{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Clear AD"],"funding":["NCI NIH HHS"],"pagination":["270-285"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7517009"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(10)"],"pubmed_abstract":["RAD52 is a structurally and functionally conserved component of the DNA double-strand break (DSB) repair apparatus from budding yeast to humans. We recently showed that expressing the human gene, <i>HsRAD52</i> in <i>rad52</i> mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that <i>HsRAD52</i> supports DSB repair by a mechanism of HRR that conserves genome structure and is independent of the canonical HR machinery. In this study we report that naturally occurring variants of <i>HsRAD52</i>, one of which suppresses the pathogenicity of <i>BRCA2</i> mutations, were unable to suppress the IR sensitivity and HRR defects of <i>rad52</i> mutant yeast cells, but fully suppressed a d"],"journal":["Microbial cell (Graz, Austria)"],"pubmed_title":["Variants of the human <i>RAD52</i> gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast."],"pmcid":["PMC7517009"],"funding_grant_id":["R01 CA184585","R50 CA211280"],"pubmed_authors":["Clear AD","Negritto MC","Lewis O","Wolf EW","Owens S","Bailis AM","Xu J","Manthey GM","Perry JJP","Adamson AW","Rico R","Kenjic N","Neuhausen SL","Lopez IY"],"additional_accession":[]},"is_claimable":false,"name":"Variants of the human <i>RAD52</i> gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast.","description":"RAD52 is a structurally and functionally conserved component of the DNA double-strand break (DSB) repair apparatus from budding yeast to humans. We recently showed that expressing the human gene, <i>HsRAD52</i> in <i>rad52</i> mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that <i>HsRAD52</i> supports DSB repair by a mechanism of HRR that conserves genome structure and is independent of the canonical HR machinery. In this study we report that naturally occurring variants of <i>HsRAD52</i>, one of which suppresses the pathogenicity of <i>BRCA2</i> mutations, were unable to suppress the IR sensitivity and HRR defects of <i>rad52</i> mutant yeast cells, but fully suppressed a d","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Jul","modification":"2025-04-05T12:57:33.315Z","creation":"2025-04-05T12:57:33.315Z"},"accession":"S-EPMC7517009","cross_references":{"pubmed":["33015141"],"doi":["10.15698/mic2020.10.732"]}}