E-MTAB-5775
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-5775 | ExpressionAtlas | 2017-06-15
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:In this study, we analyzed global liver gene expression in MICU1 knock-down (KD) mice. To generate liver-specific MICU1 KD mice, MICU1loxp/loxp male mice were treated with an AAV8-Cre under the control of a hepatocyte specific promoter (TBG). AAV8-TBG-Null treated littermates were used as controls. Liver samples were collected 3-5 weeks after injection. Knockdown was verified by protein and mRNA (94%, 98%, respectively). Mouse Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrays were used to obtain global gene expression data.
2016-01-10 | GSE69801 | GEO
Project description:To initially determine changes on the transcriptome level that might account for the phenotypic observations in an unbiased fashion, we performed large-scale mRNA expression profiling 8 weeks after treatment with an AAV harboring a control or GAbpa-specific miRNA under the LP1 promoter. Mice were subjected to 16 h fasting or a 16 h fasting + 6 h refeeding cycle before termination of the experiment. All 8 AAV-injected experimental groups as NC and GAbpα knockdown samples for the different conditions (wt or db/db; fasting or refeeding) were included.
2017-05-31 | E-MTAB-5775 | biostudies-arrayexpress
Project description:S23 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E11.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E11.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 220 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E10.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 221 experiment: Our research has shown that heterozygous deletion of the miRNA processing enzyme Dicer leads to developmental delay of the thymus in mouse embryos. We sought to identify the microRNAs (miRNAs) affected by the loss of a single copy of Dicer in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring a floxed allele of Dicer, Cre-recombinase under the control of the Wnt1 NCC-specific promoter, and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) cells from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos via FACS and compared the relative expression of miRNAs in the Dicer-heterozygotes compared to Dicer-wildtypes by miRNA microarray.
2010-11-10 | GSE25256 | GEO
Project description:In this study, we analyzed global liver gene expression in MICU1 knock-down (KD) mice. To generate liver-specific MICU1 KD mice, MICU1loxp/loxp male mice were treated with an AAV8-Cre under the control of a hepatocyte specific promoter (TBG). AAV8-TBG-Null treated littermates were used as controls. Liver samples were collected 3-5 weeks after injection. Knockdown was verified by protein and mRNA (94%, 98%, respectively). Mouse Gene 2.0 ST (Affymetrix, Santa Clara, CA) arrays were used to obtain global gene expression data. Gene expression was profiled in control and in liver-specific Micu1 knockdown mice liver samples; 4 biological replicates per condition.
2016-01-10 | E-GEOD-69801 | biostudies-arrayexpress
Project description:In this study, we analyzed global liver gene expression in MCU knock-down (KD) mice. MCUloxp/loxp male mice were treated with an AAV8-Cre under the control of a hepatocyte specific promoter (TBG) to generate liver-specific MCU KD mice. AAV8-TBG-Null treated littermates were used as controls. Knockdown was verified 3 weeks after injection by protein and mRNA (80%). 5 weeks after injection mice were subjected to 70% partial hepatectomy and liver semples were collected 30h after the sugery. Mouse Clariom S (Affymetrix, Santa Clara, CA) arrays were used to obtain global gene expression data from pooled liver samples (pools of 4 biological replicates per array).
2020-01-01 | GSE137891 | GEO
Project description:We previously demonstrated that antisense oligonucleotide (ASO)-mediated knockdown of Mboat7, the gene encoding Membrane Bound O-Acyltransferase 7, in the liver and adipose tissue of mice promoted high fat diet-induced hepatic steatosis, hyperinsulinemia, and systemic insulin resistance. Thereafter, other groups showed that hepatocyte-specific genetic deletion of Mboat7 promoted striking fatty liver and NAFLD progression in mice but does not alter insulin sensitivity, suggesting the potential for cell autonomous roles. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. We generated floxed Mboat7 mice and created hepatocyte- and adipocyte-specific knockout mice using Cre-recombinase mice under the control of the albumin and adiponectin promoter, respectively. After chow and high fat diet feeding (60% kCal fat), mice were subjected to metabolic phenotyping and tissues to molecular workup and analysis. Here, we show that MBOAT7 function in adipocytes contributes to diet-induced metabolic disturbances including hyperinsulinemia and systemic insulin resistance. The expression of Mboat7 in white adipose tissue closely correlates with diet-induced obesity across a panel of ~100 inbred strains of mice fed a high fat/high sucrose diet. Moreover, we found that adipocyte-specific genetic deletion of Mboat7 is sufficient to promote hyperinsulinemia, systemic insulin resistance, and mild fatty liver. Unlike in the liver, where Mboat7 plays a relatively minor role in maintaining arachidonic acid (AA)-containing PI pools, Mboat7 is the major source of AA-containing PI pools in adipose tissue. Our data demonstrate that MBOAT7 is a critical regulator of adipose tissue PI homeostasis, and adipocyte MBOAT7-driven PI biosynthesis is closely linked to hyperinsulinemia and insulin resistance in mice.
2023-05-10 | PXD039894 | Pride
Project description:We have previously shown that the HyD-LIR-Venus probe can specifically inhibit selective autophagy by suppressing the interaction of LIR-containing selective autophagy substrates and receptors with ATG8-family proteins in vivo. We generated hepatocyte-specific HyD-LIR-Venus-expressing mice (HyD-LIRflox/flox; Alb-Cre) by crossing HyD-LIRflox/flox mice, in which HyD-LIR-Venus is expressed under CAG promoter in a Cre-recombinase-dependent manner, with Alb-Cre transgenic mice that express Cre under the control of the Albumin promoter. We performed quantitative proteomic analysis of the livers of 5-week-old HyD-LIRflox/flox and HyD-LIRflox/flox; Alb-Cre mice using the RTS-SPS-MS3 method on Tribrid mass spectrometry.
2023-04-24 | PXD037013 | JPOST Repository
Project description:The gene expression of normal and tumor tissues isolated from WT mice were compared with tumor tissues isolated from mice harboring liver specific deletion of HMGB1
2018-06-06 | GSE89689 | GEO
Project description:S23 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E11.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E11.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 220 experiment: We sought to identify the microRNAs (miRNAs) enriched in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring Cre-recombinase under the control of the Wnt1 NCC-specific promoter and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) and YFP- (non-NCCs) from E10.5 Wnt1Cre-R26R mouse embryos via FACS and compared the relative enrichment of miRNAs in the YFP+ population by miRNA microarray. 221 experiment: Our research has shown that heterozygous deletion of the miRNA processing enzyme Dicer leads to developmental delay of the thymus in mouse embryos. We sought to identify the microRNAs (miRNAs) affected by the loss of a single copy of Dicer in the neural crest cell (NCC) population from E10.5 mouse embryos. To accomplish this, we utilized a transgenic mouse line harboring a floxed allele of Dicer, Cre-recombinase under the control of the Wnt1 NCC-specific promoter, and also carrying the R26R-YFP allele. We sorted YFP+ (NCCs) cells from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos via FACS and compared the relative expression of miRNAs in the Dicer-heterozygotes compared to Dicer-wildtypes by miRNA microarray. S23 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E11.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from five E11.5 embryos were sorted into YFP+ and YFP- populations and pooled. 220 experiment: RNA from YFP+ (NCCs) and YFP- (non-NCCs) cells sorted by FACS from E10.5 Wnt1Cre-R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten E10.5 embryos were sorted into YFP+ and YFP- populations and pooled. 221 experiment: RNA from YFP+ (NCCs) cells sorted by FACS from E10.5 Dicerfl/+,Wnt1Cre,R26R and Dicer+/+,Wnt1Cre,R26R mouse embryos was isolated and hybridized to Exiqon miRNA microarrays v10. Cells from ten embryos were sorted into YFP+ populations and pooled for each genotype.
2010-11-10 | E-GEOD-25256 | biostudies-arrayexpress
Project description:Cre-recombinase expression under control of an albumin promoter in the presence of floxed alleles is a highly effective and specific way to target gene mutations in hepatocytes. However, some concerns have been raised regarding off-target and/or toxic effects of cre itself, possibly confounding the interpretation of studies employing this approach. We have now used this tool to succesfully target gene deletions in hepatocytes during pneumonia, a condition which results in significant remodeling of the hepatic transcriptome. The goal of this study was to determine what effects, if any, cre expression alone has on hepatic gene expression during bacterial pneumonia. Mutant mice expressed CRE-recombinase under control of an albumin promoter. Results from mutants were compared to wild-type mice on the same genetic background (C57BL/6). Microarray analysis was performed on liver RNA collected from both genotypes of mice in the absence and presence of pneumococcal pneumonia.
2012-02-16 | GSE35515 | GEO