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accession-icon GSE54890
Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Early B cell factor 1 regulates adipocyte morphology and lipolysis in white adipose tissue.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE42680
Early B-cell Factor 1 Regulates Adipocyte Morphology and Lipolysis in White Adipose Tissue [expression profiling]
  • organism-icon Homo sapiens
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st), Illumina HiSeq 2000

Description

To investgate the role of EBF1 in human adipocyte, we performed global expression profiling in human adipocytes transfected with siRNA targeting EBF1.

Publication Title

Early B cell factor 1 regulates adipocyte morphology and lipolysis in white adipose tissue.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE25402
Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity
  • organism-icon Homo sapiens
  • sample-icon 119 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

Adipose tissue microRNAs as regulators of CCL2 production in human obesity.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

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accession-icon GSE25401
Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity [gene expression]
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity.

Publication Title

Adipose tissue microRNAs as regulators of CCL2 production in human obesity.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE25910
Adipose Tissue MicroRNAs as Regulators of CCL2 Production in Human Obesity (differentiation data)
  • organism-icon Homo sapiens
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We used an unbiased systems biology approach to study the regulation of gene expression in human adipose tissue focusing on inflammation. We show that microRNAs play a major role as regulators of CCL2 production in obesity.

Publication Title

Adipose tissue microRNAs as regulators of CCL2 production in human obesity.

Sample Metadata Fields

Sex, Age, Specimen part, Subject

View Samples
accession-icon GSE94753
Global transcriptome profiling identifies KLF15 and SLC25A10 as regulators of adipocytes insulin sensitivity in obese women
  • organism-icon Homo sapiens
  • sample-icon 70 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st), Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Global transcriptome profiling identifies KLF15 and SLC25A10 as modifiers of adipocytes insulin sensitivity in obese women.

Sample Metadata Fields

Sex, Specimen part, Disease

View Samples
accession-icon GSE94752
Global transcriptome profiling identifies KLF15 and SLC25A10 as regulators of adipocytes insulin sensitivity in obese women [WAT]
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

The aim of this study was to identify new genes controlling insulin sensitivity in adipocytes from obese women with either insulin-resistant (OIR) or -sensitive (OIS) adipocytes.

Publication Title

Global transcriptome profiling identifies KLF15 and SLC25A10 as modifiers of adipocytes insulin sensitivity in obese women.

Sample Metadata Fields

Sex, Specimen part, Disease

View Samples
accession-icon GSE94751
Global transcriptome profiling identifies KLF15 and SLC25A10 as regulators of adipocytes insulin sensitivity in obese women [siRNA]
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st), Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

The aim of this study was to identify new genes controlling insulin sensitivity in adipocytes from obese women with either insulin-resistant (OIR) or -sensitive (OIS) adipocytes.

Publication Title

Global transcriptome profiling identifies KLF15 and SLC25A10 as modifiers of adipocytes insulin sensitivity in obese women.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE36683
Gene Regulation by Estrogen Signaling and DNA Methylation in MCF7 Breast Cancer Cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

Estrogen signaling and epigenetic modifications, in particular DNA methylation, are involved in regulation of gene expression in breast cancers. Here we investigated a potential regulatory cross-talk between these two pathways by identifying their common target genes and exploring potential underlying molecular mechanisms in human MCF7 breast cancer cells. Principal Findings: Gene expression profiling revealed that the expression of approximately 150 genes was influenced by both 17-estradiol (E2) and a hypomethylating agent 5-aza-2-deoxycytidine (DAC). Based on gene ontology (GO), CpG island prediction analysis and previously reported estrogen receptor (ER) binding regions, we selected six genes for further analysis (BTG3, FHL2, PMAIP1, BTG2, CDKN1A and TGFB2). GO analysis suggests that these genes are involved in intracellular signaling cascades, regulation of cell proliferation and apoptosis, while CpG island prediction of promoter regions reveals that the promoters of these genes contain at least one CpG island. Using chromatin immunoprecipitation, we show that ER is recruited to CpG islands in promoters, but neither in an E2- nor in a DAC-dependent fashion. DAC treatment reactivates the expression of all selected genes although only the promoters of BTG3 and FHL2 genes are methylated, with E2 treatment showing no effect on the methylation status of these promoters. Conclusions: We identified a set of genes regulated by both estrogen signaling and DNA methylation. However, our data does not support a direct molecular interplay of mediators of estrogen and epigenetic signaling at promoters of regulated genes.

Publication Title

Global identification of genes regulated by estrogen signaling and demethylation in MCF-7 breast cancer cells.

Sample Metadata Fields

Cell line

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accession-icon GSE65495
Induction of USP17 by combining BET and HDAC inhibitors in breast cancer cells.
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

Members of bromodomain and extra-C terminal (BET) domain family and the histone deacetylase (HDAC) enzyme family efficiently regulate the expression of important oncogenes and tumor suppressors. HDACs induce histone hypoacetylation meanwhile BET proteins bind to acetylated lysines on histones to regulate gene transcription. Here we show that the BET inhibitor JQ1 inhibited proliferation and induced apoptosis of both triple negative and estrogen receptor positive breast cancer cells. Consistent with the critical role of histone acetylation in the regulation of gene expression, microarray analysis revealed broad transcriptional changes after JQ1 or HDAC inhibitor treatment. By examining the molecular pathways affected by the epigenetic inhibitors we found that both BET and HDAC inhibitors are suppressing similar genes that were involved in cell cycle regulation. Combining JQ1 with HDAC inhibitors, we found that the combination significantly decreased cell viability. This effect was partly mediated by the more efficient suppression of genes essential for cell-cycle progression. Furthermore, we detected a dramatic increase in the expression of several members of the USP17 family of deubiquitinating enzymes in response to the single agent treatment, which further increased by the combination treatment. Since constitutive expression of USP17 has been reported to block the Ras/MAPK pathway, our data also suggest that the blockade of the Ras/MAPK pathway might also be involved in the synergistic effect of the combination treatment. In conclusion, this study suggests that co-treatment with BET inhibitors and HDAC inhibitors could be an effective treatment regime in future breast cancer therapy.

Publication Title

Induction of USP17 by combining BET and HDAC inhibitors in breast cancer cells.

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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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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