ArticleNucleic acids research2015
FANCD2 and REV1 cooperate in the protection of nascent DNA strands in response to replication stress.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 44 citations in OpenAlex.
- REV1 Loss Triggers a G2/M Cell-Cycle Arrest Through Dysregulation of Mitotic Regulators.Genes · 2025Article
- SART3 promotes homologous recombination repair by stimulating DNA-RNA hybrids removal and DNA end resection.Nature communications · 2025Article
- VGLL3 modulates chemosensitivity through promoting DNA double-strand break repair.Science advances · 2024Article
- REV1 coordinates a multi-faceted tolerance response to DNA alkylation damage and prevents chromosome shattering in Drosophila melanogaster.PLoS genetics · 2024Article
- Article
- Drug Discovery Targeting Post-Translational Modifications in Response to DNA Damages Induced by Space Radiation.International journal of molecular sciences · 2023Review
- MAD2L2 promotes replication fork protection and recovery in a shieldin-independent and REV3L-dependent manner.Nature communications · 2022Article
- HIV-1 exploits the Fanconi anemia pathway for viral DNA integration.Cell reports · 2022Article
- REV1 promotes lung tumorigenesis by activating the Rad18/SERTAD2 axis.Cell death & disease · 2022Article
- REV1: A novel biomarker and potential therapeutic target for various cancers.Frontiers in genetics · 2022Article
- A fork in the road: Where homologous recombination and stalled replication fork protection part ways.Seminars in cell & developmental biology · 2021Review
- A Novel Germline Compound Heterozygous Mutation ofFrontiers in genetics · 2021Article
- Targeting translesion synthesis (TLS) to expose replication gaps, a unique cancer vulnerability.Expert opinion on therapeutic targets · 2021Review
- The FANC/BRCA Pathway Releases Replication Blockades by Eliminating DNA Interstrand Cross-Links.Genes · 2020Review
- Sml1 Inhibits the DNA Repair Activity of Rev1 in Saccharomyces cerevisiae during Oxidative Stress.Applied and environmental microbiology · 2020Article
- WRNIP1 Protects Reversed DNA Replication Forks from SLX4-Dependent Nucleolytic Cleavage.iScience · 2019Article
- Article
- Role of Y-family translesion DNA polymerases in replication stress: Implications for new cancer therapeutic targets.DNA repair · 2019Review
- Mechanisms for stalled replication fork stabilization: new targets for synthetic lethality strategies in cancer treatments.EMBO reports · 2018Review
- RPA and RAD51: fork reversal, fork protection, and genome stability.Nature structural & molecular biology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
REV1 is a eukaryotic member of the Y-family of DNA polymerases involved in translesion DNA synthesis and genome mutagenesis. Recently, REV1 is also found to function in homologous recombination. However, it remains unclear how REV1 is recruited to the sites where homologous recombination is processed. Here, we report that loss of mammalian REV1 results in a specific defect in replication-associated gene conversion. We found that REV1 is targeted to laser-induced DNA damage stripes in a manner dependent on its ubiquitin-binding motifs, on RAD18, and on monoubiquitinated FANCD2 (FANCD2-mUb) that associates with REV1. Expression of a FANCD2-Ub chimeric protein in RAD18-depleted cells enhances REV1 assembly at laser-damaged sites, suggesting that FANCD2-mUb functions downstream of RAD18 to recruit REV1 to DNA breaks. Consistent with this suggestion we found that REV1 and FANCD2 are epistatic with respect to sensitivity to the double-strand break-inducer camptothecin. REV1 enrichment at DNA damage stripes also partially depends on BRCA1 and BRCA2, components of the FANCD2/BRCA supercomplex. Intriguingly, analogous to FANCD2-mUb and BRCA1/BRCA2, REV1 plays an unexpected role in protecting nascent replication tracts from degradation by stabilizing RAD51 filaments. Collectively these data suggest that REV1 plays multiple roles at stalled replication forks in response to replication stress.
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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.