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Homo sapiens
3 Downloadable Samples
IlluminaGenomeAnalyzerIIx
Description
We carried out a genome-wide investigation of the primary transcriptional targets of 1a,25(OH)2D3 in breast epithelial cancer cells using RNA-Seq technology. We identified early transcriptional targets of 1a,25(OH)2D3 involved in adhesion, growth regulation, angiogenesis, actin cytoskeleton regulation, hexose transport, inflammation and immunomodulation, apoptosis, endocytosis and signaling. Furthermore, we found several transcription factors to be regulated by 1a,25(OH)2D3 that subsequently amplify and diversify the transcriptional output driven by 1a,25(OH)2D3 leading finally to a growth arrest of the cells. Moreover, we could show that 1a,25(OH)2D3 elevates the trimethylation of histone H3 lysine 4 at several target gene promoters. Our present transcriptomic analysis of differential expression after 1a,25(OH)2D3 treatment provides a resource of primary 1a,25(OH)2D3 targets that might drive the antiproliferative action in breast cancer epithelial cells.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 18 Downloadable Samples
- IlluminaHiSeq2000
Description
investigation of lncRNAs deregulated in oncogenic induced senescence.
Publication Title
No associated publication
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 12 Downloadable Samples
Affymetrix Mouse Expression 430A Array (moe430a)
Description
The neuronal ceroid lipofuscinoses (NCL) are a group of childhood inherited neurodegenerative disorders characterized by blindness, early dementia and pronounced cortical atrophy. The similar pathological and clinical profiles of different forms of NCL suggest that common disease mechanisms may be involved. Here, we have performed quantitative gene expression profiling of cortex from targeted knock out mice produced for Cln1 and Cln5 to explore NCL-associated molecular pathways. Combined microarray datasets from both mouse models exposed a common affected pathway: genes regulating cytoskeletal dynamics and neuronal growth cone stabilization display similar aberrations. We analyzed locus specific gene expression and showed regional clustering of Cln1 and three major genes of this pathway, further supporting a close functional relationship between the corresponding gene products, Cap1, Ptprf and Ptp4a2. The evidence from the gene expression data was substantiated by immunohistochemical staining data of Cln1-/- and Cln5-/- cortical neurons. These primary neurons displayed abnormalities in beta-tubulin and actin as well as abnormal intracellular distribution of growth cone associated proteins GAP-43, synapsin and Rab3. Our data provide the first evidence for a common molecular pathogenesis behind neuronal degeneration in CLN1 and CLN5. Since CLN1 and CLN5 code for proteins with distinct functional roles these data may have implications for other forms of NCL.
Publication Title
Brain gene expression profiles of Cln1 and Cln5 deficient mice unravels common molecular pathways underlying neuronal degeneration in NCL diseases.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Saccharomyces cerevisiae
- 338 Downloadable Samples
- Illumina HiSeq 2500
Description
WT cells and mutants during growth on low phosphate levels and recovery
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Disease, Cell line
View Samples- Saccharomyces cerevisiae
- 200 Downloadable Samples
- Illumina HiSeq 2500
Description
WT and mutants cells during growth in low phosphate levels and recovery into 20mM phosphate
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Disease, Cell line
View Samples- Mus musculus
- 17 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Bronchial asthma is associated with type 2 immune responses induced by components of adaptive as well as innate immunity. Although innate cytokines such as IL-25 have been shown to play key roles in development of airway hyperreactivity (AHR), little is known of innate molecules that regulate IL-25-mediated airway inflammation. We found that blockade of repulsive guidance molecule b (RGMb) in an experimental murine model of asthma blocked the development of AHR, a cardinal feature of asthma, and that RGMb is expressed on F4/80+CD11b+CD11cneg macrophages (RGMb+ macrophages), which accumulated in the lungs of OVA-sensitized and challenged mice, but not in nave mice. Moreover, we found that a large fraction of the RGMb+ macrophages expressed the IL-25 receptor IL-17RB and produced IL-13. IL-25 was critical for the development of AHR in our model, since mice deficient in IL-17RB did not develop AHR. Finally, treatment with anti-RGMb mAb during the challenge phase of the protocol after allergen sensitization effectively prevented the development of AHR and airway inflammation, suggesting for the first time that RGMb+ cells, including RGMb+ macrophages, play critical roles in allergen-induced asthma.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- Illumina HiSeq 2000
Description
It is currently debated as to whether liver macrophage (LM) activation from an anti-inflammatory to pro-inflammatory phenotype contributes to obesity-induced metabolic diseases. Here we report that LMs do not undergo a pro-inflammatory phenotype switch in obesity-induced insulin resistance in mice and humans. Remarkably, immune response related genes remained also unchanged in fly immune cells (haemocytes) upon high fat feeding. However, unbiased transcriptomic analyses revealed that LMs produce non-inflammatory factors, such as insulin like growth factor binding protein 7 (Igfbp7), that directly regulate liver metabolism. Using a unique method to manipulate gene expression only in LMs in vivo, we discovered that IGFBP7 specifically produced by LMs binds the insulin receptor and induces lipogenesis and gluconeogenesis, two major pathways increased in metabolic diseases. This study shows that macrophages could contribute to insulin resistance independently of their inflammatory status and that targeting non-inflammatory factors produced by macrophages might represent a better strategy than anti-inflammatory drugs to tackle metabolic diseases.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
The goal of this study was to examine how miR-21 upregulation influences T cell responses. miR-21 was antagonized by lentiviral overexpression of anti-sense miR-21 during activation of naive CD4 T cells from healthy adults. On day 5 after activation, libraries of miR-21 high and miR-21 low cells were prepared using the Ovation Human FFPE RNA-Seq Library Systems (NuGEN) and sequenced on an Illumina HiSeq 2500.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part
View Samples
SRP195476- Mus musculus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
RNA sequencing data from liver macrophages isolated from ob/ob mice.
Publication Title
No associated publication
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
the functions of nucleolar protein 66 in satellite cells
Publication Title
No associated publication
Sample Metadata Fields
Sex, Specimen part, Cell line
View Samples