<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Remeseiro S</submitter><funding>NIGMS NIH HHS</funding><pagination>2076-89</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3343459</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(9)</volume><pubmed_abstract>Cohesin is a protein complex originally identified for its role in sister chromatid cohesion, although increasing evidence portrays it also as a major organizer of interphase chromatin. Vertebrate cohesin consists of Smc1, Smc3, Rad21/Scc1 and either stromal antigen 1 (SA1) or SA2. To explore the functional specificity of these two versions of cohesin and their relevance for embryonic development and cancer, we generated a mouse model deficient for SA1. Complete ablation of SA1 results in embryonic lethality, while heterozygous animals have shorter lifespan and earlier onset of tumourigenesis. SA1-null mouse embryonic fibroblasts show decreased proliferation and increased aneuploidy as a result of chromosome segregation defects. These defects are not caused by impaired centromeric cohesion</pubmed_abstract><journal>The EMBO journal</journal><pubmed_title>Cohesin-SA1 deficiency drives aneuploidy and tumourigenesis in mice due to impaired replication of telomeres.</pubmed_title><pmcid>PMC3343459</pmcid><funding_grant_id>R01 GM045751</funding_grant_id><funding_grant_id>GM045751</funding_grant_id><pubmed_authors>Drosopoulos WC</pubmed_authors><pubmed_authors>Remeseiro S</pubmed_authors><pubmed_authors>Carretero M</pubmed_authors><pubmed_authors>Martinez P</pubmed_authors><pubmed_authors>Canamero M</pubmed_authors><pubmed_authors>Schildkraut CL</pubmed_authors><pubmed_authors>Cuadrado A</pubmed_authors><pubmed_authors>Blasco MA</pubmed_authors><pubmed_authors>Losada A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cohesin-SA1 deficiency drives aneuploidy and tumourigenesis in mice due to impaired replication of telomeres.</name><description>Cohesin is a protein complex originally identified for its role in sister chromatid cohesion, although increasing evidence portrays it also as a major organizer of interphase chromatin. Vertebrate cohesin consists of Smc1, Smc3, Rad21/Scc1 and either stromal antigen 1 (SA1) or SA2. To explore the functional specificity of these two versions of cohesin and their relevance for embryonic development and cancer, we generated a mouse model deficient for SA1. Complete ablation of SA1 results in embryonic lethality, while heterozygous animals have shorter lifespan and earlier onset of tumourigenesis. SA1-null mouse embryonic fibroblasts show decreased proliferation and increased aneuploidy as a result of chromosome segregation defects. These defects are not caused by impaired centromeric cohesion</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 May</publication><modification>2025-04-04T09:12:49.028Z</modification><creation>2019-03-27T00:53:01Z</creation></dates><accession>S-EPMC3343459</accession><cross_references><pubmed>22415365</pubmed><doi>10.1038/emboj.2012.11</doi></cross_references></HashMap>