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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

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accession-icon GSE7091
Microarray Analysis of Hepatic Genes Differentially Expressed in the Presence of the Maslinic Acid in Olive Oil
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Two olive oils only differing in the presence of maslinic acid were prepared. Using DNA microarrays, hepatic gene expression was analysed in apoE-deficient mice with a C57BL/6J genetic background

Publication Title

Apolipoprotein E determines the hepatic transcriptional profile of dietary maslinic acid in mice.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP144983
LPS Sensing Mounts an Adaptive MSC Response Enhancing Neutrophil Activation and Wound Healing
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We here addressed the question whether the unique capacity of mesenchymal stromal/stem cells (MSCs) to re-establish tissue homeostasis depends on their potential to sense pathogen associated molecular pattern (PAMP) and, in consequence, mount an adaptive response in the interest of tissue repair. After injection of MSCs which had been primed with the bacterial wall component LPS into murine wounds, an unexpected acceleration of healing occurred, clearly exceeding that of non-primed MSCs. This correlates with a fundamental reprogramming of the transcriptome in LPS treated MSCs as deduced from RNA-seq analysis and its validation. A network of genes mediating the adaptive response through the TLR-4 pathway responsible for neutrophil activation (GCP- 2, ENA-78, IL-1ß IL-8) and MSC protection (SOX6) profoundly contributes to enhanced wound healing. In fact, silencing of either TRL-4, or IRAK3, a downstream effector of TRL-4, or SOX6 suppressed wound healing most likely due to suppression of neutrophil extracellular trap formation and suppression of the enhanced microbicidal release of reactive oxygen species (ROS), key features of neutrophil activation. This previously unreported results uncover SOX6 which protects MSCs at the wound site from enhanced oxidative stress. This unprecedented findings hold substantial promise to refine current MSC-based therapies for difficult-to-treat wounds. Overall design: Transcriptome profiling of MSCs

Publication Title

TLR4-dependent shaping of the wound site by MSCs accelerates wound healing.

Sample Metadata Fields

Treatment, 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

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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

View Samples
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

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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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accession-icon SRP122893
Gene expression analyses of GI eosinophils under homeostatic conditions
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

RNA-seq was performed on eosinophils isolated from colons of naive C57/BL6 mice. Overall design: 2 samples of naive colonic eosinophils

Publication Title

Reuse of public, genome-wide, murine eosinophil expression data for hypotheses development.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP155519
Reprogram-Seq: A platform for single-cell combinatorial reprogramming [VI]
  • organism-icon Mus musculus
  • sample-icon 1 Downloadable Sample
  • 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
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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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