Targeted Inactivation of Mouse RAD52Reduces Homologous Recombination but Not Resistance to Ionizing Radiation
| العنوان: | Targeted Inactivation of Mouse RAD52Reduces Homologous Recombination but Not Resistance to Ionizing Radiation |
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| المؤلفون: | Petra P. H. Van Sloun, Albert Pastink, Tonnie Rijkers, Willy M. Baarends, Bruno Morolli, Jody Van Den Ouweland, A. Rolink, Paul H.M. Lohman |
| المساهمون: | Developmental Biology |
| المصدر: | Molecular and Cellular Biology, 18(11), 6423-6429. American Society for Microbiology |
| بيانات النشر: | Informa UK Limited, 1998. |
| سنة النشر: | 1998 |
| مصطلحات موضوعية: | DNA Repair, Cell Survival, DNA damage, T-Lymphocytes, Saccharomyces cerevisiae, Mutant, RAD52, Conserved sequence, Mice, Radiation, Ionizing, Animals, Cell Growth and Development, Molecular Biology, Gene, Mice, Knockout, Recombination, Genetic, B-Lymphocytes, biology, Stem Cells, X-Rays, fungi, Cell Biology, Flow Cytometry, biology.organism_classification, Molecular biology, Immunoglobulin Switch Region, Rad52 DNA Repair and Recombination Protein, DNA-Binding Proteins, enzymes and coenzymes (carbohydrates), Phenotype, Homologous recombination, Recombination, DNA Damage |
| الوصف: | 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. |
| تدمد: | 1098-5549 0270-7306 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::778b5d08db434438de237658a4d0e611Test https://doi.org/10.1128/mcb.18.11.6423Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....778b5d08db434438de237658a4d0e611 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10985549 02707306 |
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