ArticleMolecular and cellular biology1998
Targeted inactivation of mouse RAD52 reduces homologous recombination but not resistance to ionizing radiation.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 papers.
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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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Who cites it
155 citing papers in PubMed, 318 citations in OpenAlex.
- Mechanism of single-strand annealing from native mass spectrometry and cryo-EM structures of RAD52 homolog Mgm101.Nucleic acids research · 2026Article
- Mutations altering the DNA binding domains of the human RAD52 protein exert distinct effects on homologous recombination repair in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2026Article
- The alternative lengthening of telomeres pathway through a DNA repair lens: mechanism and therapeutic opportunities.NAR cancer · 2025Review
- AtMCM10 facilitates SDSA-mediated intermolecular homologous recombination repair via liquid-liquid phase separation in DNA damage response.Nature communications · 2025Article
- Article
- Transcriptomics and Proteomics Analysis of the Liver ofInternational journal of molecular sciences · 2025Article
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- An integrative structural study of the human full-length RAD52 at 2.2 Å resolution.Communications biology · 2024Article
- New Horizons of Synthetic Lethality in Cancer: Current Development and Future Perspectives.Journal of medicinal chemistry · 2024Review
- Characterization and regulation of cell cycle-independent noncanonical gene targeting.Nature communications · 2024Article
- Human RAD52 stimulates the RAD51-mediated homology search.Life science alliance · 2024Article
- Analysis of the indispensable RAD51 cofactor BRCA2 inLife science alliance · 2024Article
- Alternative lengthening of telomeres: mechanism and the pathogenesis of cancer.Journal of clinical pathology · 2024Article
- Article
- Novel Insights into RAD52's Structure, Function, and Druggability for Synthetic Lethality and Innovative Anticancer Therapies.Cancers · 2023Review
- Repair of DNA double-strand breaks in plant meiosis: role of eukaryotic RecA recombinases and their modulators.Plant reproduction · 2023Review
- Roles of homologous recombination in response to ionizing radiation-induced DNA damage.International journal of radiation biology · 2023Review
- A moving target for drug discovery: Structure activity relationship and many genome (de)stabilizing functions of the RAD52 protein.DNA repair · 2022Review
- Critical DNA damaging pathways in tumorigenesis.Seminars in cancer biology · 2022Review
- Rad52 mediates class-switch DNA recombination to IgD.Nature communications · 2022Article
95 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
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAD52 epistasis group is required for recombinational repair of double-strand breaks (DSBs) and shows strong evolutionary conservation. In Saccharomyces cerevisiae, RAD52 is one of the key members in this pathway. Strains with mutations in this gene show strong hypersensitivity to DNA-damaging agents and defects in recombination. Inactivation of the mouse homologue of RAD52 in embryonic stem (ES) cells resulted in a reduced frequency of homologous recombination. Unlike the yeast Scrad52 mutant, MmRAD52(-/-) ES cells were not hypersensitive to agents that induce DSBs. MmRAD52 null mutant mice showed no abnormalities in viability, fertility, and the immune system. These results show that, as in S. cerevisiae, MmRAD52 is involved in recombination, although the repair of DNA damage is not affected upon inactivation, indicating that MmRAD52 may be involved in certain types of DSB repair processes and not in others. The effect of inactivating MmRAD52 suggests the presence of genes functionally related to MmRAD52, which can partly compensate for the absence of MmRad52 protein.
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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.