Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
2 · The registry
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Shannon J Ceballos *Department of Microbiology & Molecular Genetics, University of California, Davis, CA, USA.
Shih-Hsun HungDepartment of Microbiology & Molecular Genetics, University of California, Davis, CA, USA.
Giordano ReginatoInstitute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera italiana (USI), Bellinzona, Switzerland.ORCID http://orcid.org/0009-0002-5284-4339
Maria I Cano-LinaresCentro Andaluz de Biología Molecular y Medicina Regenerativa -CABIMER; Consejo Superior de Investigaciones Científicas; Universidad de Sevilla; Universidad Pablo de Olavide, Seville, Spain.ORCID http://orcid.org/0000-0002-7632-5421
Katarzyna H MaslowskaCancer Research Center of Marseille: Team DNA Damage and Genome Instability, CNRS, Aix Marseille Univ, Inserm, Institut Paoli-Calmettes, Marseille, France.ORCID http://orcid.org/0000-0003-3393-8225
Florencia VillafañezCancer Research Center of Marseille: Team DNA Damage and Genome Instability, CNRS, Aix Marseille Univ, Inserm, Institut Paoli-Calmettes, Marseille, France.
Clare FaschingDepartment of Microbiology & Molecular Genetics, University of California, Davis, CA, USA.
Christopher EdeDepartment of Microbiology & Molecular Genetics, University of California, Davis, CA, USA.
Vincent PagèsCancer Research Center of Marseille: Team DNA Damage and Genome Instability, CNRS, Aix Marseille Univ, Inserm, Institut Paoli-Calmettes, Marseille, France.ORCID http://orcid.org/0000-0002-3059-2903
Felix PradoCentro Andaluz de Biología Molecular y Medicina Regenerativa -CABIMER; Consejo Superior de Investigaciones Científicas; Universidad de Sevilla; Universidad Pablo de Olavide, Seville, Spain.ORCID http://orcid.org/0000-0001-9805-782X
Petr CejkaInstitute for Research in Biomedicine, Faculty of Biomedical Sciences, Università della Svizzera italiana (USI), Bellinzona, Switzerland.ORCID http://orcid.org/0000-0002-9087-032X
Wolf-Dietrich HeyerDepartment of Microbiology & Molecular Genetics, University of California, Davis, CA, USA. wdheyer@ucdavis.edu.ORCID http://orcid.org/0000-0002-7774-1953
Funding
Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI KC KENT LLOYD · 2002 to 2026
$84.9M
UC Davis MCB T32 Administrative Supplement to Recognize Excellence in Diversity, Equity, Inclusion, and Accessibility (DEIA) MentorshipT32GM007377 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI CHEDIN, FREDERIC LOUIS · 1985 to 2023
$9.9M
RECOMBINATIONAL MECHANISMS OF DNA REPAIR IN EUKARYOTESR01GM058015 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI HEYER, WOLF-DIETRICH · 2000 to 2025
$8.8M
Training Program in Oncogenic Signals and Chromosome BiologyT32CA108459 · NCI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HEYER, WOLF-DIETRICH · 2006 to 2020
$3.6M
Role of Sgs1 in homologous recombination: Dissolution of branched DNA substratesF32GM083509 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FASCHING, CLARE L · 2008 to 2010
$149k
NCI NIH HHS P30 CA093373NCI NIH HHS T32 CA108459NIGMS NIH HHS F32 GM083509NIGMS NIH HHS R01 GM058015NIGMS NIH HHS T32 GM007377U.S. Department of Health & Human Services | National Institutes of Health (NIH) CA093373U.S. Department of Health & Human Services | National Institutes of Health (NIH) GM131037U.S. Department of Health & Human Services | National Institutes of Health (NIH) GM58015
6 · The paper itself
Abstract
Stalled replication forks are processed in post-replication repair by homologous recombination, fork regression, and translesion DNA synthesis. However, the regulation of pathway usage is not fully understood. Rad51 protein maintains genomic stability through its roles in recombination and in protecting stalled replication forks. We report isolation of mutations in Saccharomyces cerevisiae Rad51 that shift post-replication repair from recombination to alternate pathways including mutagenic translesion synthesis. Rad51-E135D and Rad51-K305N show near normal in vitro recombination despite changes in their DNA binding profiles, in particular to dsDNA. The mutants lead to a defect in Rad51 recruitment to stalled forks in vivo as well as a defect in the protection of dsDNA from degradation by Dna2-Sgs1 and Exo1 in vitro. Together, the evidence suggests that Rad51 binding to duplex DNA is critical to control pathway usage at stalled replication forks.
Indexed as
DNA RepairDNA ReplicationRad51 RecombinaseSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA-Binding ProteinsDNA, FungalDNA HelicasesExodeoxyribonucleasesMutationRecQ HelicasesTranslesion DNA SynthesisDNA2 protein, S cerevisiaeDNA-Binding ProteinsDNA, FungalDNA Helicasesexodeoxyribonuclease IExodeoxyribonucleasesRAD51 protein, S cerevisiaeRad51 RecombinaseRecQ HelicasesSaccharomyces cerevisiae ProteinsSGS1 protein, S cerevisiae
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.
Rad51 determines pathway usage in post-replication repair. · full record | OpenQuestion