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Gene expression in IRfl/fl Cre- and IRfl/fl Cre+ mice

ABSTRACT: The floxed insulin receptor was specifically targetted for deletion in the mammary gland using a mouse strain bearing Cre recombinase under the BLG promoter. Data analysis: Genespring was used for data analysis All entities (28853) were filtered on variance between samples, eliminating from further analysis of genes whose coefficient of variation was greater than 50%. The remaining 2239 genes were filtered on expression levels between 20 and 20,000 intensity units An unpaired T-test was used to find genes that differed significantly (P<0.05) between experimentals and controls The remaining 2014 genes were filtered for a 1.1 absolute fold change between experimentals and controls. Of the remaining expression of 890 genes was down in the Cre+ mice and expression was up for 457 genes in the Cre+ mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE48009 | GEO | 2013/06/18

SECONDARY ACCESSION(S): PRJNA208629

REPOSITORIES: GEO

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Gene expression in IRfl/fl Cre- and IRfl/fl Cre+ mice

Project description:The floxed insulin receptor was specifically targetted for deletion in the mammary gland using a mouse strain bearing Cre recombinase under the BLG promoter. Data analysis: Genespring was used for data analysis All entities (28853) were filtered on variance between samples, eliminating from further analysis of genes whose coefficient of variation was greater than 50%. The remaining 2239 genes were filtered on expression levels between 20 and 20,000 intensity units An unpaired T-test was used to find genes that differed significantly (P<0.05) between experimentals and controls The remaining 2014 genes were filtered for a 1.1 absolute fold change between experimentals and controls. Of the remaining expression of 890 genes was down in the Cre+ mice and expression was up for 457 genes in the Cre+ mice. Mouse strains containing a floxed insulin receptor (IRfl/fl) were crossed with a mouse expressing Cre recombinase from a BLG promoter RNA was applied to Affymetrix MoGene_1_0-st-v1 chips Three replicates from each strain were used for analysis.

2013-06-18 | E-GEOD-48009 | biostudies-arrayexpress

Expression data from LysMCre/Cre and KLF2∆/∆ (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with LPS for 6hours

Project description:Gene expression profile of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2∆/∆ primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation.

2012-04-16 | GSE26727 | GEO

Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach vs. Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP) mouse stomach microarray

Project description:We wished to investigate the role of E-cadherin loss in our mouse parietal cell/pre-parietal cell E-cadherin knock-out, p53 knock-out, oncogenic Kras induced model of gastric cancer. As such, we isolated RNA from stomach tissue from our E-cadherin knock-out model (Atp4b-Cre;Cdh1(fl/fl);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)) and our E-cadherin heterozygous model (Atp4b-Cre;Cdh1(fl/+);Kras(LSL-G12D/+);Trp53(fl/fl);Rosa26(LSL-YFP/LSL-YFP)). We then performed a microarray on this stomach tissue from four independent mice of each genotype. Differentially expressed genes were identified and gene set overlap analysis was used to identify pathways enriched in one model over the other.

2018-05-01 | E-MTAB-5833 | biostudies-arrayexpress

RNA-seq analysis of Mettl3fl/fl and LysM-cre, Mettl3fl/fl MDSC Transcriptomes

Project description:To comprehensively learn about the mechanisms of METTL3-mediated pro-tumoral functions, we performed RNA-sequencing to identify differentially expressed genes in isolated MDSC in Mettl3fl/fl (WT) and LysM-cre, Mettl3fl/fl (KO) MC38-bearing mice

2022-01-01 | GSE182864 | GEO

Hepatic transcriptome analysis of PRDX1fl/fl and Alb-Cre；PRDX1fl/fl mice on MCD

Project description:The etiology of non-alcoholic steatohepatitis (NASH) has been complicated. An increasing body of literature has indicated that hepatic oxidative stress exerts a causal role in driving NASH. Nevertheless, how the anti-oxidant defense system guards against oxidative stress and NASH remains unclear. In this study, we sought to investigate how the peroxidase peroxiredoxin 1 protects against NASH. To this end, we fed WT and hepatic PRDX1 knockout (Alb-Cre;Prdx1fl/fl) a methionine and choline deficient diet (MCD) for 5 weeks and collected liver samples for RNA sequencing analysis. As revealed by gene-set enrichment analysis (GSEA) and KEGG pathway enrichment analysis, there was an enrichment of genes involved in JAK-STAT signaling. Further, we observed that the expression of many genes involved in JAK-STAT signaling such as Pdgfb and Pdgfra was significantly increased in Alb-Cre;Prdx1fl/fl mice. Collectively, these results suggest that increased JAK-STAT signaling accounts for the deteriorated NASH phenotypes in Alb-Cre;Prdx1fl/fl mice.

2023-08-14 | GSE201030 | GEO

RNA seq of vhlfl/fl cd4 cre, hif1afl/fl vhlfl/fl cd4 cre and WT CD4 T cells before and after anti-CD3/CD28 stimulation

Project description:Purpose: We compared the transcriptomes of murine CD4 T cells lacking either the vhl gene ( vhlfl/fl cd4 cre (vhl cKO) ) or both vhl and hif1a (hif1afl/fl vhlfl/fl cd4 cre (dcKO)) with WT controls before and 24 h after T cell receptor stimulation using anti-CD3/CD28. Results: Using an optimized data analysis workflow, about 45-60 million sequence reads per sample to the mouse genome (build mm10) and identified ca 12500 transcripts in the CD4 T cells of WT and mutant mice after performing HISAT2 alignements to the mm10 reference. Conclusion: the segregation of the transcriptome of unstimulated WT CD4 T cells as compared to the other groups. Within the TCR-stimulated groups the gene expression of vhl cKO CD4 T cells differed to that of WT and vhl hif1a dcKO CD4 T cells which showed in comparison important similarity between them

2022-06-01 | GSE190791 | GEO

Transcriptional profiling of E14.5 control and Tbr2 fl/fl;Foxg1::Cre cortices

Project description:The abscence of TBR2 gene in human leads to microcephaly. This condition is mimicked by the specific ablation of the murine gene in developing cerebral cortex. Herein we compared gene expression in control and Tbr2 cKO in E14.5 cerebral cortices. This approach represents a useful tool to identify the molecular mechanisms at the basis of the phenotype. 6 samples, 3x Tbr2 +/+;Foxg1::Cre (control) and 3x Tbr2 fl/fl;Foxg1::Cre

2016-09-08 | E-GEOD-63619 | biostudies-arrayexpress

Transcription profiling by array of LysMCre/Cre and KLF2?/? (LysMCre/Cre: KLF2 FL/FL) primary peritoneal macrophages treated with lipopolysaccharide (LPS) for 6 hours

Project description:Gene expression profile of LysMCre/Cre and KLF2?/? primary peritoneal macrophages following 6 hours of LPS treatment. We used microarrays to detail the global program of gene expression following LPS stimulation of LysMCre/Cre and KLF2?/? primary peritoneal macrophages. We identified distinct classes of genes that were altered following LPS stimulation. We injected 3 pairs of LysMCre/Cre (n=3) and KLF2?/? (n=3) mice with 2 ml of thioglycolate broth intraperitoneally. After 72 hours of thioglycolate injection, total cell suspension from peritoneal cavity were collected. These cells were seeded on 100mm tissue culture plates. Cells were allowed to attach for 4 hours and unattached cells were removed by washing with cell culture medium. These cells were placed in humidified incubator for additional 24 hours before LPS treatment. LPS was diluted to final concentration of 100ng/ml in culture medium and this medium was placed on peritoneal macrophages derived from LysM Cre/Cre and KLF2?/? mice for 6hours. Cells were lysed and total RNA was isolated and subjected to hybridization on Affymetrix microarrays.

2012-04-15 | E-GEOD-26727 | biostudies-arrayexpress

Expression analyses of E12.5 embryonic brains from Nestin Cre+, Rest GTi/GTi, p53 fl/fl vs Rest GTi/GTi, p53 fl/fl littermates

Project description:We use mice containing a gene trap in the first intron of the Rest gene, which effectively eliminates transcription from all coding exons, to prematurely remove REST from neural progenitors. We find catastrophic DNA damage that occurs during S-phase of the cell cycle, with consequences including abnormal chromosome separation, apoptosis, and smaller brains. Further support for persistent effects is the latent appearance of proneural glioblastomas in adult mice also lacking the tumor suppressor, p53. A Rest deficient mouse line generated previously, using a conventional gene targeting approach, does not exhibit these phenotypes, likely due to a remaining C terminal peptide that still binds chromatin and recruits REST chromatin modifiers.Our results indicate that REST-mediated chromatin remodeling is required for proper S-phase dynamics, prior to its well-established role in relieving repression of neuronal genes at terminal differentiation. extract RNA from E12.5 brain in triplicates, compare gene expression profile between Gene Trap REST knockout mice and control littermates

2015-08-01 | E-GEOD-68368 | biostudies-arrayexpress