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DYRK1B deletion allograft

ABSTRACT: DYRK1B deletion allograft

PROVIDER: PRJEB71502 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	ERR12387555.fastq.gz	Fastqsanger.gz
	ERR12387556.fastq.gz	Fastqsanger.gz
	ERR12387557.fastq.gz	Fastqsanger.gz
	ERR12387558.fastq.gz	Fastqsanger.gz
	ERR12387559.fastq.gz	Fastqsanger.gz

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Mouse bone-marrow-derived macrophages treated with supernatant of DYRK1B-deletion / Wildtype mKpc4 cells

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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DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis

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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DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis

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DYRK1B deletion allograft

Project description:Gene expression pattern in s.c. allografted DYRK1BKO-mKpc4 cells

2024-05-29 | E-MTAB-13667 | biostudies-arrayexpress

RNA-sequencing explores the transcriptional profile of Wild Type and DYRK1B transgenic hearts

Project description:Here, we investigates the effects of dual-specificity tyrosine-regulated kinase 1B (DYRK1B) on mitochondrial bioenergetics, cardiac hypertrophy, and heart failure.We engineered DYRK1B transgenic and the effects of DYRK1B and its downstream mediators were subsequently elucidated using RNA-seq analysis. In this dataset, we inquire the transcriptional profile of WT and DYRK1B transgenic hearts at 3-day and 8-week old.

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DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis

Project description:Dual-specificity tyrosine phosphorylation-regulated kinase 1B (DYRK1B), a member of the CMGC group of kinase, is associated with metabolic syndrome. However, the molecular mechanisms involved remain elusive. In this study, we demonstrate that Dyrk1b expression is induced in liver by fasting and in diabetic mice. Using both in vivo and in vitro studies, we show that DYRK1B promotes hepatic gluconeogenesis and glucose intolerance. Liver-specific Dyrk1b conditional knockout mice were protected from diet-induced hyperglycemia. Mechanistically, DYRK1B interacts with and phosphorylates FOXO1, primarily at Thr467/Ser468, which is essential for its nuclear localization. Additionally, DYRK1B inhibits AKT mediated FOXO1 phosphorylation at Thr24 and Ser256, thereby enhancing its nuclear retention. DYRK1B mediated phosphorylation enhances the expression of gluconeogenic genes and promotes gluconeogenesis. Further, a pharmacological inhibitor of DYRK1B significantly reduced blood glucose levels in diabetic mice. Collectively, these findings offer new insights into DYRK1B’s role in the glucose metabolism and identify it as a new therapeutic target for treating diabetes.

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Mouse bone-marrow-derived macrophages treated with supernatant of DYRK1B-deletion / Wildtype mKpc4 cells

Project description:Mouse bone-marrow-derived macrophages treated with supernatant of DYRK1B-deletion / Wildtype mKpc4 cells

| PRJEB71503 | ENA

Inhibition of DYRK1B suppresses inflammation in allergic contact dermatitis model and Th1/Th17 immune response

Project description:To investigate the inhibition effect of DYRK1B kinase function on human naïve CD4+ T cell differetionation which stimulated under Treg polarizing condition for 24 hours.

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Screen Identifies DYRK1B Network as Mediator of Transcription Repression on Damaged Chromatin

Project description:The uploaded data are described within "Screen Identifies DYRK1B Network as Mediator of Transcription Repression on Damaged Chromatin". In short, peptides from RPE1 epithelial cells with either normal expression of DYRK1B, over expression, of knockout of the kinase were TMT11 plex labeled and enriched by tandem phosphopeptide enrichment.

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Project description:DYRK1B phosphorylates FOXO1 to promote hepatic gluconeogenesis

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