E-GEOD-50028
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA202289PRJNA215841PRJNA232748
PROVIDER: E-GEOD-50028 | ExpressionAtlas | 2015-07-27
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-50028-analysis-methods.tsv | Tabular | |||
| E-GEOD-50028-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-50028-configuration.xml | Xml | |||
| E-GEOD-50028-percentile-ranks.tsv | Tabular | |||
| E-GEOD-50028.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 89 |
Similar Datasets
Project description:Gene expression data of untreated and RA-treated wild type and RXRα-deficient mice liver
| PRJNA215841 | ENA
Project description:Liver transcriptional profiles of untreated or LPS/GalN-treated wild-type and TMX-/- mice.
2012-05-01 | GSE28438 | GEO
Project description:Our project focuses on retinoic acid (RA) effect on hepatic lipid homeostasis. Even though RA has more than one receptor including retinoids x receptor (RXR) and retinoic acid receptor (RAR), most probably, RA effect on lipid homeostasis is mediated by RXR and its partners such as PXR, FXR, and PPAR. So we treated the wild type and RXRα-knockout mice by retinoic acid to check the global gene expression especially for lipid homeostasis genes. We used microarrays to observe the global gene expression underlying hepatic lipid homeostasis. We treated both the wild type and RXRα-KO mice with normal diet and RA-containing diet for 7 days. For each group, three replicates were done. Liver total RNA were used to test global gene expression by microarray.
2013-08-21 | E-GEOD-50028 | biostudies-arrayexpress
Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.
2013-01-02 | E-GEOD-32421 | biostudies-arrayexpress
Project description:To identify RA regulated genes in endoderm, we did microarray analysis comparing gene expression levels between wild-type and RA-deficient embryos, which were treated with BMS453 at the beginning of gastrulation and were collected at stages 23.
2014-01-24 | E-MTAB-1419 | biostudies-arrayexpress
Project description:The pathogenesis of rheumatoid arthritis (RA) is complicated and involves both innate and adaptive immunity [5]. The innate immunity such as macrophages or fibroblast-like synoviocytes (FLS) in the synovium can generate inflammatory mediators, including TNF-α, IL-1, IL-6, IL-17, IFN-γ, and chemo kines that lead to synovial inflammation, bone erosion, and cartilage damage [6-8]. The IL-17 signaling mediates the autoantibody production in collagen-induced arthritis (CIA) model [9]. However, the treatment response with an anti-IL17 monoclonal antibody in RA patients shows a high degree of heterogeneity [10]. The inhibitors of the Janus kinase (JAK) pathway are approved for RA patients [11]. These data suggest that the targeted multiple cytokines through the JAK pathway are useful for RA treatment. Disturbance of type I IFNs (IFNs-I) signaling and production drive autoimmune development [12]. The presymptomatic RA patients display an increase of IFNs-I before the onset of symptoms [13]. The RA patients also show the elevation of IFN- α in the synovial fluid and high expression of IFNs-I regulated gene in peripheral blood mononuclear cells (PBMC) [14]. However, the role of IFNs-I in arthritis and bone homeostasis has suggested the accelerating effect of arthritis and bone damage. The interferon-alpha receptor knockout mice develop arthritis severity higher than wild-type mice in the model of antigen-induced arthritis [15]. IFNs-I also affects the bone homeostasis by inhibiting osteoclastogenesis via receptor activator of nuclear factor-kappa B (RANK) pathway, and reduction of c-FOS expression [16-18]. Therefore, the goal of RA treatment with antagonizing the IFNs-I pathway has to be optimized between efficacy and potentially adverse effect. STING is a cytosolic DNA sensor that initiates the production of IFNs-I. STING functions have been reported as both pro-inflammatory signaling and negative regulator against inflammation [19-21]. The mutation in exon 5 of the STING gene results in gain function leading to initiate inflammation and cause the Sting associated vasculopathy with onset in infancy (SAVI) [22]. Loss of STING function rescues DNaseII-deficient mice from lethality and polyarthritis [23]. However, Sting-deficient lupus mice (MRL/Lpr mice) show higher and earlier mortality than Sting-sufficient MRL/Lpr mice [24]. The pathology also shows lymphoid hypertrophy with a higher amount of macrophages and granulocytes infiltration, autoantibodies, and cytokine [24]. The objective of this study was to identify the role of STING in the pathogenesis of rheumatoid arthritis using collagen-induced arthritis (CIA) model as a representative model of the human RA.
2020-06-26 | PXD018652 | Pride
Project description:Mucopolysaccharidosis Type II is a hereditary lysosomal storage disease characterized by deficiency in the enzyme iduronate 2-sulfatase (IDS). IDS is critical in the breakdown of sulfated glycosaminoglycans and its deficiency leads to an accumulation of these compounds across various tissue types resulting in multisystemic dysfunction. Intravenous administration of recombinant IDS (idursulfase) substantially improves patients’ quality and length of life. However, recombinant IDS delivered intravenously is sequestered in the liver and respiratory failure remains as the leading cause of death for patients independent of idursulfase treatment, which suggests insufficient delivery to the lungs. This study aimed to assess a novel method of idursulfase administration by nebulizer in combination with intravenous treatment and determine if this route of administration may improve lung delivery of idursulfase and overall pathology. To fulfill this aim, whole body IDS knockout mice underwent twelve weeks of intravenous or combination treatment. Liver and lung tissue were harvested seven days after the last treatment. IDS activity, histological markers, and global proteomics from treated groups were compared to untreated knockouts or wild-type mice. Increased enzyme activity and histological measurements indicated augmented delivery to the liver with the combined treatment, but lung enzyme activity with each treatment was similar to untreated animals. However, proteomics data demonstrated that both treatments attenuated key features of the disease, although it is unclear whether the addition of nebulized administration improved efficacy in the lungs.
2025-06-09 | PXD054411 | Pride
Project description:Expression data of metformin treated wild type and parietal cell- specific AMPK-deficient mice
| PRJNA594351 | ENA
Project description:To confirm the effect of Bcl6 on the liver sex difference, we performed the gene expression analysis in male and female wild type mice and male and female liver specific Bcl-6 deficient mice.
2017-11-29 | GSE107435 | GEO