Mouse bone-marrow-derived macrophages treated with supernatant of DYRK1B-deletion / Wildtype mKpc4 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB71503 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12387566.fastq.gz | Fastqsanger.gz | |||
| ERR12387567.fastq.gz | Fastqsanger.gz | |||
| ERR12387568.fastq.gz | Fastqsanger.gz | |||
| ERR12387569.fastq.gz | Fastqsanger.gz |
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Project description:Mus musculus macrophages were derived from bone marrow, and treated with the supernatant of of DYRK1B-deletion (multiple clones) or Wildtype mKpc4 cells.
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Project description:One of the causes of hyperglycemia in type 2 diabetes is elevated hepatic glucose production. AKT-FOXO1 pathway is primarily involved in the hormonal upregulation of this process, and pharmacological or genetic inhibition of this pathway prevents diabetes in animal models. Here we report that DYRK1B regulates FoxO1 function through phosphorylation to regulate hepatic glucose metabolism. DYRK1B expression is induced by fasting and in diabetic mice. DYRK1B promoted hepatic gluconeogenesis and glucose intolerance in in vivo and in vitro model systems. Liver-specific DYRK1B conditional knockout mice were protected from diet-induced hyperglycemia. Mechanistically, DYRK1B interacted with and phosphorylated FoxO1, primarily at T467S468, which is required for its nuclear localization. DYRK1B inhibited AKT mediated FoxO1 phosphorylation at T24 and S256 and enhanced its nuclear retention. DYRK1B mediated phosphorylation of FoxO1 enhanced the expression of gluconeogenic genes and promoted gluconeogenesis. Treatment with DYRK1B pharmacological inhibitor AZ191 significantly lowered blood glucose levels in diabetic mice. We conclude that DYRK1B is a regulator of glucose metabolism, and its pharmacological inhibition could serve as therapeutic target for treating diabetes.
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