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GSE43959
Caenorhabditis elegans
18 Downloadable Samples
Affymetrix C. elegans Genome Array (celegans)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Diet-induced developmental acceleration independent of TOR and insulin in C. elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 9 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Analysis of wildtype (N2) C. elegans fed different diets: E. coli OP50, E. coli HT115 and Comamonas DA1877
Publication Title
Diet-induced developmental acceleration independent of TOR and insulin in C. elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 9 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Analysis of wildtype (N2) C. elegans fed different diets: E. coli OP50, Comamonas DA1877, and Diluted Comamonas (1:1000 Comamonas DA1877:E. coli OP50)
Publication Title
Diet-induced developmental acceleration independent of TOR and insulin in C. elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Caenorhabditis elegans
- 9 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Analysis of wildtype C. elegans (N2) and pcca-1(ok2282) and metr-1(ok521) mutants fed Comamonas DA1877
Publication Title
Integration of metabolic and gene regulatory networks modulates the C. elegans dietary response.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [probe set (exon) version (huex10st)
Description
Oesophageal exposure to duodenogastroesophageal refluxate is implicated in the development of Barretts Metaplasia, with increased risk of progression to oesophageal adenocarcinoma. The literature proposes that reflux exposure activates NF-kB, driving the aberrant expression of intestine-specific caudal-related homeobox genes. However, early events in the pathogenesis of Barretts Metaplasia from a normal epithelium are poorly understood. To investigate this, our study subjected a 3D model of the normal human oesophageal mucosa to repeated, pulsatile exposure to specific bile components and examined changes in gene expression. Initial 2D experiments with a range of bile salts observed that taurochenodeoxycholate (TCDC) impacted upon NF-kB activation without causing cell death. Informed by this, the 3D human oesophageal model was repeatedly exposed to TCDC in the presence and absence of acid, and the epithelial cells underwent gene expression profiling. We identified ~300 differentially expressed genes following each treatment, with a large and significant overlap between treatments. Enrichment analysis (Broad GSEA, DAVID and Metacore, GeneGo Inc) identified multiple gene sets related to cell signalling, inflammation, proliferation, differentiation and cell adhesion. Specifically NF-kB activation, Wnt signalling, cell adhesion and targets for the transcription factors PTF1A and HNF4 were highlighted. CDX1/2 transcription factors are believed to play a role in BM development; however, in this study their targets were not enriched, suggesting that CDX1/2 activation may not be the one of the initial events for BM formation. Our findings highlight new areas for investigation in the earliest stages of BM pathogenesis of oesophageal diseases and new potential therapeutic targets.
Publication Title
Pulsatile exposure to simulated reflux leads to changes in gene expression in a 3D model of oesophageal mucosa.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 49 Downloadable Samples
Illumina HiSeq 2000
Description
The goal was to capture the transcriptional activity due to over-expression of AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) genes .Overexpressions were validated using Western Blots. Illumina RNA-Seq technology was used to capture the downstream transcriptional activity. Reads were 101 base pairs long and single ended. An R open source package “Rsubread” was used to align and quantify the read using UCSC hg19 annotation. The integer-based gene counts were later normalized in TPM . Overall design: Profiles of gene expression, downstream of AKT, BAD, ERBB2, IGF1R, RAF1 and KRAS(G12V) over-expression, were generated in cells derived from breast and used to generate a gene-expression signatures.
Publication Title
Activity of distinct growth factor receptor network components in breast tumors uncovers two biologically relevant subtypes.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
- Illumina HiSeq 2000
Description
CD133+ and CD133- cells were FACS islated from GBML8 cells to find gene signatures upregulated in cancer stem cells Overall design: After surface immuno staining, CD133+ and CD133- cells were FACS isolated and subjected to RNA isolation. Experiment represent averaged data of 2 independent FACS isolations.
Publication Title
GPR133 (ADGRD1), an adhesion G-protein-coupled receptor, is necessary for glioblastoma growth.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 48 Downloadable Samples
Sentrix MouseRef-8 Expression BeadChip (Target ID), Rosetta/Merck Mouse TOE 75k Array 1 microarray
Description
A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.
Publication Title
Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 16 Downloadable Samples
- Sentrix MouseRef-8 Expression BeadChip (Target ID)
Description
A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.
Publication Title
Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 14 Downloadable Samples
- Sentrix MouseRef-8 Expression BeadChip (Target ID)
Description
A major task in dissecting the genetics of complex traits is to identify causal genes for disease phenotypes. We previously developed a method to infer causal relationships among genes through the integration of DNA variation, gene transcription, and phenotypic information. Here we validated our method through the characterization of transgenic and knockout mouse models of candidate genes that were predicted to be causal for abdominal obesity. Perturbation of eight out of the nine genes, with Gas7, Me1 and Gpx3 being novel, resulted in significant changes in obesity related traits. Liver expression signatures revealed alterations in common metabolic pathways and networks contributing to abdominal obesity and overlapped with a macrophage-enriched metabolic network module that is highly associated with metabolic traits in mice and humans. Integration of gene expression in the design and analysis of traditional F2 intercross studies allows high confidence prediction of causal genes, and identification of involved pathways and networks.
Publication Title
Validation of candidate causal genes for obesity that affect shared metabolic pathways and networks.
Sample Metadata Fields
No sample metadata fields
View Samples