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Identification of regulator of DYRK2

ABSTRACT: We used microarrays to identified new factor that regulates key factors in siRNA DYRK2 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75917 | GEO | 2016/08/23

SECONDARY ACCESSION(S): PRJNA305707

REPOSITORIES: GEO

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Identification of regulator of DYRK2

Project description:We used microarrays to identified new factor that regulates key factors in siRNA DYRK2 cells. We silenced DYRK2 in MCF-7 cells (siDYRK2 cells) using siRNA. For control, non-silencing siRNA was used. We obtained expression profiles from siDYRK2 cells and sControl cells.

2016-08-23 | E-GEOD-75917 | biostudies-arrayexpress

DYRK2 regulates cancer stem cell population.

Project description:We used microarrays to identified new factor that regulates cancer stem cell population in shRNA DYRK2 cells using stable DYRK2 knockdown cells and mammosphere.

2016-08-23 | GSE75918 | GEO

DYRK2 regulates cancer stem cell population.

Project description:We used microarrays to identified new factor that regulates cancer stem cell population in shRNA DYRK2 cells using stable DYRK2 knockdown cells and mammosphere. We stably silenced DYRK2 in MCF-7 cells (shRNA-DYRK2 cells) using pSuper vector. For control, pSuper control cells were created. We obtained expression profiles from shRNA-DYRK2 cells and pSuper control cells. We also obtained RNA from mammosphere which are stably expressing pSuper vector or shRNA DYRK2.

2016-08-23 | E-GEOD-75918 | biostudies-arrayexpress

DYRK2 gene transfer suppresses liver tumorigenesis

Project description:We generated liver-specific Dyrk2 knockout mice mating Dyrk2 flox mice with Alb-cre mice and co-introduced SB13-transposase-, myrAkt-, Myc- and mutant Hras-expressing plasmids with either HA- or Dyrk2-expressing plasmid into the knockout mice by HTVi. Dyrk2-expressing suppressed tumorigenesis compared with HA-expressing.

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DYRK2 knockout mice exhibit fetal growth retardation

Project description:We generated DYRK2-deficient mice using the CRISPR/Cas9 genome editing method and demonstrated that loss of DYRK2 gene causes fetal growth retardation and neonatal lethality at birth. Total RNA from DYRK2-/- whole embryo was compared with those of WT mice by microarray.

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Positive regulation of Hedgehog signaling via phosphorylation of GLI2/GLI3 by DYRK2 kinase

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DYRK2 drives renal fibrosis through CDK1-dependent G2/M phase dysregulation in tubular epithelial cells

Project description:Renal fibrosis is a common pathological characteristic of chronic kidney disease (CKD) and serves as a critical prognostic indicator for renal outcomes. However, current therapeutic strategies targeting renal fibrosis remain limited. Here, we identify dual-specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) as a crucial driver of renal fibrosis. DYRK2 was significantly induced in the fibrotic mouse kidneys, particularly in proximal tubules, following unilateral ureter obstruction (UUO) or aristolochic acid nephropathy (AAN). Tubule-specific silencing of DYRK2 reduces the production of profibrotic cytokines and alleviates renal fibrosis in mice. In vitro, knockdown of DYRK2 reduces excessive reactive oxygen species (ROS) production, prevents the loss of epithelial phenotype in renal tubular epithelial cells (RTECs) and attenuates fibroblast activation by inhibiting G2/M arrest. Mechanistically, DYRK2 binds and phosphorylates CDK1 at Thr14, inducing G2/M arrest of RTECs and promoting tubulointerstitial fibrosis. Notably, DYRK2 upregulation was also observed in kidneys from various CKD patients, suggesting it may be a common pathogenic feature in human kidney diseases. Collectively, our studies indicate that DYRK2 could be a potential therapeutic target for renal fibrosis.

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DYRK2 gene transfer suppresses liver tumorigenesis

Project description:DYRK2 gene transfer suppresses liver tumorigenesis

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DYRK2 knockout mice exhibit fetal growth retardation

Project description:DYRK2 knockout mice exhibit fetal growth retardation

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Selective inhibition reveals the regulatory function of DYRK2 in protein synthesis and calcium entry

Project description:The dual-specificity tyrosine phosphorylation-regulated kinase DYRK2 has emerged as a key regulator of cellular processes such as proteasome-mediated protein degradation. To gain further insights into its function, we took a chemical biology approach and developed C17, a potent small-molecule DYRK2 inhibitor, through multiple rounds of structure-based optimization guided by a number of co-crystallized structures. C17 displayed an effect on DYRK2 at a single-digit nanomolar IC50 and showed outstanding selectivity for the human kinome containing 467 other human kinases. Using C17 as a chemical probe, we further performed quantitative phosphoproteomic assays and identified several novel DYRK2 targets, including eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) and stromal interaction molecule 1 (STIM1). DYRK2 phosphorylated 4E-BP1 at multiple sites, and the combined treatment of C17 with AKT and MEK inhibitors showed synergistic 4E-BP1 phosphorylation suppression. The phosphorylation of STIM1 by DYRK2 substantially increased the interaction of STIM1 with the ORAI1 channel, and C17 impeded the store-operated calcium entry process. Collectively, these studies further expand our understanding of DYRK2 and provide a valuable tool to further pinpoint its biological function.

2021-03-26 | MSV000087106 | MassIVE

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