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GSE36601
Saccharomyces cerevisiae
10 Downloadable Samples
Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Background
Publication Title
Distinct roles of the Gcn5 histone acetyltransferase revealed during transient stress-induced reprogramming of the genome.
Sample Metadata Fields
Treatment
View Samples- Saccharomyces cerevisiae
- 10 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
The data provide information expression profile in yeast for 5 different physioloigcal conditions during stress adpatation and stress recovery (normal growth, during stress adaptation, after stress adaptation, under stress recovery, after stress recovery) in yeast. The purpose of the study is to understand how histone acetyltransferase HATs (Gcn5) apply it is function in gene regulation by changing global or local histone acetylation level under different physiological conditions.
Publication Title
Distinct roles of the Gcn5 histone acetyltransferase revealed during transient stress-induced reprogramming of the genome.
Sample Metadata Fields
Treatment
View Samples- Mus musculus
- 8 Downloadable Samples
Illumina HiSeq 2000
Description
We recently identified pathogenic KIF1Bb mutations in sympathetic nervous system malignancies that are defective in developmental apoptosis. Here we deleted KIF1Bb in the mouse sympathetic nervous system based on a cre recombination system driven by the dopamine beta hydroxylase (DBH) promoter. We observed impaired sympathetic nervous function and misexpression of genes required for sympathoadrenal lineage differentiation in KIF1Bb deficient sympathetic ganglia. Overall design: We analyzed superior cervical ganglia from post-natal day 1 mice. We compared ganglia from four wild-type control animals (KIF1Bb fl/fl) with ganglia from four animals with conditional knockout of KIF1Bb (KIF1Bb fl/fl : DBHcre +/-).
Publication Title
Neuroblast differentiation during development and in neuroblastoma requires KIF1Bβ-mediated transport of TRKA.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 1120 Downloadable Samples
- Illumina HiSeq 2000
Description
Naïve CD4 T cells differentiate into functionally diverse subsets of T helper (Th) cells. Gene expression profiling has the capacity to pinpoint factors that regulate subset differentiation and function, however obtaining transcriptional profiles of pure populations has been challenging. We performed single cell RNA-Sequencing (scRNA-Seq) of T helper cells from lymph node, lung and airways in a mouse model of asthma. scRNA-Seq resolved transcriptional profiles of naïve CD4 T, Th1, Th2, Treg cells and various activated states including a population responding to type I interferons. A trajectory for Th2 cell differentiation was delineated over time, with Th2 cells acquiring follicular T helper cell characteristics in the lung-draining lymph node before undergoing further modifications in the lung. A feature of airway Th2 cells was their enrichment for genes associated with lipid metabolism and experiments with blockers of key metabolic pathways supported roles for glucose and lipid metabolism in Th2 cell differentiation. Overall design: Mice were sentized and challanged with HDM extract intranasally. scRNA-Seq was performed in 384-well format. The relevant organs (either BAL, lung or mLN) were isolated, rapidly processed, stained for a panel of surface markers and single cell sorted within approximately 90 minutes of organ harvest. In total 764 memory T helper cells (CD3+CD4+CD44+) were sorted directly into lysis buffer using a BD Influx from two independent mice 15 days after sensitization and challenge with HDM as described above. In addition, 50 naïve T Helper cells (CD3+CD4+CD62LhiCD44lo), 50 Treg cells (CD3+CD4+CD25hi) from mLN of a mouse not exposed to HDM; 200 ST2+ mLN and 82 ST2+ lung T helper cells (CD3+CD4+CD44+ST2+CD25-) were sort purified at day 10 of the HDM model. SMART-Seq2 libraries were prepared using the method described in Picelli et al. (Nature Methods 2013) by the Eukaryotic Single Cell Genomics national facility at SciLife Laboratory, Stockholm.
Publication Title
Single-Cell RNA Sequencing of the T Helper Cell Response to House Dust Mites Defines a Distinct Gene Expression Signature in Airway Th2 Cells.
Sample Metadata Fields
Specimen part, Subject
View Samples- Macaca mulatta
- 48 Downloadable Samples
- Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
The etiology of the central nervous system (CNS) alterations after human immunodeficiency virus (HIV) infection, such as dementia and encephalitis, remains unknown. We have used microarray analysis in a monkey model of neuroAIDS to identify 98 genes, many previously unrecognized in lentiviral CNS pathogenesis, whose expression is significantly up-regulated in the frontal lobe of simian immunodeficiency virus-infected brains. Further, through immunohistochemical illumination, distinct classes of genes were found whose protein products localized to infiltrating macrophages, endothelial cells and resident glia, such as CD163, Glut5, and ISG15. In addition we found proteins induced in cortical neurons (ie, cyclin D3, tissue transglutaminase, 1-antichymotrypsin, and STAT1), which have not previously been described as participating in simian immunodeficiency virus or HIV-related CNS pathology. This molecular phenotyping in the infected brains revealed pathways promoting entry of macrophages into the brain and their subsequent detrimental effects on neurons. These data support the hypothesis that in HIV-induced CNS disease products of activated macrophages and astrocytes lead to CNS dysfunction by directly damaging neurons, as well as by induction of altered gene and protein expression profiles in neurons themselves which are deleterious to their function.
Publication Title
Induction of pathogenic sets of genes in macrophages and neurons in NeuroAIDS.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 10 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented.
Publication Title
Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 116 Downloadable Samples
Description
Skeletal muscle is one of the primary tissues involved in the development of type 2 diabetes (T2D). Obesity is tightly associated with T2D, making it challenging to isolate specific effects attributed to the disease alone. By using an in vitro myocyte model system we were able to isolate the inherent properties retained in myocytes originating from donor muscle precursor cells, without being confounded by varying extracellular factors present in the in vivo environment of the donor. We generated and characterized transcriptional profiles of myocytes from 24 human subjects, using a factorial design with two levels each of the factors T2D (healthy or diseased) and obesity (non-obese or obese), and determined the influence of each specific factor on genome-wide transcription. We identified a striking similarity of the transcriptional profiles associated independently with T2D or obesity. Obesity thus presents an inherent phenotype in skeletal myocytes, similar to that induced by T2D. Through bioinformatics analysis we found a candidate epigenetic mechanism, H3K27me3 histone methylation, mediating the observed transcriptional signatures. Functional characterization of the expression profiles revealed dysregulated myogenesis and down-regulated muscle function in connection with T2D and obesity, as well as up-regulation of genes involved in inflammation and the extracellular matrix. Further on, we identified a metabolite subnetwork involved in sphingolipid metabolism and affected by transcriptional up-regulation in T2D. Collectively, these findings pinpoint transcriptional changes that are hard-wired in skeletal myocytes in connection with both obesity and T2D. Overall design: Isolated skeletal muscle precursor cells from 24 males and females (6 normal glucose tolerant, 6 obese, 6 type 2 diabetic, and 6 obese and type 2 diabetic) were differentiated in vitro and stimulated with insulin. RNA from fully differentiated myotubes sampled at 0, 0.5, 1, and 2 hours after insulin stimulation was quantified using RNA-seq (96 samples in total). The 6 base-line (0h) samples from normal glucose tolerant individuals are available under the submission GSE63887, the remaining 90 samples are contained in this submission.
Publication Title
Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 7 Downloadable Samples
- IlluminaHiSeq2500, IlluminaHiSeq2000
Description
Skeletal myocytes are metabolically active and susceptible to insulin resistance, thus implicated in type 2 diabetes (T2D). This complex disease involves systemic metabolic changes and their elucidation at the systems level requires genome-wide data and biological networks. Genome-scale metabolic models (GEMs) provide a network-context to integrate high-throughput data. We generated myocyte-specific RNA-seq data and investigated their correlation with proteome data. These data were then used to reconstruct a comprehensive myocyte GEM. Next, we performed a meta-analysis of six studies comparing muscle transcription in T2D versus healthy subjects. Transcriptional changes were mapped on the myocyte GEM, revealing extensive transcriptional regulation in T2D, particularly around pyruvate oxidation, branched-chain amino acid catabolism, and tetrahydrofolate metabolism, connected through the down-regulated dihydrolipoamide dehydrogenase. Strikingly, the gene signature underlying this metabolic regulation successfully classifies the disease state of individual samples, suggesting that regulation of these pathways is a ubiquitous feature of myocytes in response to T2D. Overall design: Isolated skeletal muscle precursor cells from six normal glucose tolerant and non-obese males and females were differentiated in vitro. RNA from fully differentiated myotubes was sequenced using RNA-seq.
Publication Title
Type 2 diabetes and obesity induce similar transcriptional reprogramming in human myocytes.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 42 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Importance of Comprehensive Molecular Profiling for Clinical Outcome in Children With Recurrent Cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 42 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
to explore possible treatment targets and reasons for agressive children cacners by comprehensive molecular profiling on several platforms
Publication Title
Importance of Comprehensive Molecular Profiling for Clinical Outcome in Children With Recurrent Cancer.
Sample Metadata Fields
No sample metadata fields
View Samples