ArticleThe EMBO journal2013
Rad51 replication fork recruitment is required for DNA damage tolerance.
Article in The EMBO journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 94 citations in OpenAlex.
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- The bacterial MRE11-RAD50 and DNA2-WRN homologs process replication forks at distinct and separate loci on the chromosome.FEBS letters · 2026Article
- Rad51 determines pathway usage in post-replication repair.Nature communications · 2026Article
- Analyzing DNA Replication Fork Stability and Collapse Using Chromatin Fiber Analysis and the R-ODD-BLOBS Program.Computational and structural biotechnology journal · 2026Article
- The chromatin regulator HELLS mediates SSB repair and responses to DNA alkylation damage.Nucleic acids research · 2025Article
- Somatic mutations in IRE1α regulate keratinocyte migration and survival by differentially activating Rho GTPases.Journal of cell science · 2025Article
- S-phase checkpoint protects from aberrant replication fork processing and degradation.Nucleic acids research · 2025Article
- A Rfa1-MN-based system reveals new factors involved in the rescue of broken replication forks.PLoS genetics · 2025Article
- Post-replicative lesion processing limits DNA damage-induced mutagenesis.Nucleic acids research · 2025Article
- Ubiquitin protease Ubp1 cooperates with Ubp10 and Ubp12 to revert lysine-164 PCNA ubiquitylation at replication forks.Nucleic acids research · 2025Article
- Review
- BRCA1/BARD1 ubiquitinates PCNA in unperturbed conditions to promote continuous DNA synthesis.Nature communications · 2024Article
- Physical interactions between specifically regulated subpopulations of the MCM and RNR complexes prevent genetic instability.PLoS genetics · 2024Article
- APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability.Science advances · 2024Article
- The translocated virulence protein VirD5 causes DNA damage and mutation duringScience advances · 2022Article
- Changes in the architecture and abundance of replication intermediates delineate the chronology of DNA damage tolerance pathways at UV-stalled replication forks in human cells.Nucleic acids research · 2022Article
- RAD51 is a druggable target that sustains replication fork progression upon DNA replication stress.PloS one · 2022Article
- Review
- RAD51: Beyond the break.Seminars in cell & developmental biology · 2021Review
- Complex Mechanisms of Antimony Genotoxicity in Budding Yeast Involves Replication and Topoisomerase I-Associated DNA Lesions, Telomere Dysfunction and Inhibition of DNA Repair.International journal of molecular sciences · 2021Article
6 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
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homologous recombination (HR) is essential for genome integrity. Recombination proteins participate in tolerating DNA lesions that interfere with DNA replication, but can also generate toxic recombination intermediates and genetic instability when they are not properly regulated. Here, we have studied the role of the recombination proteins Rad51 and Rad52 at replication forks and replicative DNA lesions. We show that Rad52 loads Rad51 onto unperturbed replication forks, where they facilitate replication of alkylated DNA by non-repair functions. The recruitment of Rad52 and Rad51 to chromatin during DNA replication is a prerequisite for the repair of the non-DSB DNA lesions, presumably single-stranded DNA gaps, which are generated during the replication of alkylated DNA. We also show that the repair of these lesions requires CDK1 and is not coupled to the fork but rather restricted to G2/M by the replicative checkpoint. We propose a new scenario for HR where Rad52 and Rad51 are recruited to the fork to promote DNA damage tolerance by distinct and cell cycle-regulated replicative and repair functions.
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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.