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accession-icon GSE66039
Global analysis of androgen-signaling reveals the function of miRNAs for the epigenomic regulation in prostate cancer cells
  • organism-icon Homo sapiens
  • sample-icon 8 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

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE66038
Effects of miRNA-mediated TET2 in prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Prostate cancer is the most common cancer in men. We identified that miR-29 family is the most androgen-responsive miRNA in hormone-refractory prostate cancer cells. For the screening of miR-29b target, we performed microarray analysis in two prostate cancer cells. Because TET2 is the primary target of miR-29 family by our analysis, we also performed TET2 signaling by microarray.

Publication Title

TET2 repression by androgen hormone regulates global hydroxymethylation status and prostate cancer progression.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE15461
Insufficiency of Copper Ion Homeostasis Causes Freeze-Thaw Injury of Yeast Cells
  • organism-icon Saccharomyces cerevisiae
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

Saccharomyces cerevisiae is exposed to freeze-thaw stress in commercial processes including frozen dough baking. The cell viability and fermentation activity after freeze-thaw were dramatically decreased due to freeze-thaw injury. Because freeze-thaw injury involves complex phenomena, the mechanisms of it are not fully understood. We attempted to analyze the mechanisms of freeze-thaw injury by indirect gene expression analysis during post-thaw incubation after freeze-thaw treatment using DNA microarray profiling. The results showed that a high frequency of the genes involved in the homeostasis of metal ions were up-regulated depending on the freezing period. The phenotype of the deletion mutants of the up-regulated genes extracted by indirect gene expression analysis was assessed. The deletion strains of the MAC1 and CTR1 genes involved in copper ion homeostasis exhibited freeze-thaw sensitivity, suggesting that copper ion homeostasis is required for freeze-thaw tolerance. Supplementation with copper ions during post-thaw incubation increased intracellular superoxide dismutase activity. Inverse correlated with intracellular superoxide dismutase activity, intracellular levels of reactive oxygen species were decreased. Moreover, cell viability increased by supplementation with copper ions under specific assessment conditions. This study suggested that insufficiency of copper ion homeostasis may be one of the causes of freeze-thaw injury.

Publication Title

Insufficiency of copper ion homeostasis causes freeze-thaw injury of yeast cells as revealed by indirect gene expression analysis.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE65350
Expression data from mouse embryo
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To understand the molecular mechanism by which regulate skeletal development, we attempted to identify transcription factors that were highly expressed in developing cartilage during the embryonic stage.

Publication Title

The transcription factor Foxc1 is necessary for Ihh-Gli2-regulated endochondral ossification.

Sample Metadata Fields

Specimen part

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accession-icon GSE37431
Endothelial cell-enriched genes expression in mouse embryo
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The early blood vessels of the embryo and yolk sac in mammals develop by aggregation of de novo forming angioblasts into a primitive vascular plexus, which then undergoes a complex remodeling process. Angiogenesis is also important for disease progression in the adult. However, the precise molecular mechanism of vascular development remains unclear.

Publication Title

Genome-wide identification of endothelial cell-enriched genes in the mouse embryo.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7501
Genes in nonpermissive temperature-induced cell growth arrest and differentiation of astrocyte RCG-12 cells
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in astrocyte RCG-12 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Astrocyte RCG-12 cells used in this study were derived from primary cultured rat cortical glia cells infecting with a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation. Of the 15,923 probe sets analyzed, nonpermissive temperature differentially expressed 556 probe sets by >2.0-fold.

Publication Title

Identification of genetic networks involved in the cell growth arrest and differentiation of a rat astrocyte cell line RCG-12.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE8444
Genes in nonpermissive temperature-induced cell growth arrest and differentiation of tracheal epithelial RTEC11 cells
  • organism-icon Rattus norvegicus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Expression 230A Array (rae230a)

Description

We performed global scale microarray analysis to identify detailed mechanisms by which nonpermissive temperature induces cell growth arrest and differentiation in tracheal epithelial RTEC11 cells harboring temperature-sensitive simian virus 40 large T-antigen by using an Affymetrix GeneChip system. Tracheal epithelial RTEC11 cells used in this study were derived from transgenic rats harboring a temperature-sensitive simian virus 40 large T-antigen. Although the cells grew continuously at the permissive temperature, the nonpermissive temperature led to cell growth arrest and differentiation.

Publication Title

Establishment and functional characterization of a tracheal epithelial cell line RTEC11 from transgenic rats harboring temperature-sensitive simian virus 40 large T-antigen.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE21306
Expression data from RECK-overexpressing HT1080 fibrosarcoma cells
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

RECK, a glycosylphosphatidylinositol-anchored glycoprotein, inhibits the enzymatic activities of some matrix metalloproteinases (MMP), thereby suppressing tumor cell metastasis; however, the detailed mechanism is still obscure. In this study, we compared the gene expression profiles between mock- and RECK-transfected HT1080 cells.

Publication Title

RECK negatively regulates matrix metalloproteinase-9 transcription.

Sample Metadata Fields

Cell line

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accession-icon GSE67272
Nitric oxide signaling and its role in oxidative stress response in Schizosaccharomyces pombe
  • organism-icon Schizosaccharomyces pombe
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Yeast Genome 2.0 Array (yeast2)

Description

In examining NO signaling in the fission yeast Schizosaccharomyces pombe, we found that the putative NO dioxygenase SPAC869.02c (named Yhb1) and the S-nitrosoglutathione reductase Fmd2 cooperatively reduced intracellular NO levels as NO-detoxification enzymes. Although both protein levels were increased with exogenous NO, their expression patterns were different during growth phases. While expression of Yhb1 in the log phase was abrogated by treatment with an NO synthase inhibitor, induction of Fmd2 in the stationary phase was correlated with elevated mitochondrial respiratory chain (MRC) activity and reactive oxygen species (ROS) generation. Moreover, NO was localized in the mitochondria specifically in the stationary phase, suggesting that there are at least two distinctive types of NO signaling in S. pombe cells. For mitochondrial NO signaling, pretreatment with an NO donor effectively rescued the cell viability by repressing generation of ROS under oxidative stress. DNA microarray analysis revealed that exogenous NO contributes to tolerance to hydrogen peroxide (H2O2) stress by (i) inhibition of Fe3+ to Fe2+conversion, (ii) upregulation of the H2O2-detoxifying enzymes, and (iii) downregulation of the MRC genes. Therefore, NO is suggested to play a pivotal role in the negative feedback system to regulate ROS levels under oxidative stress in S. pombe cells.

Publication Title

Nitric oxide signaling and its role in oxidative stress response in Schizosaccharomyces pombe.

Sample Metadata Fields

Treatment

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accession-icon GSE23343
Expression data from human liver with or without type 2 diabetes
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The liver may regulate glucose homeostasis by modulating the sensitivity/resistance of peripheral tissues to insulin, by way of the production of secreted proteins, termed hepatokines.

Publication Title

A liver-derived secretory protein, selenoprotein P, causes insulin resistance.

Sample Metadata Fields

Sex, Specimen part, Disease

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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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