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Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Promoter hypermethylation and transcriptional silencing is a common epigenetic mechanism of tumour suppressor inactivation in cancer, including malignant brain tumours.
Publication Title
Epigenetic genome-wide analysis identifies BEX1 as a candidate tumour suppressor gene in paediatric intracranial ependymoma.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st), Affymetrix Human Gene 2.0 ST Array (hugene20st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Epithelial to mesenchymal transition (EMT) is activated during cancer invasion and metastasis, enriches for cancer stem cells (CSCs), and contributes to therapeutic resistance and disease recurrence. The epithelial cell line MCF7, can be induced to undergo EMT with the induction of PKC by PMA. 5-10% of the resulting cells have a CSC phenotype. This study looks at the transcriptome of these cells and how it differs from cells with a non-CSC phenotype.
Publication Title
Chromatinized protein kinase C-θ directly regulates inducible genes in epithelial to mesenchymal transition and breast cancer stem cells.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 1 Downloadable Sample
- Illumina human-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Identification of biologically relevant enhancers in human erythroid cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 1 Downloadable Sample
- Illumina human-6 v2.0 expression beadchip
Description
Identification of cell-type specific enhancers is important for understanding the regulation of programs controlling cellular development and differentiation. Enhancers are typically marked by the co-transcriptional activator protein p300 or by groups of cell-expressed transcription factors. We hypothesized that a unique set of enhancers regulates gene expression in human erythroid cells, a highly specialized cell type evolved to provide adequate amounts of oxygen throughout the body. Using chromatin immunoprecipitation followed by massively parallel sequencing, genome-wide maps of candidate enhancers were constructed for p300 and four transcription factors, GATA1, NF-E2, KLF1, and SCL, using primary human erythroid cells. These data were combined with gene expression analyses and candidate enhancers identified. Consistent with their predicted function as candidate enhancers, there was statistically significant enrichment of p300 and combinations of co-localizing erythroid transcription factors within 1-50 kb of the TSS of genes highly expressed in erythroid cells. Candidate enhancers were also enriched near genes with known erythroid cell function or erythroid cell phenotypes. Candidate enhancers exhibited only moderate conservation with mouse and minimal conservation with nonplacental vertebrates. Candidate enhancers were mapped to a data set of erythroid-associated, biologically relevant, SNPs from the GWAS catalog of the NHGRI. Fourteen candidate enhancers, representing 10 genetic loci, mapped to sites associated with biologically relevant erythroid traits. Fragments from these loci directed statistically significant expression in reporter gene assays. Identification of enhancers in human erythroid cells will allow a better understanding of erythroid cell development, differentiation, structure, and function, and provide insights into inherited and acquired hematologic disease.
Publication Title
Identification of biologically relevant enhancers in human erythroid cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 27 Downloadable Samples
Illumina HiSeq 3000
Description
We recently reported that single-cell derived isogenic subclones of SKMEL5 cells have differential initial sensitivity to BRAF-inhibitors. In order to probe differences among these subclones, we selected three subclones with unique drug responses: progressing (SK-MEL-5 SC10), stationary (SK-MEL-5 SC07), and regressing (SK-MEL-5 SC01) and performed RNASeq. This study examines differentially expressed genes (DEGs) among the subclones to identify the molecular basis for initial differences in drug sensitivity. Overall design: Transcriptomics analysis between single-cell derived isogenic subclones of BRAF-mutated melanoma cell line, SK-MEL-5
Publication Title
A Nonquiescent "Idling" Population State in Drug-Treated, BRAF-Mutated Melanoma.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Expression profiling of mRNA abundance in the adult mouse olfactory epithelium during replacement of OSNs forced by the bilateral ablation of the olfactory bulbs. The experiment was done on 6 week old male C57Bl/6 mice. Olfactory epithelium tissue samples were collected on days 1, 5, and 7 after bulbectomy. The cellular processes activated by bulbectomy include apoptosis of mature olfactory sensory neurons, infiltration of macrophages and dendritic cells, stimulation of proliferation of basal cell progenitors, and differentation of new sensory neurons.
Publication Title
Transcriptional changes during neuronal death and replacement in the olfactory epithelium.
Sample Metadata Fields
No sample metadata fields
View Samples- Sus scrofa
- 83 Downloadable Samples
- Illumina HiSeq 2000
Description
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection of 3rd trimester pregnant pigs can result in transmission of the virus to the fetus and ultimately death in utero or postnatally. Little is known about the immune response to infection at the maternal-fetal interface and in the fetus itself, or the molecular events behind virus transmission and disease progression in the fetus. To investigate these processes, RNA-sequencing of two tissues, uterine endothelium adjacent to the umbilical attachment site and fetal thymus, was performed 21 days post challenge on four groups of fetuses selected from a large PRRSV challenge experiment of pregnant gilts. Overall design: RNA-seq experiment compared gene expression between four different groups of fetuses (n=12 per group): control (CON-uninfected fetuses from mock inoculated gilts), UNINF (uninfected fetuses from PRRSV-inoculated gilts), INF (infected fetuses from PRRSV-inoculated gilts), and meconium-stained fetuses (MEC-meconium-stained fetuses from PRRSV-inoculated gilts) and investigated two tissues: uterine endometrium (with adherent placental tissue) at the site of umbilical attachment and fetal thymus (96 samples in total). Three contrasts were performed for the differential expression (edgeR) and network (WGCNA) analyses: UNINF v CON, INF v UNINF, and MEC v INF.
Publication Title
Genome-wide analysis of the transcriptional response to porcine reproductive and respiratory syndrome virus infection at the maternal/fetal interface and in the fetus.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 1000
Description
Pulmonary fibrosis (PF) is associated with many chronic lung diseases including Systemic sclerosis (SSc), Idiopathic Pulmonary Fibrosis (IPF) and Cystic Fibrosis (CF) which are characterized by the progressive accumulation of stromal cells and formation of scar tissue. Pulmonary fibrosis is a dysregulated response to alveolar injury which causes a progressive decline in lung function and refractory to current pharmacological therapies. Airway and alveolar epithelial cells and stromal cells contribute to pulmonary fibrosis but the cell-specific pathways and gene networks that are responsible for the pathophysiology are unknown. Recent animals models generated in our lab demonstrate clinical phenotypes seen in human fibrotic disease. The mouse model of transforming growth factor-a (TGFa)-induced fibrosis include conditionally expressing TGFa in the lung epithelium under control of the CCSP promoter driving rtTA expression (CCSP/TGFa). This allow the TGFa is only expressed in airway and alveolar epithelial cells and only when mice fed doxycycline (Dox). Similar to PF in humans, TGFa mice on Dox developed a progressive and extensive adventitial, interstitial and pleural fibrosis with a decline in lung mechanics. Thus, the TGFa transgenic mouse is a powerful model to determine lung cell-specific molecular signatures involved in pulmonary fibrosis. In this study, we sought to determine changes in the transcriptome during TGFa-induced pulmonary fibrosis. Our results showed that several pro-fibrotic genes increased in the lungs of TGFa mice. This study demonstrates that WT1 network gene changes associated with fibrosis and myfibroblast accumulation and thus may serve as a critical regulator fibrotic lung disease. Overall design: mRNA profiles of CCSP/- and CCSP/TGFalpha mice treated with Dox
Publication Title
Fibrocytes Regulate Wilms Tumor 1-Positive Cell Accumulation in Severe Fibrotic Lung Disease.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE49132- Mus musculus
- 8 Downloadable Samples
- Illumina MouseWG-6 v2.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Function of GATA factors in the adult mouse liver.
Sample Metadata Fields
Specimen part, Treatment
View Samples