Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.

2013-04-30 | GSE46246 | GEO

Exon level expression data from the liver of adult control and Dhx32 homozygous mutant mice

Project description:We compared the whole mRNA transcript expression from control and homozygous mutant Dhx32 mice by Affymetrix Mouse Exon ST 1.0 Array ST to identify alternatively spliced mRNA transcripts We include exon level expression data from the liver of three control and three Dhx32 homozygous mutant mice

2011-11-17 | GSE15133 | GEO

Mus musculus

Project description:A strong anti-inflammatory signature revealed by liver transcription profiling of Tmprss6-/- mice

| PRJNA198530 | ENA

[E-MEXP-3786] IGF-I-induced chronic gliosis and retinal stress lead to neurodegeneration in an animal model of retinopathy

2013-04-30 | E-GEOD-46246 | biostudies-arrayexpress

Mus musculus

Project description:Transcription profiling of liver from farnesoid X receptor knockout mice

| PRJNA237019 | ENA

Vitamin C alters the amount of specific endoplasmic reticulum associated proteins involved in lipid metabolism in the liver of mice synthesizing a nonfunctional WRN mutant protein

Project description:Werner syndrome (WS) is a premature aging disorder caused by mutations in a DNA helicase/exonuclease. Mice lacking the helicase domain of the Wrn protein orthologue exhibit transcriptomic and metabolic alterations, some of which are reversed by vitamin C. Recent studies on the liver of these animals indicated that the Wrn mutant protein is associated with the endoplasmic reticulum (ER) resulting in an ER stress response. In this study, we identified liver proteins that exhibit actual level differences in the ER fraction between wild type and Wrn mutant mice using quantitative proteomic profiling with label-free Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS). Multiple Reaction Monitoring (MRM) and immunoblotting were performed to validate findings in a secondary independent cohort of wild type and Wrn mutant mice in the presence or absence of vitamin C in drinking water. The list of identified proteins showing significant altered expression levels was compared to transcriptomic results that were obtained in previous studies to assess the extent of correlation between the mRNA levels and their corresponding encoded protein levels in the liver of our different mouse cohorts.

2018-03-02 | PXD007758 | Pride

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