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GSE8442
Bos taurus, Homo sapiens, Rattus norvegicus
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Angiotensin II (Ang-II) regulates adrenal steroid production and gene transcription through several signaling pathways. Changes in gene transcription occur within minutes after Ang-II stimulation, causing an acute increase in aldosterone production and subsequent increase in the overall capacity to produce aldosterone. Our goal was to compare the Ang-II regulation of early gene expression and confirm the upregulation of selected genes using quantitative real-time RT-PCR (qPCR) across three species: human, bovine, and rat.
Publication Title
Angiotensin-II acute regulation of rapid response genes in human, bovine, and rat adrenocortical cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Sus scrofa
- 12 Downloadable Samples
- Affymetrix Porcine Genome Array (porcine)
Description
Previous results from a genome scan in a F2 Iberian by Meishan intercross showed several chromosome regions associated with litter size traits. In order to identify candidate genes underlying these QTL we have performed an ovary gene expression analysis during pregnancy. F2 sows were ranked by their estimated breeding values for prolificacy, the six sows with higher EBV (HIGH prolificacy) and the six with lower EBV (LOW prolificacy) were selected. Samples were hybridized to Affymetrix porcine expression microarrays. The statistical analysis with a mixed-model approach identified 221 differentially expressed probes, representing 189 genes. These genes were functionally annotated in order to identify the genetic pathways overrepresented. Among the most represented functional groups the first one was immune system response activation against external stimulus. The second group was made up of genes which regulate the maternal homeostasis by complement and coagulation cascades. The last group was involved on lipid and fatty acid enzymes of metabolic processes, which participate in steroidogenesis pathway. In order to identify powerful candidate genes for prolificacy, the second approach of this study was merging microarray data with position information of QTL affecting litter size, previously detected in the same experimental cross. According to this, we have identified 27 differentially expressed genes co-localized with QTL for litter size traits, which fulfill the biological, positional and functional criteria.
Publication Title
Differential gene expression in ovaries of pregnant pigs with high and low prolificacy levels and identification of candidate genes for litter size.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Microarray analysis of Myd88-/-Trif-/- and Myd88-/-Rip2-/- macrophage responses to WT or dotA mutant L. pneumophila.
Publication Title
Type IV secretion-dependent activation of host MAP kinases induces an increased proinflammatory cytokine response to Legionella pneumophila.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
Illumina HiSeq 2500
Description
We used RNA-seq as a method of next generation sequencing (NGS) to identify RIPK1 dependent inflammatory mediators and pathways in LPS injected mice. Overall design: Mice were divided intro 3 groups - control (n=2), LPS (n=2) and LPS/Nec-1 (n=2). BM cells were isolated by FACS as described for qPCR analysis. Total RNAs were isolated using Qiagen RNeasy kit according to the manufacturer's protocol
Publication Title
RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Gene level expression estimate using the Whole Transcript (WT) Assay approach of the Gene 1.0 ST Array System for Mouse. This assay was done to identify the RIPK1-dependent gene expression changes in mouse BMDMs.
Publication Title
RIPK1 and RIPK3 Kinases Promote Cell-Death-Independent Inflammation by Toll-like Receptor 4.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Histidine-rich glycoprotein (HRG) is a 75 kDa heparin-binding plasma protein which has been implicated in regulation of tumor angiogenesis and growth. To exert some of its biological functions, HRG acts on macrophages.This study was performed to assess changes in gene expression in peritoneal macrophages treated with HRG using oligonucleotide microarrays
Publication Title
Genetic deficiency in plasma protein HRG enhances tumor growth and metastasis by exacerbating immune escape and vessel abnormalization.
Sample Metadata Fields
Specimen part, Disease, Treatment, Time
View Samples- Homo sapiens
- 28 Downloadable Samples
- Illumina human-6 v2.0 expression beadchip
Description
Patients with febrile malaria were recruited in order to determine Peripheral Blood Mononuclear Cell (PBMC) gene expression during malaria. Blood was harvested from patients during the acute phase of the illness, and then patients were given a curative regimen of antimalarials. Three to four weeks after treatment, patients returned to the malaria clinic and blood was collected again, in order that each patient could serve as his or her own control. PBMC were isolated at the time of blood collection and forzen in RNA extraction buffer. At the end of the study, each patient was arrayed for ~47,000 transcripts, comparing gene expression at the end of therapy to that at the beginning. The goal was to determine which genes were altered as a result of disease at least 2 fold in a statistically significant manner and to assess if the genes involved could be related to Toll-like receptor signaling pathways. Approximately 60 genes involved in inflammation were confirmed by qPCR.
Publication Title
Malaria primes the innate immune response due to interferon-gamma induced enhancement of toll-like receptor expression and function.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 8 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Brain tumor neurospheres (BTCSs) are cancer cells with neural stem cell-like properties found in the fatal brain tumor glioblastoma multiforme (GBM). These cells account for less than 1% of total tumor cells, are poorly differentiated and are believed to be involved in tumor induction, progression, treatment resistance and relapse. Specific miRNAs play important roles in modulating the proliferation and differentiation of neural stem cells, therefore, we aimed to identify miRNAs controlling differentiation in GBM-BTSCs through high throughput screening miRNA array profiling. We compared the miRNA expression profiles at the neurosphere state and upon 4 and 14days of differentiation by using LIMMA, finding 21 differentially expressed miRNAs : hsa-miR-103, hsa-miR-106a, hsa-miR-106b, hsa-miR-15b, hsa-miR-17, hsa-miR-19a, hsa-miR-20a, hsa-miR-25, hsa-miR-301a and hsa-miR-93 were found up-regulated upon differentiation, while hsa-miR-100, hsa-miR-1259, hsa-miR-21, hsa-miR-22, hsa-miR-221, hsa-miR-222, hsa-miR-23b, hsa-miR-27a, hsa-miR-27b, hsa-miR-29a and hsa-miR-29b were down-regulated. Expression of 11 of the 21 miRNAs was examined by qPCR and 7 of them were validated: hsa-miR-21, hsa-miR-29a, hsa-miR-29b, hsa-miR-221 and hsa-miR-222 increased their expression upon differentiation, while hsa-miR-93 and hsa-miR-106a were inhibited. Functional studies demonstrated that miR-21 over-expression induced the expression of glial and/or neuronal cell markers in the neurospheres, possibly due to SPRY1 targeting by miR-21 in these cells, while miR-221 and miR-222 inhibition at the differentiated state reduced the expression of those differentiation markers. On the other hand, miR-29a and miR-29b targeted MCL1 in the GBM neurospheres and increased apoptotic cell death.
Publication Title
Involvement of miRNAs in the differentiation of human glioblastoma multiforme stem-like cells.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Glioblastoma multiforme is one of the most devastating cancers and presents unique challenges to therapy due to its aggressive behaviour. Cancer stem cells have been described to be the only cell population with tumorogenic capacity in glioblastoma. Therefore, effective therapeutic strategies targeting these cells may be beneficial. We have established different cultures of glioblastoma stem cells (GSCs) derived from surgical specimens and found that, after induction of differentiation, NFB was activated, which allows intermediate tumor precursor cells to remain cycling. We also showed that blockade of NFB signaling in differentiating GSCs by different genetic strategies or treatment with small molecule inhibitors, promoted replication arrest, progression to a mature phenotype, mainly neuronal cells, and senescence. This effect was partly mediated by downregulation of the NFB target gene cyclin D1. Furthermore, intravenous treatment of immunodeficient mice bearing human GSC-derived tumors with a novel small-molecule inhibitor of the NFB pathway induced senescence of tumor cells but no ultraestructural alterations of the brain parenchymal cells were detected. These findings reveal that activation of NFB may keep differentiating GSCs from acquiring a mature postmitotic phenotype, thus allowing cell proliferation, and support the rationale for therapeutic strategies aimed at promoting premature senescence in GSCs undergoing differentiation.
Publication Title
Blockade of the NFκB pathway drives differentiating glioblastoma-initiating cells into senescence both in vitro and in vivo.
Sample Metadata Fields
Specimen part, Disease
View Samples- Homo sapiens
- 121 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
We sought to identify genes and gene signatures which correlate with progression by sampling human melanomas from nevi, primary, and metastatic tumors. The large number of samples also permits analysis within groups.
Publication Title
Integrative genome comparison of primary and metastatic melanomas.
Sample Metadata Fields
Sex, Specimen part, Disease, Race, Subject
View Samples