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- W2004197063 abstract "Objectives: The peptide hormone glucagon is a biological antagonist of insulin and it stimulates glucose output from the liver. Insulin inhibits glucagon secretion and the glucagon gene transcription, whose abnormal expression leads to hyperglucagonemia contributing to impaired glucose tolerance in diabetes mellitus type 2. Previous studies suggest that the insulin-induced inhibition of the glucagon gene involves glycogen synthase kinase 3β (GSK3β). CBP was shown to be crucial for the activation of the glucagon gene in the alpha cells and to be phosphorylated by GSK3β on its C-terminal end. In this study, the GSK3β phosphorylation sites within the C-terminus of CBP were mapped." @default.
- W2004197063 created "2016-06-24" @default.
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- W2004197063 date "2007-03-29" @default.
- W2004197063 modified "2023-09-26" @default.
- W2004197063 title "Identification of a GSK3β phosphorylation sites within the C-terminus of the transcriptional coactivator CBP" @default.
- W2004197063 doi "https://doi.org/10.1055/s-2007-972375" @default.
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