ArticleProceedings of the National Academy of Sciences of the United States of America2012
Bioinformatic identification of genes suppressing genome instability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- The role of the nuclear pore complex in the stability of disease-related short tandem DNA repeats.Nucleic acids research · 2026Article
- Both genome instability and replicative senescence stem from the shortest telomere in telomerase-negative cells.Nature communications · 2026Article
- Unraveling the role of coagulation-related genes in esophageal squamous cell carcinoma: development of a prognostic model and exploration of potential clinical significance.Frontiers in oncology · 2025Article
- Interstitial telomeric sequences promote gross chromosomal rearrangement via multiple mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of different classes of genome instability suppressor genes through analysis of DNA damage response markers.G3 (Bethesda, Md.) · 2024Article
- FEN1 endonuclease as a therapeutic target for human cancers with defects in homologous recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Elongation Factor TFIIS Prevents Transcription Stress and R-Loop Accumulation to Maintain Genome Stability.Molecular cell · 2019Article
- EssentialProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Review
- Cdc73 suppresses genome instability by mediating telomere homeostasis.PLoS genetics · 2018Article
- Pathways and Mechanisms that Prevent Genome Instability inGenetics · 2017Review
- Forks on the Run: Can the Stalling of DNA Replication Promote Epigenetic Changes?Frontiers in genetics · 2017Review
- Guinier peak analysis for visual and automated inspection of small-angle X-ray scattering data.Journal of applied crystallography · 2016Article
- A Network of Conserved Synthetic Lethal Interactions for Exploration of Precision Cancer Therapy.Molecular cell · 2016Article
- A genetic network that suppresses genome rearrangements in Saccharomyces cerevisiae and contains defects in cancers.Nature communications · 2016Article
- Yeast Assay Highlights the Intrinsic Genomic Instability of Human PML Intron 6 over Intron 3 and the Role of Replication Fork Proteins.PloS one · 2015Article
- Review
- SET-ting the stage for DNA repair.Nature structural & molecular biology · 2014Article
- Mutational landscape of yeast mutator strains.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Do mutator mutations fuel tumorigenesis?Cancer metastasis reviews · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Unbiased forward genetic screens for mutations causing increased gross chromosomal rearrangement (GCR) rates in Saccharomyces cerevisiae are hampered by the difficulty in reliably using qualitative GCR assays to detect mutants with small but significantly increased GCR rates. We therefore developed a bioinformatic procedure using genome-wide functional genomics screens to identify and prioritize candidate GCR-suppressing genes on the basis of the shared drug sensitivity suppression and similar genetic interactions as known GCR suppressors. The number of known suppressors was increased from 75 to 110 by testing 87 predicted genes, which identified unanticipated pathways in this process. This analysis explicitly dealt with the lack of concordance among high-throughput datasets to increase the reliability of phenotypic predictions. Additionally, shared phenotypes in one assay were imperfect predictors for shared phenotypes in other assays, indicating that although genome-wide datasets can be useful in aggregate, caution and validation methods are required when deciphering biological functions via surrogate measures, including growth-based genetic interactions.
Indexed as
Identifiers
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.