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accession-icon GSE42253
Gene expression data from T cells and NK cells with and without treatment with Hsp90 inhibitor (Geldanamycin)
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Hsp90 is critical for regulation of the phenotype and functional activity of human T lymphocytes and natural killer (NK) cells.

Publication Title

Heat shock protein 90 is critical for regulation of phenotype and functional activity of human T lymphocytes and NK cells.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE65476
B-catenin deficiency, but not c-Myc deletion, suppresses the immediate phenotypes of Apc loss in the liver
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dysregulated Wnt signalling is seen in approximately 30% of hepatocellular cancers, thus finding pathways downstream of activation of Wnt signalling is key. Using cre lox technology we have deleted the the adenomatous polyposis coli tumour suppressor protein (Apc) within the adult mouse liver and observed a rapid increase in nuclear beta-catenin and C-Myc. This is associated with an induction of proliferation leading to hepatomegally within 4 days of gene deletion. To investigate the downstream pathways responsible for these phenotypes we analysed the impact of inactivating Apc in the context of deficiency of the potentially key effectors beta-catenin and c-Myc. beta-catenin loss rescues both the proliferation and hepatomegally phenotypes following Apc loss. However c-Myc deletion, which rescues the phenotypes of Apc loss in the intestine, had no effect on the phenotypes of Apc loss. The consequences of deregulation the Wnt pathway within the liver are therefore strikingly different to those observed within the intestine, with the vast majority of Wnt targets beta-catenin dependent but c-Myc independent in the liver.

Publication Title

B-catenin deficiency, but not Myc deletion, suppresses the immediate phenotypes of APC loss in the liver.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE90607
Fibrostenotic phenotype of fibroblasts in Crohn's disease is dependent on tissue stiffness and reversed by LOX inhibition
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The results of this study indicate that stenotic fibroblasts exhibit an aberrant response to tissue stiffness with reduced MMP activity, leading to a perpetuous vicious circle of ever more fibrosis formation. Altering the microenvironment by LOX inhibition increases MMP activity and decreases ECM contraction, resulting in a potential anti-fibrotic agent for Crohns disease.

Publication Title

Fibrostenotic Phenotype of Myofibroblasts in Crohn's Disease is Dependent on Tissue Stiffness and Reversed by LOX Inhibition.

Sample Metadata Fields

Sex, Specimen part, Disease, Subject

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accession-icon GSE16728
Characterization of whole blood gene expression profiles in sickle-cell disease patients using globin mRNA reduction
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Room temperature whole blood mRNA stabilization procedures, such as the PAX gene system, are critical for the application of transcriptional analysis to population-based clinical studies. Global transcriptome analysis of whole blood RNA using microarrays has proven to be challenging due to the high abundance of globin transcripts that constitute 70% of whole blood mRNA in the blood. This is a particular problem in patients with sickle-cell disease, secondary to the high abundance of globin-expressing nucleated red blood cells and reticulocytes in the circulation . In order to more accurately measure the steady state whole blood transcriptome in sickle-cell patients, we evaluated the efficacy of reducing globin transcripts in PAXgene stabilized RNA samples for genome-wide transcriptome analyses using oligonucleotide arrays. We demonstrate here by both microarrays and Q-PCR that the globin mRNA depletion method resulted in 55-65 fold reduction in globin transcripts in whole blood collected from healthy volunteers and sickle-cell disease patients. This led to an improvement in microarray data quality with increased detection rate of expressed genes and improved overlap with the expression signatures of isolated peripheral blood mononuclear (PBMC) preparations. The differentially modulated genes from the globin depleted samples had a higher correlation coefficient to the 112 genes identified to be significantly altered in our previous study on sickle-cell disease using PBMC preparations. Additionally, the analysis of differences between the whole blood transcriptome and PBMC transcriptome reveals important erythrocyte genes that participate in sickle-cell pathogenesis and compensation. The combination of globin mRNA reduction after whole-blood RNA stabilization represents a robust clinical research methodology for the discovery of biomarkers for hematologic diseases and in multicenter clinical trials investigating a wide range of nonhematologic disorders where fractionation of cell types is impracticable.

Publication Title

Characterization of whole blood gene expression profiles as a sequel to globin mRNA reduction in patients with sickle cell disease.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE28466
Induction of ER stress in the colon cancer cell line LS174 with SubAB
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

To assess the effect of activation of the unfolded protein response (UPR) in colon cancer cell lines, we treated cells with the AB5 subtilase cytotoxin (SubAB). This proteolytically cleaves the 78-kDa glucose-regulated protein (GRP78; also known as HSPA5 or BiP) inside the endoplasmic reticulum. We find that the WNT signaling pathway is highly affected upon treatment with SubAB.

Publication Title

ER stress causes rapid loss of intestinal epithelial stemness through activation of the unfolded protein response.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE103172
Indian Hedgehog suppresses a stromal cell driven intestinal immune response
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Indian Hedgehog Suppresses a Stromal Cell-Driven Intestinal Immune Response.

Sample Metadata Fields

Specimen part, Time

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accession-icon SRP155526
Reprogram-Seq: A platform for single-cell combinatorial reprogramming [I]
  • organism-icon Mus musculus
  • sample-icon 49 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.

Publication Title

Rational Reprogramming of Cellular States by Combinatorial Perturbation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP155525
Reprogram-Seq: A platform for single-cell combinatorial reprogramming [II]
  • organism-icon Mus musculus
  • sample-icon 36 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq.

Publication Title

Rational Reprogramming of Cellular States by Combinatorial Perturbation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon SRP155523
Reprogram-Seq: A platform for single-cell combinatorial reprogramming [III]
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Reprogram-Seq leverages organ-specific cell atlas data with single-cell perturbation and computational analysis to predict, evaluate, and optimize TF combinations that reprogram a cell type of interest. Overall design: Focusing on the cardiac system, we performed Reprogram-Seq on P0 mouse heart cells to generate a reference transcriptomic map. Based on the reference map, we selected TF candidates and tests 1000s of TF cocktails for direct lineage conversion by scRNA-Seq. This series includes uninfected, non-transformed MEFs.

Publication Title

Rational Reprogramming of Cellular States by Combinatorial Perturbation.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE16755
Gene expression in macrophages treated with IFNalpha
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To study effects of IFNalpha treatment on monocyte-derived macrophages which may influence susceptibility or resistance to HIV.

Publication Title

Interleukin-27 inhibition of HIV-1 involves an intermediate induction of type I interferon.

Sample Metadata Fields

Specimen part

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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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