Expression of human RAD52 confers resistance to ionizing radiation in mammalian cells.
Processing of mutagenic DNA damages by the double strand breaks (DSB) in eukaryotes is most likely achieved by multiple pathways, including homologous recombination. Although RAD52 has been shown to be important for DSB repair in yeasts, its role in DSB repair in mammalian cells has not been demonstrated. This study reports for the first time that the overexpression of human RAD52 confers enhanced resistance to gamma-rays and induces homologous intrachromosomal recombination in cultured monkey cells. Recombination frequency synergistically increased by the combination of overexpression of RAD52 and ionizing radiation. These observations suggest that homologous recombination mediated by RAD52 is involved in double-stranded break repair in mammalian cells.
Park
M S
MS
Life Sciences Division, Los Alamos National Laboratory, New Mexico 87545, USA.
D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D002460:Cell Line; D003001:Cloning, Molecular; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000235:genetics*; D000882:Haplorhini; D006801:Humans; D008969:Molecular Sequence Data; D051721:Rad52 DNA Repair and Recombination Protein; D011836:Radiation Tolerance; D011995:Recombination, Genetic; D017386:Sequence Homology, Amino Acid
D004268:DNA-Binding Proteins; C497194:RAD52 protein, human; D051721:Rad52 DNA Repair and Recombination Protein