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• W2158300687 abstract "Proliferation of pancreatic islet β cells is an important mechanism for self-renewal and for adaptive islet expansion. Increased expression of the Ink4a/Arf locus, which encodes the cyclin-dependent kinase inhibitor p16 INK4a and tumor suppressor p19 Arf , limits β-cell regeneration in aging mice, but the basis of β-cell Ink4a/Arf regulation is poorly understood. Here we show that Enhancer of zeste homolog 2 (Ezh2), a histone methyltransferase and component of a Polycomb group (PcG) protein complex, represses Ink4a/Arf in islet β cells. Ezh2 levels decline in aging islet β cells, and this attrition coincides with reduced histone H3 trimethylation at Ink4a/Arf , and increased levels of p16 INK4a and p19 Arf . Conditional deletion of β-cell Ezh2 in juvenile mice also reduced H3 trimethylation at the Ink4a/Arf locus, leading to precocious increases of p16 INK4a and p19 Arf . These mutant mice had reduced β-cell proliferation and mass, hypoinsulinemia, and mild diabetes, phenotypes rescued by germline deletion of Ink4a/Arf . β-Cell destruction with streptozotocin in controls led to increased Ezh2 expression that accompanied adaptive β-cell proliferation and re-establishment of β-cell mass; in contrast, mutant mice treated similarly failed to regenerate β cells, resulting in lethal diabetes. Our discovery of Ezh2-dependent β-cell proliferation revealed unique epigenetic mechanisms underlying normal β-cell expansion and β-cell regenerative failure in diabetes pathogenesis." @default.
• W2158300687 created "2016-06-24" @default.
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• W2158300687 date "2009-04-15" @default.
• W2158300687 modified "2023-10-17" @default.
• W2158300687 title "Polycomb protein Ezh2 regulates pancreatic β-cell <i>Ink4a/Arf</i> expression and regeneration in diabetes mellitus" @default.
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• W2158300687 doi "https://doi.org/10.1101/gad.1742509" @default.
• W2158300687 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2675862" @default.
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• W2158300687 hasPublicationYear "2009" @default.
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