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• W2078291208 abstract "Werner syndrome (WS) is a premature aging disorder caused by WRN protein deficiency. Here, we report on the generation of a human WS model in human embryonic stem cells (ESCs). Differentiation of WRN-null ESCs to mesenchymal stem cells (MSCs) recapitulates features of premature cellular aging, a global loss of H3K9me3, and changes in heterochromatin architecture. We show that WRN associates with heterochromatin proteins SUV39H1 and HP1α and nuclear lamina-heterochromatin anchoring protein LAP2β. Targeted knock-in of catalytically inactive SUV39H1 in wild-type MSCs recapitulates accelerated cellular senescence, resembling WRN-deficient MSCs. Moreover, decrease in WRN and heterochromatin marks are detected in MSCs from older individuals. Our observations uncover a role for WRN in maintaining heterochromatin stability and highlight heterochromatin disorganization as a potential determinant of human aging." @default.
• W2078291208 created "2016-06-24" @default.
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• W2078291208 date "2015-06-05" @default.
• W2078291208 modified "2023-10-14" @default.
• W2078291208 title "A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging" @default.
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• W2078291208 doi "https://doi.org/10.1126/science.aaa1356" @default.
• W2078291208 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4494668" @default.
• W2078291208 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25931448" @default.
• W2078291208 hasPublicationYear "2015" @default.
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