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Molecular Profiling of glucokinase-expressing cells from mouse hypothalamus

ABSTRACT: Analysis of genes from glucokinase-expressing cells following immunoprecipitation of hypothalamic EGFP-tagged L10 ribosomal protein from Glucokinase-cre/Elongation factor 1 alpha 1 - lox stop lox - EGFPL10 mice

ORGANISM(S): Mus musculus

PROVIDER: GSE49868 | GEO | 2013/09/13

SECONDARY ACCESSION(S): PRJNA215178

REPOSITORIES: GEO

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Molecular Profiling of glucokinase-expressing cells from mouse hypothalamus

Project description:Analysis of genes from glucokinase-expressing cells following immunoprecipitation of hypothalamic EGFP-tagged L10 ribosomal protein from Glucokinase-cre/Elongation factor 1 alpha 1 - lox stop lox - EGFPL10 mice mRNA obtained by immunoprecipitation in adult Gck-cre/EF1A1-LSL-EGFPL10 mice

2013-09-13 | E-GEOD-49868 | biostudies-arrayexpress

RNAseq data from mouse beta-cells expressing mutant (GCK Y214C) versus wild-type Glucokinase

Project description:The goal of this study is to compare the transcriptome of mouse beta-cells expressing mutant constitutively active Glucokinase versus wild-type Glucokinase.

2016-10-15 | GSE86949 | GEO

Citrullination of glucokinase is linked to autoimmune diabetes

Project description:Inflammation, including reactive oxygen species and inflammatory cytokines in tissues amplify various post-translational modifications (PTMs) of self-proteins. A number of PTMs have been identified as autoimmune biomarkers in the initiation and progression of Type 1 diabetes (T1D). In this study, we have identified the citrullination of pancreatic glucokinase (GK) as a result of inflammation, triggering autoimmunity and affecting GK biological functions. Glucokinase is expressed in hepatocytes to regulate glycogen synthesis, and in pancreatic beta cells as a glucose sensor to initiate glycolysis and insulin signaling. We identify autoantibodies and autoreactive CD4+ T cells to glucokinase epitopes in the circulation of T1D patients and NOD mice. Finally, citrullination alters GK biologic activity (Km) and suppresses glucose-stimulated insulin secretion. Our studies define glucokinase as a T1D biomarker, providing new insights of how inflammation drives PTMs to create both neoautoantigens and affect beta cell metabolism.

2022-03-17 | PXD028825 | Pride

Beta cell-targeted glucokinase overexpression

Project description:Beta cell-targeted glucokinase overexpression

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Expression profiling on lactation day 2 mammary epithelial cells from constitutive miR-150 expressing mice compared to controls.

Project description:Constitutive expression of miR-150 in mammary epithelium causes severe lactation defects. Mammary epithelial cells (MECs) at lactation day 2 were isolated from four homozygous ROSA26-lox-STOP-lox-miR-150 (Stop-150) mice with WAP-driven Cre (WAP-Cre) and compared to MECs from four WAP-Cre control mice. Statistical analysis of the mRNA changes between the two genotypes identified supression of many lipid and cholesterol synthesis genes due to constitutive expression of miR-150.

2016-10-01 | GSE80666 | GEO

Gene expression profiles in glucokinase activator (GKA)-treated pancreatic islets

Project description:To identify the target genes of glucokinase activator (GKA) in islet, GKA-induced gene expression in mouse pancreatic islets was measured at 24 hours after treatment of 30 microM GKA or vehicle.

2012-10-02 | GSE41248 | GEO

Gene expression profiles in glucokinase activator (GKA)-treated pancreatic islets

2012-10-02 | GSE41248 | GEO

Multiplexed assessment of human glucokinase variant activity

Project description:Multiplexed assessment of human glucokinase variant activity

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Label-free differential proteomics analysis of Ba/F3 expressing WT and mutant R98S RPL10

Project description:We recently identified a recurrent mutation in the ribosomal gene RPL10 that results in substitution of residue arginine 98 by a serine (R98S) of the ribosomal protein L10 (RPL10) in the contest of T-cell acute lymphoblastic leukemia (T-ALL). To gain insights into the mechanisms by which the RPL10 R98S mutation contributes to T-ALL development, we screened for proteins that are differentially expressed between RPL10 wild type (WT) and RPL10 R98S (R98S) expressing cells. These experiments were conducted in the mouse pro-B Ba/F3 cell line, a well-established hematopoietic model for oncogenic studies.

2017-11-28 | PXD005995 | Pride

Lin28 expression affect embryonic lung development

Project description:Lin28A and its paralog Lin28B are RNA binding proteins that regulate gene expression by inhibition of the maturation of the Per/Pri Let-7 miRNAs family and also via Let-7 independent mechanism. To study the effect of Lin28A ectopic-expression on mouse embryonic development we used a transgenic mice strain that combine a Cre-Lox system and a Tet-On system (herein Lox-stop-Lox-TetOn-Lin28A mice) and enable spatial and temporal control of transgenic Lin28A over-expression. Here we show that global Lin28A over-expression (by crossing Lox-stop-Lox-TetOn-Lin28A males with VasaCre females) in the mouse embryo prevents embryonic lung development. To study the precise developmental stage affected by Lin28A expression we preformed RNA sequencing analysis for transgenic and control lungs from E12.5, E14.5, E16.5 and E18.5 embryos. This analysis revealed that the development of the lung was delayed but not completely abrogated by Lin28A expression. We further showed that the effect of Lin28A expression in the mesenchymal cells (by crossing Lox-stop-Lox-TetOn-Lin28A males with Wt1Cre females) of the lung leads to the same phenotype as global Lin28A expression while expression in the lung epithelial cells (by crossing the Lox-stop-Lox-TetOn-Lin28A males with Nkx2.1Cre females) result in a milder developmental phenotype.

2019-09-22 | GSE122919 | GEO

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