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GSE18602
Mus musculus
12 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Microglia are resident CNS immune cells that are active sensors in healthy brain and versatile effectors under pathological conditions. Cerebral ischemia induces a robust neuroinflammatory response that includes marked changes in the gene expression and phenotypic profile of a variety of endogenous CNS cell types (astrocytes, neurons, microglia) as well as an influx of leukocytic cells (neutrophils, macrophages, T-cells) from the periphery. Many molecules and conditions can trigger a transformation of resting (or surveying) microglia to an activated (alerted/reactive) state. Here we review recent developments in the literature that relate to microglial activation in the experimental setting of in vitro and in vivo ischemia. We also present new data from our own laboratory demonstrating the direct effects of in vitro ischemic conditions on the microglial phenotype and genomic profile. Emphasis is placed on the role of specific molecular signaling systems such as hypoxia inducible factor-1 (HIF-1) and toll-like receptor-4 (TLR4) in regulating the microglial response in this setting. We then review histological and recent novel radiological data that confirms a key role for microglial activation in the setting of ischemic stroke in humans. We discuss recent progress in the pharmacological and molecular targeting of microglia in acute ischemic stroke. Finally, we explore how recent studies on ischemic preconditioning have increased interest in preemptively targeting microglial activation in order to reduce stroke severity.
Publication Title
Microglia in ischemic brain injury.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 97 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 97 diploid invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Patient stratification was performed according to axillary lymph node status (node-negative, pN0; node-positive, pN1) and overall survival (>8-year survivors; breast cancer-specific mortality within 8 years of diagnosis). Array-CGH results was validated by FISH using tumors showing HER2/neu gene amplification and expression profiling was confirmed using qPCR for 16 transcripts.
Publication Title
Clinical implications of gene dosage and gene expression patterns in diploid breast carcinoma.
Sample Metadata Fields
Disease, Disease stage
View Samples- Homo sapiens
- 97 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
Genomic and expression profiling using 38K BAC array-CGH and Illumina HT-12 beadchips were performed on 97 diploid invasive breast tumors to assess the impact of gene dosage on gene expression patterns and the effect of other mechanisms on transcriptional levels. Patient stratification was performed according to axillary lymph node status (node-negative, pN0; node-positive, pN1) and overall survival (>8-year survivors; breast cancer-specific mortality within 8 years of diagnosis). Array-CGH results was validated by FISH using tumors showing HER2/neu gene amplification and expression profiling was confirmed using qPCR for 16 transcripts.
Publication Title
Clinical implications of gene dosage and gene expression patterns in diploid breast carcinoma.
Sample Metadata Fields
Disease, Disease stage
View Samples- Homo sapiens
- 53 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
Transcriptomic profiling of human breast tumors.
Publication Title
Clinical implications of gene dosage and gene expression patterns in diploid breast carcinoma.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 42 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Analysis of gene expression in 17 low-grade fibromyxoid sarcoma (LGFMS) samples compared to that of histologically similar tumors. LGFMS is characterized by the specific translocations t(7;16)(q33;p11) or t(11;16)(p11;p11) and corresponding fusion genes FUS-CREB3L2 or FUS-CREB3L1.
Publication Title
FUS-CREB3L2/L1-positive sarcomas show a specific gene expression profile with upregulation of CD24 and FOXL1.
Sample Metadata Fields
Specimen part, Disease
View Samples- Arabidopsis thaliana
- 24 Downloadable Samples
Illumina HiSeq 2500
Description
In plants, apical meristems allow continuous growth along the body axis. Within the root apical meristem (RAM), a group of slowly dividing quiescent center (QC) cells is thought to limit stem cell activity to directly neighboring cells (Cowels, 1956; van den Berg et al., 1997), thus endowing them with unique properties, distinct from displaced daughters. This binary identity of the stem cells stands in apparent contradiction with the more gradual changes in cell division potential (Bennett and Scheres, 2010) and differentiation (Yamaguchi et al., 2008; 2010; Furuta et al, 2014; Geldner, 2013; Masucci et al., 1996; Dolan and Costa, 2001) that occur as cells move further away from the QC. To address this paradox and to infer molecular organization of the root meristem, we used a whole-genome approach to determine dominant transcriptional patterns along root ontogeny zones. We found that the prevalent patterns are expressed in two opposing gradients. One is characterized by genes associated with development, the other enriched in differentiation genes. We confirmed these transcript gradients, and demonstrate that these translate to gradients in protein accumulation and gradual changes in cellular properties. We also show that gradients are genetically controlled through multiple pathways. Based on these findings, we propose that cells in the Arabidopsis root meristem gradually transition from 'stemness' towards differentiation. Overall design: This study contains high-resolution datasets from cell populations from the enitre root meristem and xylem-specific cell populations. Using fluorescence activated cell sorting, three cell populations were isolated based on their GFP expression intensity. Two-Three replicates were used per sample
Publication Title
Framework for gradual progression of cell ontogeny in the <i>Arabidopsis</i> root meristem.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Characteristic extinguishing of B-cell phenotype in cHL is believed to be a result of transcription factor network deregulation due to the overexpression of repressor proteins ID2 and ABF-1. KLF4 is a versatile transcription factor, participating in regulation of differentiation processes in various tissues. Epigenetic silencing of KLF4 in cHL hints that KLF4 is involved in the complex mechanism of extinguishing of B-cell phenotype in cHL.
Publication Title
KLF4 is a tumor suppressor in B-cell non-Hodgkin lymphoma and in classic Hodgkin lymphoma.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus.
Publication Title
Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 4 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Early invasive growth and metastasis are features of pancreatic cancer that rely on resistance to anoikis, an apoptosis program activated upon loss of adequate matrix anchorage. Re-expression of the tumor suppressor p16 reversed anoikis resistance of pancreatic cancer cells. This conversion to an anoikis-susceptible phenotype was found to be associated with a striking loss of GNE mRNA expression, prompting us to address the role of GNE in pancreatic cancer in more detail. GNE catalyzes a rate-limiting key step of the sialic acid biosynthesis and may have additional functions in the nucleus.
Publication Title
Loss of UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase (GNE) induces apoptotic processes in pancreatic carcinoma cells.
Sample Metadata Fields
Specimen part, Cell line
View Samples