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accession-icon GSE15320
Microarray analysis of therapeutic (GM4) and non therapeutic (GM) NOD DC
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)

Description

We have previously demonstrated that bone marrow-derived DC can prevent diabetes development and halt progression of insulitis in NOD mice, the mouse model of type 1 diabetes (T1D). The DC population that was most effective in this therapy had a mature phenotype, expressed high levels of costimulatory molecules and secreted low levels of IL-12p70. The protective DC therapy induced regulatory Th2 cells that shifted the dominant Th1 environment, present in NOD mice, to a mixed Th1/Th2 milieu. Microarray analysis of therapeutic and non-therapeutic DC populations revealed several novel molecules that could play important roles in the observed DC-mediated therapy. The therapeutic DC population expressed a unique pattern of costimulatory molecules and chemokines, which were confirmed by flow cytometry and ELISA assays. We have performed in vitro chemotaxis assays that demonstrated the therapeutic DC preferentially attracted Th2 cells, as compared to Th1, Treg or nave T cells. In addition we quantified the in vivo migration of activated islet-specific T cells to the pancreas using novel cell labeling techniques and 19F nuclear magnetic resonance. A subcutaenous injection of therapeutic DC alters the migration of both Th1 and Th2 cells to the pancreas, and Th1 cells appeared in the lymph node draining the site of DC injection. These results suggest that the therapeutic function of DC is mediated in part by the chemoattractive properties of these DC for diabetogenic Th1 cells.

Publication Title

Gene expression analysis of dendritic cells that prevent diabetes in NOD mice: analysis of chemokines and costimulatory molecules.

Sample Metadata Fields

Sex

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accession-icon GSE42133
Disrupted functional neworks in autism underlie early brain maldevelopment and provide accurate classification
  • organism-icon Homo sapiens
  • sample-icon 147 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

The disrupted genetic mechanisms underlying neural abnormalities in Autism Spectrum Disorder remain mostly unknown and speculative. No biological marker nor genetic signature is currently available to assist with early diagnosis.

Publication Title

Prediction of autism by translation and immune/inflammation coexpressed genes in toddlers from pediatric community practices.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE10658
IL-9/mast cell-mediated intestinal permeability predispose to oral antigen hypersensitivity
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Small intestine of a pool of three Wt mice and a pool of 3 IL-9tg mice in a balb/c backround.

Publication Title

IL-9- and mast cell-mediated intestinal permeability predisposes to oral antigen hypersensitivity.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP092911
The molecular basis of CD4 T-cell help for the cytotoxic T-cell response
  • organism-icon Mus musculus
  • sample-icon 22 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500, Illumina HiSeq 2000

Description

CD4+ T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes, resulting from CD4+ T-cell help during priming, as apparent in effector CTLs. This gene expression signature reveals that CD4+ T-cell help optimizes CTLs in the expression of cytotoxic effector molecules, but also in many other functions that ensure optimal efficacy of CTLs throughout their life cycle. Overall design: Whole transcriptome analysis of effector CD8 T cells primed in the presence or absence of CD4 T cell help after vaccination or virus infection, or treated with agonistic CD27 or blocking CD70 antibody after vaccination.

Publication Title

CD4<sup>+</sup> T Cell Help Confers a Cytotoxic T Cell Effector Program Including Coinhibitory Receptor Downregulation and Increased Tissue Invasiveness.

Sample Metadata Fields

Specimen part, Cell line, Subject

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accession-icon SRP067567
Genome-wide responses to extracellular actin in Drosophila
  • organism-icon Drosophila melanogaster
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We report the transcriptional changes in Drosophila after administration of Actin or buffer control Overall design: Examination of transcriptional responses to actin versus buffer injected flies at 3,6 and 24 hours post injection (each time point includes triplicate samples)

Publication Title

Actin is an evolutionarily-conserved damage-associated molecular pattern that signals tissue injury in <i>Drosophila melanogaster</i>.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE10191
Human colon expression in healthy controls and UC
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Activation of inflammatory pathways in human IBD. Leukocyte recruitment pathways including those for eosiniphils are activated in the affected colon in IBD. However, the functional implications of this are not known. We hypothesized that pro-inflammatory eotaxin (CCL11) dependent networks would be up regulated in the colon of pediatric patients with Ulcerative Colitis (UC), and that these would regulate eosinophil recruitment to the gut. These experiments tested differential colon gene expression relative to these pathways in healthy and UC samples. Colon biopsy samples were obtained from UC patients at diagnosis, and healthy controls. The global pattern of gene expression was determined using GeneSpring software, and biological networks were identified using Ingenuity software. Data suggested that a leukocyte recruitment network which includeds CCL11 is up regulated in pediatric UC at diagnosis. The degree of up regulation of these genes compared to healthy controls was remarkably conserved within the UC patient group, suggesting common mechanisms of mucosal inflammation.

Publication Title

Intestinal macrophage/epithelial cell-derived CCL11/eotaxin-1 mediates eosinophil recruitment and function in pediatric ulcerative colitis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE61256
Obesity accelerates epigenetic aging of human liver
  • organism-icon Homo sapiens
  • sample-icon 133 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Obesity accelerates epigenetic aging of human liver.

Sample Metadata Fields

Sex, Age, Disease, Subject

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accession-icon GSE61260
Human liver gene expression data from subjects of varying ages
  • organism-icon Homo sapiens
  • sample-icon 133 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

N=134 human liver samples from morbidly obese patients and healthy controls were analysed by array-based mRNA expression profiling. Liver messenger RNA expression datasets from the German patients were generated on the HuGene 1.1 ST gene array The purpose of the study was to correlate these gene expression data with body mass index and with an epigenetic measure of age acceleration based on DNA methylation data.

Publication Title

Obesity accelerates epigenetic aging of human liver.

Sample Metadata Fields

Sex, Age, Disease, Subject

View Samples
accession-icon GSE18454
Analysis of normal lung cells treated with 5-aza-dC to induce DNA demethylation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Analysis of 2 cultured normal lung cell lines, Normal Human Bronchial Epithelial (NHBE) and Human Small Airway Epithelial (SAEC) cells (Lonza, Walkersville, MD), following treatment with 5-aza-dC to induce DNA demethylation. These results provide insight into the role of epigenetic alterations, specifically demethylation, in differential gene expression in various lung neoplasms.

Publication Title

Integrative discovery of epigenetically derepressed cancer testis antigens in NSCLC.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE48452
Human liver biopsy of different phases from control to NASH
  • organism-icon Homo sapiens
  • sample-icon 72 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disorder in industrialized countries. Liver samples from morbidly obese patients (N=45) with all stages of NAFLD and controls (N=18) were analysed by array-based DNA methylation and mRNA expression profiling. NAFLD-specific expression and methylation differences were seen for nine genes coding for key enzymes in intermediate metabolism (including PC, ACLY, PLCG1) and insulin/insulin-like signalling (including IGF1, IGFBP2, PRKCE) and replicated by bisulfite pyrosequening (independent N=39). Transcription factor binding sites at NAFLD-specific CpG sites were >1000-fold enriched for ZNF274, PGC1A and SREBP2. Intra-individual comparison of liver biopsies before and after bariatric surgery showed NAFLD-associated methylation changes to be partially reversible. Post-bariatric and NAFLD-specific methylation signatures were clearly distinct both in gene-ontology and transcription factor binding site analyses, with >400-fold enrichment of NRF1, HSF1 and ESRRA sites. Our findings provide one of the first examples of treatment-induced epigenetic organ remodelling in humans.

Publication Title

DNA methylation analysis in nonalcoholic fatty liver disease suggests distinct disease-specific and remodeling signatures after bariatric surgery.

Sample Metadata Fields

Sex, Age, Specimen part

View Samples

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)

fund-icon Fund the CCDL

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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