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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.

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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.

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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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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

Project description:To understand the molecular mechanisms underlying developmental abnormalities in Dyrk2-/- mice, we performed comprehensive whole-genome RNA sequencing of the MEFs from wild-type and Dyrk2-/- embryos

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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

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

2021-01-21 | MSV000086745 | MassIVE

Interactome of DYRK2 by using BioID proximity labeling

Project description:In this study, DYRK2 was found to be an important regulator of Hedgehog signaling. To identify DYRK2 interacting proteins, we performed interactome using BioID proximity labeling. NIH3T3 cells containing Dox-inducible DYRK2-BioID2-HA construct were cultured in the media with or without Doxycycline for DYRK2-BioID2-HA expression, followed by proximity labeling. The lysates from Doxycycline induction (DYRK2) and without induction (Mock) were subjected to streptavidin pull-down and the proteins were identified by LC-MS/MS.

2024-07-01 | PXD043445 | JPOST Repository

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