<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lee M</submitter><funding>Medical Research Council</funding><funding>CIHR</funding><pagination>3360-9</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3145889</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>30(30)</volume><pubmed_abstract>The inactivation of BRCA2, a suppressor of breast, ovarian and other epithelial cancers, triggers instability in chromosome structure and number, which are thought to arise from defects in DNA recombination and mitotic cell division, respectively. Human BRCA2 controls DNA recombination via eight BRC repeats, evolutionarily conserved motifs of ∼35 residues, that interact directly with the recombinase RAD51. How BRCA2 controls mitotic cell division is debated. Several studies by different groups report that BRCA2 deficiency affects cytokinesis. Moreover, its interaction with HMG20b, a protein of uncertain function containing a promiscuous DNA-binding domain and kinesin-like coiled coils, has been implicated in the G2-M transition. We show here that HMG20b depletion by RNA interference distur</pubmed_abstract><journal>Oncogene</journal><pubmed_title>A mitotic function for the high-mobility group protein HMG20b regulated by its interaction with the BRC repeats of the BRCA2 tumor suppressor.</pubmed_title><pmcid>PMC3145889</pmcid><funding_grant_id>G0700651</funding_grant_id><funding_grant_id>G9900064</funding_grant_id><funding_grant_id>G0600332</funding_grant_id><funding_grant_id>MC_U105359877</funding_grant_id><pubmed_authors>Venkitaraman AR</pubmed_authors><pubmed_authors>Daniels MJ</pubmed_authors><pubmed_authors>Lee M</pubmed_authors><pubmed_authors>Garnett MJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>A mitotic function for the high-mobility group protein HMG20b regulated by its interaction with the BRC repeats of the BRCA2 tumor suppressor.</name><description>The inactivation of BRCA2, a suppressor of breast, ovarian and other epithelial cancers, triggers instability in chromosome structure and number, which are thought to arise from defects in DNA recombination and mitotic cell division, respectively. Human BRCA2 controls DNA recombination via eight BRC repeats, evolutionarily conserved motifs of ∼35 residues, that interact directly with the recombinase RAD51. How BRCA2 controls mitotic cell division is debated. Several studies by different groups report that BRCA2 deficiency affects cytokinesis. Moreover, its interaction with HMG20b, a protein of uncertain function containing a promiscuous DNA-binding domain and kinesin-like coiled coils, has been implicated in the G2-M transition. We show here that HMG20b depletion by RNA interference distur</description><dates><release>2011-01-01T00:00:00Z</release><publication>2011 Jul</publication><modification>2025-05-31T22:44:38.487Z</modification><creation>2025-05-31T22:44:38.487Z</creation></dates><accession>S-EPMC3145889</accession><cross_references><pubmed>21399666</pubmed><doi>10.1038/onc.2011.55</doi></cross_references></HashMap>