Identifying PDEF regulated genes may shed light on the mechanism by which PDEF may induce breast cancer progression. To that purpose, we have used the MCF-7 human breast tumor cell line model to identify PDEF induced genes. Briefly, PDEF expression was down regulated by shRNA in MCF-7 cells and RNA probes from PDEF-down regulated and control MCF-7 cells were used to screen the Affymetrics HG-U133A Gene Chips. This analysis found 62 genes that were induced 2-fold or higher by PDEF. Further analysis of 3 of these genes namely S100A7, CEACAM6 and B7-H4 in primary breast tumors showed CEACAM6 as a frequently elevated and co-exressed gene with PDEF in these tumors.
Prostate derived Ets transcription factor and Carcinoembryonic antigen related cell adhesion molecule 6 constitute a highly active oncogenic axis in breast cancer.
Cell line
View SamplesTo identify novel genes and adaptations induced by resveratrol preconditioning that could promote long-term cerebral ischemic tolerance. After analyzing the results, we identified only 155 differentially expressed genes among which the majority of genes consisting of 126 were downregulated and only 29 genes were upregulated. The downregulated genes clustered into biological processes involved in regulating the memebrane potential, gene expression regulation, and neurotrasmitter transport secrection. While the upregulated gene included immediate early genes and genes involved in antioxidant defense. Overall design: Mice were subject to an intraperitoneal injection of vehicle or resveratrol (10mg/kg) (n=3 per group), two weeks later their cerebral cortex was collected, RNA was extracted and then sent for sequencing
Resveratrol Preconditioning Induces Genomic and Metabolic Adaptations within the Long-Term Window of Cerebral Ischemic Tolerance Leading to Bioenergetic Efficiency.
Specimen part, Cell line, Subject
View SamplesIn this study we isolated and cultured neural progenitor cells (NPCs) from human fetal brain collected during the gliogenic phase (second trimester) of aborted fetuses, we differentiated NPCs into astrocyte using different protocols (FBS or CNTF/BMP4) and utilized RNA sequencing to analyze transcriptomic changes underlying the differentiation process Overall design: Neural progenitor cells (NPCs) isolated from 4 different donors (91, 103, 110 and 114 days embryos) were differentiated for 1 week using 2.5% FBS, while 3 NPCs lines (two from 103 and one from 110 days embryo) were differentiated for 1 week in the presence of CNTF/BMP4. RNA was extracted from NPCs before and after differentiation and submitted for sequencing on the Illumina HiSeq 2000 platform
A comparative transcriptomic analysis of astrocytes differentiation from human neural progenitor cells.
No sample metadata fields
View SamplesThe data contained in this record are used to differentiate between the effects of IFN-a and IFN-b on 48h cultures of the ex vivo pbmcs of ATL patients, using Affymetrix microarrays (HuGene 1.0).
IFN-β induces greater antiproliferative and proapoptotic effects and increased p53 signaling compared with IFN-α in PBMCs of Adult T-cell Leukemia/Lymphoma patients.
Specimen part, Subject
View SamplesGlucocorticoids are first-line agents for the treatment of many eosinophil-associated disorders. However, their mechanism of action in this group of disorders remains poorly understood, including the well-known clinical observation that glucocorticoids at therapeutic doses lead to profound, transient eosinopenia within hours of administration. To gain an unbiased, genome-wide view of the early transcriptional effects of glucocorticoids on human eosinophils in vivo, and torelate them to the kinetics of glucocorticoid-induced eosinopenia, RNA sequencing was performed on purified blood eosinophils obtained before and 30, 60, and 120 minutes after administration of a single dose of oral prednisone (1 mg/kg) to healthy subjects with hypereosinophilia (hypereosinophilia of unknown significance). Overall design: Three subjects with hypereosinophilia of unknown significance were each given a single dose of oral prednisone, 1 mg/kg. Whole blood was collected before and 30 minutes, 1 hour, and 2 hours after prednisone administration. Eosinophils were purified from each peripheral blood sample. Total RNA was obtained from purified eosinophils and subject to library preparation and high-throughput sequencing.
Transcript- and protein-level analyses of the response of human eosinophils to glucocorticoids.
Specimen part, Disease, Disease stage, Treatment, Subject, Time
View SamplesBlood from subjects with cardioembolic stroke and controls was collected, and the RNA extracted was interrogated and whole genome U133 Affymetrix Arrays. Twenty-three control samples and sixty-nine cardioembolic stroke samples were assayed.
Gene expression in peripheral immune cells following cardioembolic stroke is sexually dimorphic.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Effect of Human Genetic Variability on Gene Expression in Dorsal Root Ganglia and Association with Pain Phenotypes.
Specimen part
View SamplesSingle nucleotide polymorphisms (SNP) can affect mRNA gene expression, in a tissue-specific manner. In this work we survey association of SNP alleles with mRNA gene expression in human dorsal root ganglions (DRG) to gain insights into pathophysiology of pain phenotypes.
Effect of Human Genetic Variability on Gene Expression in Dorsal Root Ganglia and Association with Pain Phenotypes.
Specimen part
View SamplesSingle nucleotide polymorphisms (SNP) can affect mRNA gene expression, in a tissue-specific manner. In this work we survey association of SNP alleles with mRNA gene expression in human dorsal root ganglions (DRG) to gain insights into pathophysiology of pain phenotypes.
Effect of Human Genetic Variability on Gene Expression in Dorsal Root Ganglia and Association with Pain Phenotypes.
Specimen part
View SamplesCD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer's disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33. Overall design: Microglia were isolated from brains of WT, 5xFAD, 5xFAD;CD33-/-, 5xFAD;TREM2-/-, and 5xFAD;CD33-/-;TREM2-/- mice at 4 and 8 months of age, using FACS sorting for CD11b and CD45. RNA was extracted using the RNeasy Plus Micro Kit (Qiagen). Libraries were prepared using the TruSeq Stranded mRNA LT Prep Kit (Illumina) and sequenced on an Illumina HiSeq 2500 sequencer using single-end 50. Reads were aligned to mouse genome mm10 using the STAR aligner. Read counts for individual genes were obtained using HTSeq.
TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease.
Age, Cell line, Subject
View Samples