<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kakarougkas A</submitter><funding>Medical Research Council</funding><funding>Canadian Institutes of Health Research</funding><pagination>9719-31</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3834810</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>41(21)</volume><pubmed_abstract>Although DNA non-homologous end-joining repairs most DNA double-strand breaks (DSBs) in G2 phase, late repairing DSBs undergo resection and repair by homologous recombination (HR). Based on parallels to the situation in G1 cells, previous work has suggested that DSBs that undergo repair by HR predominantly localize to regions of heterochromatin (HC). By using H3K9me3 and H4K20me3 to identify HC regions, we substantiate and extend previous evidence, suggesting that HC-DSBs undergo repair by HR. Next, we examine roles for 53BP1 and BRCA1 in this process. Previous studies have shown that 53BP1 is pro-non-homologous end-joining and anti-HR. Surprisingly, we demonstrate that in G2 phase, 53BP1 is required for HR at HC-DSBs with its role being to promote phosphorylated KAP-1 foci formation. BRCA</pubmed_abstract><journal>Nucleic acids research</journal><pubmed_title>Opposing roles for 53BP1 during homologous recombination.</pubmed_title><pmcid>PMC3834810</pmcid><funding_grant_id>G0500897</funding_grant_id><funding_grant_id>G0801130B</funding_grant_id><funding_grant_id>G1000050</funding_grant_id><pubmed_authors>Goodarzi AA</pubmed_authors><pubmed_authors>Jeggo PA</pubmed_authors><pubmed_authors>Shibata A</pubmed_authors><pubmed_authors>Kakarougkas A</pubmed_authors><pubmed_authors>Ismail A</pubmed_authors><pubmed_authors>Klement K</pubmed_authors><pubmed_authors>Freire R</pubmed_authors><pubmed_authors>Lobrich M</pubmed_authors><pubmed_authors>Conrad S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Opposing roles for 53BP1 during homologous recombination.</name><description>Although DNA non-homologous end-joining repairs most DNA double-strand breaks (DSBs) in G2 phase, late repairing DSBs undergo resection and repair by homologous recombination (HR). Based on parallels to the situation in G1 cells, previous work has suggested that DSBs that undergo repair by HR predominantly localize to regions of heterochromatin (HC). By using H3K9me3 and H4K20me3 to identify HC regions, we substantiate and extend previous evidence, suggesting that HC-DSBs undergo repair by HR. Next, we examine roles for 53BP1 and BRCA1 in this process. Previous studies have shown that 53BP1 is pro-non-homologous end-joining and anti-HR. Surprisingly, we demonstrate that in G2 phase, 53BP1 is required for HR at HC-DSBs with its role being to promote phosphorylated KAP-1 foci formation. BRCA</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013 Nov</publication><modification>2025-04-04T12:26:49.356Z</modification><creation>2019-03-27T03:08:58Z</creation></dates><accession>S-EPMC3834810</accession><cross_references><pubmed>23969417</pubmed><doi>10.1093/nar/gkt729</doi></cross_references></HashMap>