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accession-icon GSE100130
RNA Expression Data from developing enteric nervous system (ENS) and bowel
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The enteric nervous system (ENS) can control most essential gut functions owing to its organization into complete neural circuits consisting of a multitude of different neuronal subtypes.

Publication Title

Transcription and Signaling Regulators in Developing Neuronal Subtypes of Mouse and Human Enteric Nervous System.

Sample Metadata Fields

Specimen part

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accession-icon GSE23895
Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents
  • organism-icon Mus musculus, Rattus norvegicus
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Protein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency.

Publication Title

Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE14879
Gene expression study of anaplastic large cell lymphomas: cellular origin, pathogenesis and relation to Hodgkin lymphoma
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Anaplastic large cell lymphoma (ALCL) is a main type of T cell lymphomas and comprises three distinct entities: systemic ALK+, systemic ALK- and cutaneous ALK- ALCL. Little is known about their pathogenesis and their cellular origin, and morphological and immunophenotypical overlap exists between ALK- ALCL and classical Hodgkin lymphoma (cHL). We conducted gene expression profiling of microdissected lymphoma cells of ALK+ and ALK- systemic ALCL, cutaneous ALCL and cHL, and of eight subsets of normal T and NK cells. The analysis supports a derivation of ALCL from activated T cells, but the lymphoma cells acquired a gene expression pattern hampering an assignment to a CD4+, CD8+ or CD30+ T cell origin. Indeed, ALCL display a general down-modulation of T cell characteristic molecules. All ALCL types show significant expression of NFB target genes and upregulation of genes involved in oncogenesis (e.g. EZH2). Surprisingly few genes are differentially expressed between systemic and cutaneous ALK- ALCL despite their different clinical behaviour, and between ALK- ALCL and cHL despite their different cellular origin. ALK+ ALCL are characterized by expression of genes regulated by pathways constitutively activated by ALK. This study provides multiple novel insights into the molecular biology and pathogenesis of ALCL.

Publication Title

Gene expression profiling of isolated tumour cells from anaplastic large cell lymphomas: insights into its cellular origin, pathogenesis and relation to Hodgkin lymphoma.

Sample Metadata Fields

Specimen part

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accession-icon GSE54011
C. Elegans expression: toxic vs. adequate vs. low selenium
  • organism-icon Caenorhabditis elegans
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Genome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations

Publication Title

Toxic-selenium and low-selenium transcriptomes in Caenorhabditis elegans: toxic selenium up-regulates oxidoreductase and down-regulates cuticle-associated genes.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE85987
Inhibition of endothelial Notch signaling attenuates inflammation
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE85992
Gene expression data from endothelial cells isolated from DNFB-treated ears of mice with inducible endothelial-specific overexpression of constitutively active Notch1 intracellular domain
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip, Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Notch1 is a key regulator of endothelial cell behaviour. This experiment was designed to identify genes regulated by Notch1 signaling in inflammatory activated mouse endothelial cells.

Publication Title

Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE39180
Genes regulated/modulated by jagged1 in endothelial cells during inflammation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Proinflammatory activation of endothelial cells leads to recruitment of leukocytes by upregulation of adhesion molecules and presentation of chemoattractants. In response to such activation there is also a strong shift in the endothelial expression of Notch ligands, with downregulation of Dll4 and a upregulation of JAG1. To assess whether Jagged1 would affect the endothelial activation profile, we suppressed JAG1 expression during IL-1-induced activation by means of siRNA and performed a genome-wide transcriptome analysis. Our results show for the first time that Jagged1 modulates the transcription profile of activated endothelial cells and describe data that imply a role for Jagged1 in sharpening the inflammatory profile of the vasculature, giving it an edge towards leukocyte recruitment. These findings imply that Jagged1 might be a potential therapeutic target to attenuate inflammation and reduce tissue damage in inflammatory diseases.

Publication Title

Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE85986
Effect of Notch1 on inflammatory activation of human umbilical vein endothelial cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Inflammatory activation of endothelial cells enables leukocyte recruitment to tissues. We here investigate how Notch1 signaling affects the transcriptional profile of inflammatory activated human umbilical vein cells.

Publication Title

Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE89401
Clonal variation in drug and radiation response among glioma-initiating cells is linked to proneural-mesenchymal transition
  • organism-icon Homo sapiens
  • sample-icon 146 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20), Illumina HumanMethylation450 BeadChip (HumanMethylation450_15017482)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Clonal Variation in Drug and Radiation Response among Glioma-Initiating Cells Is Linked to Proneural-Mesenchymal Transition.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE89399
Clonal variation in drug and radiation response among glioma-initiating cells is linked to proneural-mesenchymal transition (HTA 2.0)
  • organism-icon Homo sapiens
  • sample-icon 146 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Intra-tumor heterogeneity is a hallmark of glioblastoma multiforme, and thought to negatively affect treatment efficacy. Here we establish libraries of glioma-initiating cell (GIC) clones from patient samples and find extensive molecular and phenotypic variability between clones, including a wide range of responses to radiation and drugs. This widespread variability was observed as a continuum of multitherapy resistance phenotypes linked to a proneural-to-mesenchymal shift in the transcriptome.

Publication Title

Clonal Variation in Drug and Radiation Response among Glioma-Initiating Cells Is Linked to Proneural-Mesenchymal Transition.

Sample Metadata Fields

Specimen part, Cell line

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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Developed by the Childhood Cancer Data Lab

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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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