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- W2075232662 abstract "Little is known about the mechanisms governing neonatal growth and maturation of organs. Here we demonstrate that calcineurin/Nuclear Factor of Activated T cells (Cn/NFAT) signaling regulates neonatal pancreatic development in mouse and human islets. Inactivation of calcineurin b1 (Cnb1) in mouse islets impaired dense core granule biogenesis, decreased insulin secretion, and reduced cell proliferation and mass, culminating in lethal diabetes. Pancreatic β cells lacking Cnb1 failed to express genes revealed to be direct NFAT targets required for replication, insulin storage, and secretion. In contrast, glucokinase activation stimulated Cn-dependent expression of these genes. Calcineurin inhibitors, such as tacrolimus, used for human immunosuppression, induce diabetes. Tacrolimus exposure reduced Cn/NFAT-dependent expression of factors essential for insulin dense core granule formation and secretion and neonatal β cell proliferation, consistent with our genetic studies. Discovery of conserved pathways regulating β cell maturation and proliferation suggests new strategies for controlling β cell growth or replacement in human islet diseases." @default.
- W2075232662 created "2016-06-24" @default.
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- W2075232662 creator A5039399292 @default.
- W2075232662 creator A5045108074 @default.
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- W2075232662 date "2012-07-01" @default.
- W2075232662 modified "2023-10-11" @default.
- W2075232662 title "Neonatal β Cell Development in Mice and Humans Is Regulated by Calcineurin/NFAT" @default.
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- W2075232662 doi "https://doi.org/10.1016/j.devcel.2012.05.014" @default.
- W2075232662 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3587727" @default.
- W2075232662 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22814600" @default.
- W2075232662 hasPublicationYear "2012" @default.
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