{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gonzalez DI"],"funding":["NCI NIH HHS","National Institutes of Health","NIH HHS","NIGMS NIH HHS","Vanderbilt-Ingram Cancer Center"],"pagination":["gkaf1373"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12709191"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["53(22)"],"pubmed_abstract":["Double-strand breaks (DSBs) pose a significant threat to chromosome stability and, if left unrepaired, can result in chromosome rearrangements. Canonical DNA repair pathways mitigate these risks. However, if these repair mechanisms fail to repair the DSB, alternative repair pathways, such as break-induced replication, single-strand annealing, and de novo telomere addition (dnTA), can be utilized. Yeast subtelomeric regions are hotspots of recombination, while interstitial telomere-like sites can promote dnTA. In yeast, dnTA sites, termed SiRTAs (sites of repair-associated telomere addition), require Cdc13 association. We identified the ubiquitin protease Ubp10 as a positive regulator of dnTA at SiRTAs. Loss of UBP10 reduces dnTA frequency but increases the frequency of other chromosomal re"],"journal":["Nucleic acids research"],"pubmed_title":["The ubiquitin protease Ubp10 suppresses the formation of translocations at interstitial telomere-like sites."],"pmcid":["PMC12709191"],"funding_grant_id":["R01 GM123292","P30 CA068485","T32GM137793","T32 GM137793","P30CA068485","R01GM123292"],"pubmed_authors":["Epum EA","Gonzalez DI","Friedman KL","Westerbeek AR"],"additional_accession":[]},"is_claimable":false,"name":"The ubiquitin protease Ubp10 suppresses the formation of translocations at interstitial telomere-like sites.","description":"Double-strand breaks (DSBs) pose a significant threat to chromosome stability and, if left unrepaired, can result in chromosome rearrangements. Canonical DNA repair pathways mitigate these risks. However, if these repair mechanisms fail to repair the DSB, alternative repair pathways, such as break-induced replication, single-strand annealing, and de novo telomere addition (dnTA), can be utilized. Yeast subtelomeric regions are hotspots of recombination, while interstitial telomere-like sites can promote dnTA. In yeast, dnTA sites, termed SiRTAs (sites of repair-associated telomere addition), require Cdc13 association. We identified the ubiquitin protease Ubp10 as a positive regulator of dnTA at SiRTAs. Loss of UBP10 reduces dnTA frequency but increases the frequency of other chromosomal re","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-06-09T03:08:46.849Z","creation":"2026-06-09T03:07:21.836Z"},"accession":"S-EPMC12709191","cross_references":{"pubmed":["41404807"],"doi":["10.1093/nar/gkaf1373"]}}