<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Romero-Franco A</submitter><funding>Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación)</funding><funding>Fundación Científica Asociación Española Contra el Cáncer (Scientific Foundation, Spanish Association Against Cancer)</funding><funding>Consejería de Economía, Innovación, Ciencia y Empleo, Junta de Andalucía (Ministry of Economy, Innovation, Science and Employment, Government of Andalucia)</funding><pagination>10802</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12669580</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>Genomic stability maintenance requires the repair of DNA breaks in the most accurate fashion. So, an exquisite regulatory network controls the choice between different repair mechanisms to maximize genome integrity. This relies mostly at the level of DNA end resection, the initial steps of the homologous recombination. On the other hand, numerous cellular activities follow a 24 h oscillation known as the circadian cycle. Thus, we explored the regulation of the choice between different DNA break repair pathways along the circadian cycle. Here we show that in human cells DNA resection shows a circadian oscillation, with a peak at early morning followed by a partial and progressive reduction until late afternoon. Such regulation depends on the circadian clock core component CRY1, which modula</pubmed_abstract><journal>Nature communications</journal><pubmed_title>Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.</pubmed_title><pmcid>PMC12669580</pmcid><funding_grant_id>P18-RT-1204</funding_grant_id><funding_grant_id>PID2022-136791NB-I00</funding_grant_id><funding_grant_id>PRYGN246626HUER</funding_grant_id><pubmed_authors>Miras H</pubmed_authors><pubmed_authors>Jimeno-Gonzalez S</pubmed_authors><pubmed_authors>Jimeno S</pubmed_authors><pubmed_authors>Romero-Franco A</pubmed_authors><pubmed_authors>Aguilera P</pubmed_authors><pubmed_authors>Castellano-Pozo M</pubmed_authors><pubmed_authors>Huertas P</pubmed_authors><pubmed_authors>Checa-Rodriguez C</pubmed_authors><pubmed_authors>Wals A</pubmed_authors><pubmed_authors>Lopez-Contreras AJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.</name><description>Genomic stability maintenance requires the repair of DNA breaks in the most accurate fashion. So, an exquisite regulatory network controls the choice between different repair mechanisms to maximize genome integrity. This relies mostly at the level of DNA end resection, the initial steps of the homologous recombination. On the other hand, numerous cellular activities follow a 24 h oscillation known as the circadian cycle. Thus, we explored the regulation of the choice between different DNA break repair pathways along the circadian cycle. Here we show that in human cells DNA resection shows a circadian oscillation, with a peak at early morning followed by a partial and progressive reduction until late afternoon. Such regulation depends on the circadian clock core component CRY1, which modula</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-07-15T09:13:49.152Z</modification><creation>2026-07-02T03:09:03.981Z</creation></dates><accession>S-EPMC12669580</accession><cross_references><pubmed>41326346</pubmed><doi>10.1038/s41467-025-65854-1</doi></cross_references></HashMap>