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Identification of gene expression changes in MEF cell lines with a targeted MDMX mutation that disrupts binding to CK1-alpha kinase

ABSTRACT: Identification of gene expression changes in MEF cell lines with a targeted MDMX mutation that disrupts binding to CK1-alpha kinase

PROVIDER: PRJNA623334 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11486615_1.fastq.gz	Fastqsanger.gz
	SRR11486615_2.fastq.gz	Fastqsanger.gz
	SRR11486616_1.fastq.gz	Fastqsanger.gz
	SRR11486616_2.fastq.gz	Fastqsanger.gz
	SRR11486617_1.fastq.gz	Fastqsanger.gz

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Identification of gene expression changes in MEF cell lines with a targeted MDMX mutation that disrupts binding to CK1-alpha kinase

Project description:The goal of this experiment is to identify genes differentially expressed in MEF cell lines with a targeted MDMX mutation that prevents binding and inhibition of CK1-alpha kinase.

2020-04-07 | GSE148138 | GEO

Critical role of the hydrogen peroxide-responsive nuclear kinase CK1-alpha-LS in vascular cell activation

Project description:CK1-alpha-LS was knocked down in human coronary artery smooth muscle cells. Gene level and exon level changes in expression were assessed. CK1-alpha-LS was knocked down in human coronary artery smooth muscle cells using retrovirus containing shRNA targeting the alternatively spliced L-insert.

2010-12-11 | E-GEOD-19441 | biostudies-arrayexpress

Critical role of the hydrogen peroxide-responsive nuclear kinase CK1-alpha-LS in vascular cell activation

Project description:CK1-alpha-LS was knocked down in human coronary artery smooth muscle cells. Gene level and exon level changes in expression were assessed.

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CK1

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Autophosphorylation of the CK1 kinase domain regulates enzyme activity and substrate specificity

Project description:CK1 enzymes are conserved, acidophilic serine/threonine kinases with a variety of critical cellular functions; their misregulation contributes to cancer, neurodegenerative diseases, and sleep phase disorders. Here, we describe a new mechanism of CK1 regulation conserved from yeast to human – autophosphorylation of a threonine in the mobile L-EF loop proximal to the active site – that inhibits kinase activity. Consequently, yeast and human CK1 enzymes with phosphoablating mutations at this site are hyperactive in vitro. We used quantitative phosphoproteomics to show that disruption of this regulatory mechanism rewires CK1 signaling in Schizosaccharomyces pombe. In accord, we found that a known CK1 pathway, a mitotic checkpoint, is downregulated in these mutants, while new pathways that confer heat shock resistance and suppress meiotic transcripts are upregulated. Molecular dynamics simulations demonstrated that phosphorylation on the L-EF loop alters the conformation of the substrate docking site, and we propose that this affects which CK1 substrates can be phosphorylated. Due to the functional importance of the L-EF loop, which is unique to the CK1 family of kinases, this mechanism is likely to regulate the majority of CK1 enzymes in vivo.

2023-07-20 | PXD026766 | Pride

MDMX acts as a pervasive preleukemic-to-acute myeloid leukemia transition mechanism

Project description:The p53 inhibitor MDMX is overexpressed in the vast majority of patients with acute myeloid leukemia (AML). Utilizing hematopoietic stem cells from four non-leukemic/pre-leukemic murine models, we performed bulk transcriptomic analysis to evaluate the impact of Mdmx overexpression.

2021-01-14 | GSE164838 | GEO

Effect of depletion of MDMX (aka MDM4) on gene expression in uveal melanoma cell line MEL202

Project description:To investigate the effect of MDMX depletion on the transcriptome of MEL202 cells we established 5 derivatives either containing a doxycyline- inducible Contrl shRNA or with 4 distinct MDMX -targeting shRNAs In thee biological replicates the cells were treated with doxycycline for 48 hrs after which RNA was isolated

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Tumor-derived CK1? mutations enhance MDMX inhibition of p53.

Project description:Somatic missense mutations of the CSNK1A1 gene encoding casein kinase 1 alpha (CK1?) occur in a subset of myelodysplastic syndrome (MDS) with del(5q) karyotype. The chromosomal deletion causes CSNK1A1 haplo-insufficiency. CK1? mutations have also been observed in a variety of solid and hematopoietic tumors at low frequency. The functional consequence of CK1? mutation remains unknown. Here we show that tumor-associated CK1? mutations exclusively localize to the substrate-binding cleft. Functional analysis of recurrent mutants E98K and D140A revealed enhanced binding to the p53 inhibitor MDMX, increased ability to stimulate MDMX-p53 binding, and increased suppression of p21 expression. Furthermore, E98K and D140A mutants have reduced ability to promote phosphorylation of ?-catenin, resulting in enhanced Wnt signaling. The results suggest that the CK1? mutations observed in tumors cause gain-of-function in cooperating with MDMX and inhibiting p53, and partial loss-of-function in suppressing Wnt signaling. These functional changes may promote expansion of abnormal myeloid progenitors in del(5q) MDS, and in rare cases drive the progression of other tumors.

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