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accession-icon GSE29850
Identification of Notch targets in human endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human umbilical vein endothelial cells (HUVECs) were transduced with either MIY-N1IC (Notch1 intracellular domain) or MIY vector control. The cells were sorted for YFP, and RNA was extracted using Trizol (Invitrogen) and analyzed by the Affymetrix Human Genome U133 Plus 2.0 Array. Results were analyzed using the GCRMA algorithm to identify genes with a minimum of 2-fold induction or reduction. This global gene expression study was used to identify Notch targets in the endothelium.

Publication Title

Notch initiates the endothelial-to-mesenchymal transition in the atrioventricular canal through autocrine activation of soluble guanylyl cyclase.

Alternate Accession IDs

E-GEOD-29850

Sample Metadata Fields

Specimen part

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accession-icon SRP174479
Gene expression profile of N2 and HPX-2 mutant C.elegans strains when exposed to E.coli and E.faecalis
  • organism-icon Caenorhabditis elegans
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We use RNAseq analysis as an un-biased and highly sensitive measurement of global transcriptomic changes upon the loss of HPX-2. The RNAseq result provided insights into the potential physiological processes HPX-2 is involved in. Overall design: L4 stage worms were exposed to E. faecalis or E. coli for 16 hours and total RNA was extracted for 5 biological replicates. Illumina Hiseq 4000 sequencer with 75 nt pair-ended read format was used to conduct the sequencing.

Publication Title

Heme peroxidase HPX-2 protects Caenorhabditis elegans from pathogens.

Alternate Accession IDs

GSE124372

Sample Metadata Fields

Subject

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accession-icon GSE30391
Expression data from human Wharton's jelly stem cells
  • organism-icon Homo sapiens
  • sample-icon 30 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human umbilical cord Whartons jelly stem cells (WHJSC) are gaining attention as a possible clinical source of mesenchymal stem cells for use in cell therapy and tissue engineering due to their high accessibility, expansion potential and plasticity. However, the cell viability changes that are associated to sequential cell passage of these cells are not known. In this analysis, we have identified the gene expression changes that are associated to cell passage in WHJSC.

Publication Title

Evaluation of the cell viability of human Wharton's jelly stem cells for use in cell therapy.

Alternate Accession IDs

E-GEOD-30391

Sample Metadata Fields

Specimen part

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accession-icon E-MEXP-466
Transcription profiling of two populations of non-hematopoetic stem cells (MSC and MAPC) isolated from human bone marrow
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Compare the behaviour of two populations of non-hematopoetic stem cells (MSC and MAPC) isolated from human bone marrow. The effect of culture conditions on the behaviour of MSC was also characterised by isolating MSC and then culturing the cells for 96h in MAPC growth conditions

Publication Title

Validation of COL11A1/procollagen 11A1 expression in TGF-β1-activated immortalised human mesenchymal cells and in stromal cells of human colon adenocarcinoma.

Alternate Accession IDs

None

Sample Metadata Fields

Age, Specimen part

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accession-icon SRP070204
TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-Autonomously in Caenorhabditis elegans
  • organism-icon Caenorhabditis elegans
  • sample-icon 53 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The Caenorhabditis elegans oxidative stress response transcription factor, SKN-1, is essential for the maintenance of redox homeostasis and is a functional ortholog of the Nrf family of transcription factors. The numerous levels of regulation that govern these transcription factors underscore their importance. Here, we add a thioredoxin, encoded by trx-1, to the expansive list of SKN-1 regulators. We report that loss of trx-1 promotes nuclear localization of intestinal SKN-1 in a redox-independent, cell non-autonomous fashion from the ASJ neurons. Furthermore, this regulation is not general to the thioredoxin family, as two other C. elegans thioredoxins TRX-2 and TRX-3 do not play a role in this process. Moreover, TRX-1-dependent regulation requires signaling from the p38 MAPK signaling pathway. However, while TRX-1 regulates SKN-1 nuclear localization, SKN-1 transcriptional activity remains largely unaffected. Interestingly, RNA-Seq revealed that loss of trx-1 elicits a general, organism-wide down-regulation of several classes of genes; those encoding for collagens and lipid transport and localization being most prevalent. However, one prominent lipase-related gene, lips-6, is highly up regulated upon loss of trx-1 in a skn-1-dependent manner. Together, these results uncover a novel role for a thioredoxin in regulating intestinal SKN-1 nuclear localization in a cell non-autonomous manner, thereby contributing to the understanding of the processes involved in maintaining redox homeostasis throughout an organism. Overall design: Four samples were analyzed: Two nematode strains were analyzed, each under non-stressed and stressed (10mM NaAs) conditions

Publication Title

TRX-1 Regulates SKN-1 Nuclear Localization Cell Non-autonomously in Caenorhabditis elegans.

Alternate Accession IDs

GSE77976

Sample Metadata Fields

Disease, Cell line, Subject

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accession-icon GSE77540
Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse.

Alternate Accession IDs

E-GEOD-77540

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE77539
Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Multiple myeloma (MM) remains incurable despite the introduction of novel agents and a relapsing course is observed in the majority of patients. Although the development of genomic technologies has greatly improved our understanding of MM pathogenesis, the mechanisms underlying relapse have been less investigated. In this study, an integrative analysis of DNA copy number, DNA methylation and gene expression was conducted in matched diagnosis and relapse samples from 17 MM patients. Overall, the acquisition of abnormalities at relapse was much more frequent than the lost of lesions present at diagnosis, and DNA losses were significantly more frequent at relapse than in diagnosis samples. Interestingly, copy number abnormalities involving more than 100 Mb of DNA at relapse significantly impact the gene expression of these samples, provoking a particular deregulation of IL-8 pathway. On the contrary, no relevant modifications of gene expression were observed in those samples with less than 100 Mb affected by chromosomal changes. Although different statistical approaches were used to uncover genes whose abnormal expression at relapse was regulated by DNA methylation, only two genes significantly deregulated in relapse samples (SORL1 and GLT1D1) showed a negative methylation-expression correlation. A deeper analysis demonstrated that DNA methylation was involved in regulation of SORL1 expression in MM. Finally, relevant changes in gene expression observed in relapse samples, such us downregulation of CD27 and P2RY8, were not apparently preceded by alterations in corresponding DNA. Taken together, these results showed that genomic heterogeneity, both at the DNA and RNA level, is a hallmark of MM transition from diagnosis to relapse.

Publication Title

Integrative analysis of DNA copy number, DNA methylation and gene expression in multiple myeloma reveals alterations related to relapse.

Alternate Accession IDs

E-GEOD-77539

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE29145
PKCz-mediated Gaq stimulation of the ERK5 pathway is involved in cardiac hypertrophy
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Background: Gq-coupled G protein-coupled receptors (GPCR) mediate the actions of a variety of messengers that are key regulators of cardiovascular function. Enhanced Gaq-mediated signaling plays an important role in cardiac hypertrophy and in the transition to heart failure. We have recently described that Gaq acts as an adaptor protein that facilitates PKCz-mediated activation of ERK5 in epithelial cells. Since the ERK5 cascade is known to be involved in cardiac hypertrophy, we have investigated the potential relevance of this pathway in Gq-dependent signaling in cardiac cells.

Publication Title

Protein kinase C (PKC)ζ-mediated Gαq stimulation of ERK5 protein pathway in cardiomyocytes and cardiac fibroblasts.

Alternate Accession IDs

E-GEOD-29145

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP095341
Loss of JNK in Breast Epithelium Accelerates Tumor Formation
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Members of the JNK pathway have been found to be mutated in human breast cancer. Mouse studies examining JNK loss in different tissues have demonstrated that the JNK pathway can play a role in cancer. Using and autochthonous mouse model, we found that JNK deficiency on a p53-null background resulted in more rapid tumor onset. To learn more about these tumors we generated cells lines and performed various in vitro assays, as well as RNAseq in hope of finding differentially expressed genes that may explain the differences we observed in vivo. Overall design: Tumors were harvested from mice and cells lines were established from them. RNA was isolated from established tumor cell lines.

Publication Title

The cJUN NH<sub>2</sub>-terminal kinase (JNK) signaling pathway promotes genome stability and prevents tumor initiation.

Alternate Accession IDs

GSE92560

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE83864
Gene Expression Network Analyses in Response to Air Pollution Exposures in the Trucking Industry
  • organism-icon Homo sapiens
  • sample-icon 165 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

To investigate the cellular responses induced by air pollution exposures, we performed genome-wide gene expression microarray analysis using whole blood RNA sampled at three time-points across the work weeks of 63 non-smoking employees in the trucking industry. Our objective was to identify the genes and gene networks differentially activated in response to micro-environmental measures of occupational exposure to three pollutants: PM2.5 (particulate matter 2.5 microns in diameter) and elemental carbon (EC) and organic carbon (OC).

Publication Title

Gene expression network analyses in response to air pollution exposures in the trucking industry.

Alternate Accession IDs

E-GEOD-83864

Sample Metadata Fields

No sample metadata fields

View Samples
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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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