Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA111467 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (18 months) and sex matched C57BL/6 mice. Moreover, 18months old C57BL/6 livers were hybridized with independent 18 months old C57BL/6 livers for control. Keywords: Array comparative genomic hybridization analysis (aCGH).
2009-07-29 | GSE14467 | GEO
Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (18 months) and sex matched C57BL/6 mice. Moreover, 18months old C57BL/6 livers were hybridized with independent 18 months old C57BL/6 livers for control. Keywords: Array comparative genomic hybridization analysis (aCGH). Independent HCC of AlbLTab mice were hybridized with independent C57BL/6 mice.
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Project description:Murine hepatocellular carcinoma of MCL1-/- transgenic mice and age matched alb cre mice - 12 months old.
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Project description:Atherosclerosis and pressure overload are major risk factors for the development of heart failure in patients. Cardiac hypertrophy often precedes the development of heart failure. However, underlying mechanisms are incompletely understood. To investigate pathomechanisms underlying the transition from cardiac hypertrophy to heart failure we used experimental models of atherosclerosis- and pressure overload-induced cardiac hypertrophy and failure, i.e. apolipoprotein E (apoE)-deficient mice, which develop heart failure at an age of 18 months, and non-transgenic C57BL/6J (B6) mice with heart failure triggered by 6 months of pressure overload induced by abdominal aortic constriction (AAC). The development of heart failure was monitored by echocardiography, invasive hemodynamics and histology. The microarray gene expression study of cardiac genes was performed with heart tissue from failing hearts relative to hypertrophic and healthy heart tissue, respectively. The microarray study revealed that the onset of heart failure was accompanied by a strong up-regulation of cardiac lipid metabolism genes involved in fat synthesis, storage and oxidation. Microarray gene expression profiling was performed with heart tissue isolated from (i) 18 month-old apoE-deficient mice relative to age-matched non-transgenic C57BL/6J (B6) mice, (ii) 6 month-old apoE-deficient mice with 2 months of chronic pressure overload induced by abdominal aortic constriction (AAC) relative to sham-operated apoE-deficient mice and nontransgenic B6 mice, (iii) 10 month-old B6 mice with 6 months of AAC relative to sham-operated B6 mice, and (iv) 5 month-old B6 mice with 1 month of AAC relative to age-matched B6 mice.
2010-12-03 | E-GEOD-25765 | biostudies-arrayexpress
Project description:Heart failure is a leading cause of cardiovascular mortality with limited options for treatment. We used 18 month-old apolipoprotein E (apoE)- deficient mice as a model of atherosclerosis-induced heart failure to analyze whether the anti-ischemic drug ranolazine could retard the progression of heart failure. The study showed that 2 months of ranolazine treatment improved cardiac function of 18 month-old apoE-deficient mice with symptoms of heart failure as assessed by echocardiography. To identify changes in cardiac gene expression induced by treatment with ranolazine a microarray study was performed with heart tissue from failing hearts relative to ranolazine-treated and healthy control hearts. The microarray approach identified heart failure-specific genes that were normalized during treatment with the anti-ischemic drug ranolazine. Microarray gene expression profiling was performed with heart tissue isolated from (i) untreated 18 month-old apoE-deficient mice with heart failure relative to (ii) 18 month-old apoE-deficient mice treated for two months with the anti-ischemic drug ranolazine (200 mg/kg), and (iii) age-matched non-transgenic C57BL/6J (B6) control mice.
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Project description:The complete transcriptomes of kidney cortex from 3 γ-HIF2αM3 18 month old TG+ male mice and 3 age matched wild type (WT) C57BL/6 male mice were sequenced on an Illumina HiSeq2000 Sequencer.
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Project description:Individuals expressing alpha-1-antitrypsin mutant Z protein accumulate misfolded, mutant protein in the liver and are at risk for liver diseases including cirrhosis and hepatocellular carcinoma. Transgenic PiZ mice, a model for this liver disease, display similar pathologies to humans, including inflammation, increases in proliferation, autophagy and apoptosis, accumulation of globules and develop fibrosis and hepatocellular carcinoma with age. Microarrays were used to compare the gene expressions of PiZ mice to wild-type mice in order to identify the pathways that are altered in this disorder. Pooled samples from 4 mice, 3-4 months old were used for each of 4 categories. PiZ males, PiZ females, C57Bl/6 males, C57Bl/6 females
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Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (12 months) and sex matched alb cre mice. Keywords: Array comparative genomic hybridization analysis (aCGH).
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Project description:aCGH analysis of murine transgenic liver tissues affected with HCC, hybridized with age (12 months) and sex matched alb cre mice. Keywords: Array comparative genomic hybridization analysis (aCGH). Independent HCC of MCL1-/- mice were hybridized with pooled wt mice. Mclâ1flox/flox mice (C57BL/6 background) were obtained from the Dana Farber Cancer Institute, Boston, USA (Opferman JT et al., Nature 2003) and bred to heterozygous Albumin-Cre mice (C57BL/6 background) which led to hepatocyte-specific deletion of Mcl-1. The mice develop severe chronic liver damage (Vick B et al., Hepatology, 2009).
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Project description:Olfaction is often deregulated in Alzheimer´s disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from aged Tg2576 mice (18 months of age) respect to age matched wild-type (WT) littermates
2017-11-02 | PXD007795 | Pride