{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Remeseiro S"],"funding":["NIGMS NIH HHS"],"pagination":["2076-89"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3343459"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(9)"],"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"],"journal":["The EMBO journal"],"pubmed_title":["Cohesin-SA1 deficiency drives aneuploidy and tumourigenesis in mice due to impaired replication of telomeres."],"pmcid":["PMC3343459"],"funding_grant_id":["R01 GM045751","GM045751"],"pubmed_authors":["Drosopoulos WC","Remeseiro S","Carretero M","Martinez P","Canamero M","Schildkraut CL","Cuadrado A","Blasco MA","Losada A"],"additional_accession":[]},"is_claimable":false,"name":"Cohesin-SA1 deficiency drives aneuploidy and tumourigenesis in mice due to impaired replication of telomeres.","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","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 May","modification":"2025-04-04T09:12:49.028Z","creation":"2019-03-27T00:53:01Z"},"accession":"S-EPMC3343459","cross_references":{"pubmed":["22415365"],"doi":["10.1038/emboj.2012.11"]}}