA monoubiquitination to preserve replication fork and telomerase-independent telomere stability.The EMBO journal · 2024Article
- Spatial regulation of DNA damage tolerance protein Rad5 interconnects genome stability maintenance and proteostasis networks.Nucleic acids research · 2024Article
- Structure and function of the apical PIKKs in double-strand break repair.Current opinion in structural biology · 2023Review
363 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
8 authors at 2 institutions in 2 countries.
Funding
Abstract
In response to DNA damage and blocks to replication, eukaryotes activate the checkpoint pathways that prevent genomic instability and cancer by coordinating cell cycle progression with DNA repair. In budding yeast, the checkpoint response requires the Mec1-dependent activation of the Rad53 protein kinase. Active Rad53 slows DNA synthesis when DNA is damaged and prevents firing of late origins of replication. Further, rad53 mutants are unable to recover from a replication block. Mec1 and Rad53 also modulate the phosphorylation state of different DNA replication and repair enzymes. Little is known of the mechanisms by which checkpoint pathways interact with the replication apparatus when DNA is damaged or replication blocked. We used the two-dimensional gel technique to examine replication intermediates in response to hydroxyurea-induced replication blocks. Here we show that hydroxyurea-treated rad53 mutants accumulate unusual DNA structures at replication forks. The persistence of these abnormal molecules during recovery from the hydroxyurea block correlates with the inability to dephosphorylate Rad53. Further, Rad53 is required to properly maintain stable replication forks during the block. We propose that Rad53 prevents collapse of the fork when replication pauses.
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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.