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• W3002089529 abstract "Abstract β-Cell dysfunction and reduction in β-cell mass are hallmark events of diabetes mellitus. Here we show that β-cells express abundant Kindlin-2 and deleting its expression causes severe diabetes-like phenotypes without markedly causing peripheral insulin resistance. Kindlin-2, through its C-terminal region, binds to and stabilizes MafA, which activates insulin expression. Kindlin-2 loss impairs insulin secretion in primary human and mouse islets in vitro and in mice by reducing, at least in part, Ca 2+ release in β-cells. Kindlin-2 loss activates GSK-3β and downregulates β-catenin, leading to reduced β-cell proliferation and mass. Kindlin-2 loss reduces the percentage of β-cells and concomitantly increases that of α-cells during early pancreatic development. Genetic activation of β-catenin in β-cells restores the diabetes-like phenotypes induced by Kindlin-2 loss. Finally, the inducible deletion of β-cell Kindlin-2 causes diabetic phenotypes in adult mice. Collectively, our results establish an important function of Kindlin-2 and provide a potential therapeutic target for diabetes." @default.
• W3002089529 created "2020-01-30" @default.
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• W3002089529 date "2020-01-24" @default.
• W3002089529 modified "2023-10-11" @default.
• W3002089529 title "Kindlin-2 modulates MafA and β-catenin expression to regulate β-cell function and mass in mice" @default.
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• W3002089529 doi "https://doi.org/10.1038/s41467-019-14186-y" @default.
• W3002089529 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6981167" @default.
• W3002089529 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31980627" @default.
• W3002089529 hasPublicationYear "2020" @default.
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