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• W1794578906 endingPage "2102" @default.
• W1794578906 startingPage "2090" @default.
• W1794578906 abstract "Vertebrates have two cohesin complexes that consist of Smc1, Smc3, Rad21/Scc1 and either SA1 or SA2, but their functional specificity is unclear. Mouse embryos lacking SA1 show developmental delay and die before birth. Comparison of the genome-wide distribution of cohesin in wild-type and SA1-null cells reveals that SA1 is largely responsible for cohesin accumulation at promoters and at sites bound by the insulator protein CTCF. As a consequence, ablation of SA1 alters transcription of genes involved in biological processes related to Cornelia de Lange syndrome (CdLS), a genetic disorder linked to dysfunction of cohesin. We show that the presence of cohesin-SA1 at the promoter of myc and of protocadherin genes positively regulates their expression, a task that cannot be assumed by cohesin-SA2. Lack of SA1 also alters cohesin-binding pattern along some gene clusters and leads to dysregulation of genes within. We hypothesize that impaired cohesin-SA1 function in gene expression underlies the molecular aetiology of CdLS." @default.
• W1794578906 created "2016-06-24" @default.
• W1794578906 creator A5028569390 @default.
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• W1794578906 creator A5070440139 @default.
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• W1794578906 date "2012-03-13" @default.
• W1794578906 modified "2023-10-18" @default.
• W1794578906 title "A unique role of cohesin-SA1 in gene regulation and development" @default.
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• W1794578906 doi "https://doi.org/10.1038/emboj.2012.60" @default.
• W1794578906 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3343463" @default.
• W1794578906 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22415368" @default.
• W1794578906 hasPublicationYear "2012" @default.
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