<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Orhan E</submitter><funding>SIRIC Montpellier Cancer</funding><pagination>2930</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8230762</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(12)</volume><pubmed_abstract>The RAD51 recombinase is a critical effector of Homologous Recombination (HR), which is an essential DNA repair mechanism for double-strand breaks. The RAD51 protein is recruited onto the DNA break by BRCA2 and forms homopolymeric filaments that invade the homologous chromatid and use it as a template for repair. RAD51 filaments are detectable by immunofluorescence as distinct foci in the cell nucleus, and their presence is a read out of HR proficiency. RAD51 is an essential gene, protecting cells from genetic instability. Its expression is low and tightly regulated in normal cells and, contrastingly, elevated in a large fraction of cancers, where its level of expression and activity have been linked with sensitivity to genotoxic treatment. In particular, BRCA-deficient tumors show reduced</pubmed_abstract><journal>Cancers</journal><pubmed_title>Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?</pubmed_title><pmcid>PMC8230762</pmcid><funding_grant_id>Grant INCa-DGOS-Inserm_12553</funding_grant_id><pubmed_authors>Theillet C</pubmed_authors><pubmed_authors>Sardet C</pubmed_authors><pubmed_authors>Velazquez C</pubmed_authors><pubmed_authors>Orhan E</pubmed_authors><pubmed_authors>Tabet I</pubmed_authors></additional><is_claimable>false</is_claimable><name>Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?</name><description>The RAD51 recombinase is a critical effector of Homologous Recombination (HR), which is an essential DNA repair mechanism for double-strand breaks. The RAD51 protein is recruited onto the DNA break by BRCA2 and forms homopolymeric filaments that invade the homologous chromatid and use it as a template for repair. RAD51 filaments are detectable by immunofluorescence as distinct foci in the cell nucleus, and their presence is a read out of HR proficiency. RAD51 is an essential gene, protecting cells from genetic instability. Its expression is low and tightly regulated in normal cells and, contrastingly, elevated in a large fraction of cancers, where its level of expression and activity have been linked with sensitivity to genotoxic treatment. In particular, BRCA-deficient tumors show reduced</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2026-04-08T09:18:08.878Z</modification><creation>2022-02-10T18:04:36.816Z</creation></dates><accession>S-EPMC8230762</accession><cross_references><pubmed>34208195</pubmed><doi>10.3390/cancers13122930</doi></cross_references></HashMap>