ArticleThe Journal of cell biology2015
Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells.
Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 465 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
465 citing papers in PubMed, 677 citations in OpenAlex.
- Germline polymorphisms in genes maintaining the replication fork predict the efficacy of oxaliplatin and irinotecan in patients with metastatic colorectal cancer.British journal of cancer · 2022Trial
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- RADX protects against intestinal inflammation by restraining IFI16-mediated innate immunity.EMBO molecular medicine · 2026Article
- PCNA-RECQL5-RPRD1B recruit repair components to stressed replication forks to promote survival of BRCA1-deficient cancer cells.Nucleic acids research · 2026Article
- CDT1 acts with the replisome to remodel replication forks.Science advances · 2026Article
- Nucleostemin promotes RAD51 filament assembly on double-stranded DNA to protect stalled replication forks.Nucleic acids research · 2026Article
- PARG inhibition reduces ssDNA levels and limits RPA loading upon replication fork collapse.EMBO reports · 2026Article
- Article
- RAD51 in Breast Cancer: From Vulnerability to Resistance.World journal of oncology · 2026Review
- Oxidative base damage to telomeres sensitizes cancer cells to ATR inhibition.Communications biology · 2026Article
- The BRCA1-A complex restricts replication fork reversal-dependent DNA repair in ATM deficient cells.Nature communications · 2026Article
- FET proteins and PARylation-dependent condensates promote replication fork reversal and genome stability.Nature communications · 2026Article
- Processing of reversed replication forks is required for the resolution of replication-transcription conflicts.Nucleic acids research · 2026Article
- Asymmetric attrition and secondary chromosome destabilization after double-strand breaks in human embryonic development.Nature communications · 2026Article
- FBH1 and RAD54L directly interact and cooperate to drive replication fork reversal.bioRxiv : the preprint server for biology · 2026Article
- RAD54L promotes nascent DNA degradation and radial chromosome formation in FANC-deficient cells.bioRxiv : the preprint server for biology · 2026Article
- Condensin and topoisomerases cooperate to relieve topological stress at stalled replication forks.Nature communications · 2026Article
- LIPT1 loss confers replication stress and PARP inhibitor sensitivity through PrimPol-mediated ssDNA gaps.Science advances · 2026Article
- The DNA helicase HELQ promotes replication fork reversal in coordination with BRCA2- and FANCD2-mediated repair pathways.Nucleic acids research · 2026Article
- Understanding single stranded DNA gaps: from formation to fate.The Biochemical journal · 2026Review
405 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
Replication fork reversal protects forks from breakage after poisoning of Topoisomerase 1. We here investigated fork progression and chromosomal breakage in human cells in response to a panel of sublethal genotoxic treatments, using other topoisomerase poisons, DNA synthesis inhibitors, interstrand cross-linking inducers, and base-damaging agents. We used electron microscopy to visualize fork architecture under these conditions and analyzed the association of specific molecular features with checkpoint activation. Our data identify replication fork uncoupling and reversal as global responses to genotoxic treatments. Both events are frequent even after mild treatments that do not affect fork integrity, nor activate checkpoints. Fork reversal was found to be dependent on the central homologous recombination factor RAD51, which is consistently present at replication forks independently of their breakage, and to be antagonized by poly (ADP-ribose) polymerase/RECQ1-regulated restart. Our work establishes remodeling of uncoupled forks as a pivotal RAD51-regulated response to genotoxic stress in human cells and as a promising target to potentiate cancer chemotherapy.
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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.