ArticleGenetics2002
A molecular genetic dissection of the evolutionarily conserved N terminus of yeast Rad52.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 80 citations in OpenAlex.
- In Vivo DNA Assembly inACS synthetic biology · 2025Article
- Strategic targeting of Cas9 nickase induces large segmental duplications.Cell genomics · 2024Article
- Massive contractions of myotonic dystrophy type 2-associated CCTG tetranucleotide repeats occur via double-strand break repair with distinct requirements for DNA helicases.G3 (Bethesda, Md.) · 2024Article
- Characterization of theGenes · 2023Article
- A moving target for drug discovery: Structure activity relationship and many genome (de)stabilizing functions of the RAD52 protein.DNA repair · 2022Review
- Article
- Mechanisms restraining break-induced replication at two-ended DNA double-strand breaks.The EMBO journal · 2021Article
- Catalytically inactive Cas9 impairs DNA replication fork progression to induce focal genomic instability.Nucleic acids research · 2021Article
- Improving the homologous recombination efficiency ofMetabolic engineering communications · 2020Article
- Proteomics Reveals Distinct Changes Associated with Increased Gamma Radiation Resistance in the Black YeastGenes · 2020Article
- Variants of the humanMicrobial cell (Graz, Austria) · 2020Article
- Compound F779-0434 causes synthetic lethality in BRCA2-deficient cancer cells by disrupting RAD52-ssDNA association.RSC advances · 2018Article
- Integrating Experimental and In Silico HTS in the Discovery of Inhibitors of Protein-Nucleic Acid Interactions.Methods in enzymology · 2018Article
- Genome-wide mapping of sister chromatid exchange events in single yeast cells using Strand-seq.eLife · 2017Article
- Rad52 Inverse Strand Exchange Drives RNA-Templated DNA Double-Strand Break Repair.Molecular cell · 2017Article
- Homologous recombination in budding yeast expressing the human RAD52 gene reveals a Rad51-independent mechanism of conservative double-strand break repair.Nucleic acids research · 2017Article
- Article
- Multiple Rad52-Mediated Homology-Directed Repair Mechanisms Are Required to Prevent Telomere Attrition-Induced Senescence in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- SUMOylation of Rad52-Rad59 synergistically change the outcome of mitotic recombination.DNA repair · 2016Article
- Pro-recombination Role of Srs2 Protein Requires SUMO (Small Ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction.The Journal of biological chemistry · 2016Article
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 1 institution in 1 country.
Funding
Abstract
Rad52 is a DNA-binding protein that stimulates the annealing of complementary single-stranded DNA. Only the N terminus of Rad52 is evolutionarily conserved; it contains the core activity of the protein, including its DNA-binding activity. To identify amino acid residues that are important for Rad52 function(s), we systematically replaced 76 of 165 amino acid residues in the N terminus with alanine. These substitutions were examined for their effects on the repair of gamma-ray-induced DNA damage and on both interchromosomal and direct repeat heteroallelic recombination. This analysis identified five regions that are required for efficient gamma-ray damage repair or mitotic recombination. Two regions, I and II, also contain the classic mutations, rad52-2 and rad52-1, respectively. Interestingly, four of the five regions contain mutations that impair the ability to repair gamma-ray-induced DNA damage yet still allow mitotic recombinants to be produced at rates that are similar to or higher than those obtained with wild-type strains. In addition, a new class of separation-of-function mutation that is only partially deficient in the repair of gamma-ray damage, but exhibits decreased mitotic recombination similar to rad52 null strains, was identified. These results suggest that Rad52 protein acts differently on lesions that occur spontaneously during the cell cycle than on those induced by gamma-irradiation.
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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.