ArticleMolecular cell2010
Multiple Rad5 activities mediate sister chromatid recombination to bypass DNA damage at stalled replication forks.
Article in Molecular cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 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
67 citing papers in PubMed, 116 citations in OpenAlex.
- The DNA damage tolerance factor Rad5 and telomere replication.Current genetics · 2025Review
- PCNA Unloading Is Crucial for the Bypass of DNA Lesions Using Homologous Recombination.International journal of molecular sciences · 2024Article
- Spatial regulation of DNA damage tolerance protein Rad5 interconnects genome stability maintenance and proteostasis networks.Nucleic acids research · 2024Article
- Helicase activities of Rad5 and Rrm3 genetically interact in the prevention of recombinogenic DNA lesions in Saccharomyces cerevisiae.DNA repair · 2023Article
- PARP1 recruits DNA translocases to restrain DNA replication and facilitate DNA repair.PLoS genetics · 2022Article
- Unscheduled DNA replication in G1 causes genome instability and damage signatures indicative of replication collisions.Nature communications · 2022Article
- Rad51-mediated replication of damaged templates relies on monoSUMOylated DDK kinase.Nature communications · 2022Article
- Mechanism for inverted-repeat recombination induced by a replication fork barrier.Nature communications · 2022Article
- Rad5 participates in lesion bypass through its Rev1-binding and ubiquitin ligase domains, but not through its helicase function.Frontiers in molecular biosciences · 2022Article
- Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance.EMBO reports · 2021Article
- The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.Oncogenesis · 2020Article
- Prevention of unwanted recombination at damaged replication forks.Current genetics · 2020Review
- Mechanisms of direct replication restart at stressed replisomes.DNA repair · 2020Review
- Article
- The Mgs1/WRNIP1 ATPase is required to prevent a recombination salvage pathway at damaged replication forks.Science advances · 2020Article
- Review
- SUMOylation of PCNA by PIAS1 and PIAS4 promotes template switch in the chicken and human B cell lines.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Homologous Recombination: To Fork and Beyond.Genes · 2018Review
- Regulation of HLTF-mediated PCNA polyubiquitination by RFC and PCNA monoubiquitination levels determines choice of damage tolerance pathway.Nucleic acids research · 2018Article
- Loss of Cohesin Subunit Rec8 Switches Rad51 Mediator Dependence in Resistance to Formaldehyde Toxicity inGenetics · 2018Article
7 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
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage that blocks replication is bypassed in order to complete chromosome duplication and preserve cell viability and genome stability. Rad5, a PCNA polyubiquitin ligase and DNA-dependent ATPase in yeast, is orthologous to putative tumor suppressors and controls error-free damage bypass by an unknown mechanism. To identify the mechanism in vivo, we investigated the roles of Rad5 and analyzed the DNA structures that form during damage bypass at site-specific stalled forks present at replication origins. Rad5 mediated the formation of recombination-dependent, X-shaped DNA structures containing Holliday junctions between sister chromatids. Mutants lacking these damage-induced chromatid junctions were defective in resolving stalled forks, restarting replication, and completing chromosome duplication. Rad5 polyubiquitin ligase and ATPase domains both contributed to replication fork recombination. Our results indicate that multiple activities of Rad5 function coordinately with homologous recombination factors to enable replication template switch events that join sister chromatids at stalled forks and bypass DNA damage.
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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.