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accession-icon GSE76943
RANBP6 silencing in HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Expression data from HEK293 cells expressing a doxcycline-inducible RANBP6 shRNA

Publication Title

EGFR feedback-inhibition by Ran-binding protein 6 is disrupted in cancer.

Sample Metadata Fields

Treatment

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accession-icon GSE45200
An Inhibitor of Mutant IDH1 Delays Growth and Promotes Differentiation of Glioma Cells
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An inhibitor of mutant IDH1 delays growth and promotes differentiation of glioma cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE45197
An Inhibitor of Mutant IDH1 Delays Growth and Promotes Differentiation of Glioma Cells Expression data for Xenograft Samples
  • organism-icon Homo sapiens
  • sample-icon 33 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The recent discovery of mutations in metabolic enzymes has rekindled interest in harnessing the altered metabolism of cancer cells for cancer therapy. One potential drug target is isocitrate dehydrogenase 1 (IDH1) which is mutated in multiple human cancers. Here, we examine the role of mutant IDH1 in fully transformed cells with endogenous IDH1 mutations. A selective R132H-IDH1 inhibitor (AGI-5198) identified through a high-throughput screen dose-dependently blocked the ability of the mutant enzyme (mIDH1) to produce R-2-hydroxyglutarate (R-2HG). Under conditions of near complete R-2HG inhibition, the mIDH1 inhibitor induced demethylation of histone H3K9M3 and expression of genes associated with gliogenic differentiation. Blockade of mIDH1 impaired the growth of IDH1-mutant - but not IDH1-wildtype glioma cells without appreciable changes in genome wide DNA methylation. These data suggest that mIDH1 may promote glioma growth through mechanisms beyond its well-characterized epigenetic effects.

Publication Title

An inhibitor of mutant IDH1 delays growth and promotes differentiation of glioma cells.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP074138
Human islets contain four distinct subtypes of ß cells
  • organism-icon Homo sapiens
  • sample-icon 31 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000, Illumina HiSeq 2500

Description

The transcriptomes of four subpopulations of beta cells isolated by FACS from five healthy human donors. Populations were defined using cell surface-labeling antibodies, avoiding the need for fixation. Overall design: There are 5 biological replicates of 4 different cell types. Each donor yielded all 4 subtypes.

Publication Title

Human islets contain four distinct subtypes of β cells.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE67351
Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE39186
Effect of TET1 and TET3 overexpression on the transcriptome of HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compared TET1 and TET3 overexpressing cells to uninduced cells with endogenous levels of the respective transcript to determine global gene expression changes.

Publication Title

Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE67348
Effect of the simultaneous knockdown of TET1, TET2 and TET3 on the transcriptome of HEK293 cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compared TET triple knockdown cells to control cells treated with non-targeting siRNAs to determine global gene expression changes.

Publication Title

Altering TET dioxygenase levels within physiological range affects DNA methylation dynamics of HEK293 cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE21039
Gene Expression Profiles from PBMC are Sensitive to Short Processing Delays
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In the analysis of peripheral blood gene expression, timely processing of samples is essential to ensure that measurements reflect in vivo biology, rather than ex vivo sample processing variables. The effect of processing delays on global gene expression patterns in peripheral blood mononuclear cells (PBMC) was assessed by isolating and stabilizing PBMC-derived RNA from three individuals either immediately after phlebotomy or following a 4 hour delay. RNA was labeled using NuGEN Ovation labeling and probed using the Affymetrix HG U133plus 2.0 GeneChip. Comparison of gene expression levels (p<0.05 and 2-fold expression change) identified 327 probe sets representing genes with increased expression and 46 indicating decreased expression after 4 hours. The trends in expression patterns associated with delayed processing were also apparent in an independent set of 276 arrays of RNA from human PBMC samples with varying processing times. These data indicate that the time between sample acquisition, initiation of processing, and when the RNA is stabilized should be a prime consideration when designing protocols for translational studies involving PBMC gene expression analysis.

Publication Title

Gene Expression Profiles from Peripheral Blood Mononuclear Cells Are Sensitive to Short Processing Delays.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon GSE20307
Biological Similarities Exist between Oligoarticular and Polyarticular Subtypes of JIA Based on Age at Onset
  • organism-icon Homo sapiens
  • sample-icon 149 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Objective. To identify gene expression differences in peripheral blood from patients with early and late onset juvenile idiopathic arthritis (JIA).

Publication Title

Biologic similarities based on age at onset in oligoarticular and polyarticular subtypes of juvenile idiopathic arthritis.

Sample Metadata Fields

Sex, Specimen part, Race

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accession-icon SRP168642
Neutrophil gene expression in systemic juvenile idiopathic arthritis
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIon Torrent S5

Description

Systemic juvenile idiopathic arthritis (SJIA) is a chronic childhood arthropathy with features of autoinflammation. Early inflammatory SJIA is associated with expansion and activation of neutrophils with a sepsis-like phenotype, but neutrophil phenotypes present in longstanding and clinically inactive disease (CID) are unknown. The objective of this study was to examine activated neutrophil subsets, S100 alarmin release, and gene expression signatures in children with a spectrum of SJIA disease activity. Methods: Highly-purified neutrophils were isolated using a two-step procedure of density-gradient centrifugation followed by magnetic-bead based negative selection prior to flow cytometry or cell culture to quantify S100 protein release. Whole transcriptome gene expression profiles were compared in neutrophils from children with both active SJIA and CID. Results: Patients with SJIA and active systemic features demonstrated a higher number of CD16+CD62Llo neutrophil population compared to controls. This neutrophil subset was not seen in patients with CID or patients with active arthritis not exhibiting systemic features. Using imaging flow cytometry, CD16+CD62Llo neutrophils from patients with active SJIA and features of macrophage activation syndrome (MAS) had increased nuclear hypersegmentation compared to CD16+CD62L+ neutrophils. Serum levels of S100A8/A9 and S100A12 were strongly correlated with peripheral blood neutrophil counts. Neutrophils from active SJIA patients did not show enhanced resting S100 protein release; however, regardless of disease activity, neutrophils from SJIA patients did show enhanced S100A8/A9 release upon PMA stimulation compared to control neutrophils. Furthermore, whole transcriptome analysis of highly purified neutrophils from children with active SJIA identified 214 differentially expressed genes compared to neutrophils from healthy controls. The most significantly upregulated gene pathway was Immune System Process, including AIM2, IL18RAP, and NLRC4. Interestingly, this gene set showed intermediate levels of expression in neutrophils from patients with long-standing CID yet persistent serum IL-18 elevation. Indeed, all patient samples regardless of disease activity demonstrated elevated inflammatory gene expression, including inflammasome components and S100A8. Conclusion: We identify features of neutrophil activation in SJIA patients with active disease and CID, including a proinflammatory gene expression signature, reflecting persistent innate immune activation. Taken together, these studies expand understanding of neutrophil function in chronic autoinflammatory disorders such as SJIA. Overall design: Highly purified neutrophils isolated from patients with SJIA and healthy controls

Publication Title

Neutrophils From Children With Systemic Juvenile Idiopathic Arthritis Exhibit Persistent Proinflammatory Activation Despite Long-Standing Clinically Inactive Disease.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject

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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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