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accession-icon GSE53455
Expression profiling comparisons of human CD4+ T cells treated with RORgt inhibitors
  • organism-icon Homo sapiens
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells.

Publication Title

Pharmacologic inhibition of RORγt regulates Th17 signature gene expression and suppresses cutaneous inflammation in vivo.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE87164
Gene expression in MMTV-PyMT whole tumor, CD3+ lymphocytes or CD11b+ myeloid cells with and without Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE76659
Differential gene expression in either CD3+ lymphocytes or CD11b+ myeloid cells due to Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE87163
MMTV-PyMT whole tumor gene expression with and without Class IIa HDAC inhibitor treatment
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

Publication Title

Class IIa HDAC inhibition reduces breast tumours and metastases through anti-tumour macrophages.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE58911
Gene expression in normal and tumor samples from patients with HNSCC
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Tissue samples were collected from patients diagnosed with HNSCC (oropharynx, hypopharynx, larynx). Samples were taken from the tumor site (tumor samples) and from a site distant to the tumor (normal samples) prior to therapy.

Publication Title

Prognostic biomarkers for HNSCC using quantitative real-time PCR and microarray analysis: β-tubulin isotypes and the p53 interactome.

Sample Metadata Fields

Age, Specimen part, Subject

View Samples
accession-icon GSE68009
Regulatory T cells from colonic lamina propria [array]
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

The colonic lamina propria contains a distinct population of Foxp3+ T regulatory cells (Tregs) that modulate responses to commensal microbes. Analysis of gene expression revealed that the transcriptome of colonic Tregs is distinct from splenic and other tissue Tregs. Ror and Helios in colonic Tregs mark distinct populations: Ror+Helios- or Ror-Helios+ Tregs. We uncovered an unanticipated role for Ror, a transcription factor generally considered to be antagonistic to Foxp3. Ror in colonic Tregs accounts for a small but specific part of the colon-specific Treg signature.

Publication Title

MUCOSAL IMMUNOLOGY. Individual intestinal symbionts induce a distinct population of RORγ⁺ regulatory T cells.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE7493
Mutant SOD1 rats (lobsi-affy-rat-194438)
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Missense mutations in the gene for the ubiquitously expressed superoxide dismutase-1 (SOD1) are one of the causes of familial amyotrophic lateral sclerosis (ALS), the most common adult onset motor neuron disease in humans killing selectively large motor neurons. Mice and rats overexpressing mutant SOD1 develop an adult onset neurodegenerative disease with hindlimb-paralysis and subsequent death similar to the human condition. In order to analyze the effects of mutant SOD1 expression onto the most affected cell-type in ALS, a small subpopulation of spinal cord cells, we propose to use laser microdissection to isolate mouse lumbar motor neurons and to assess the changes onto the mRNA expression profile using Affymetrix GeneChips compared to control animals. While two studies applying a genomic approach on the ALS mouse models used the entire spinal cord, contributions of changes to motor neurons were masked by the inflammatory effects of mutant SOD1 and the much larger population of non-motor neuronal cells. What is therefore needed is a cell-type specific expression profile that could reveal dysregulations in the transcriptome of the affected motor neurons.

Publication Title

Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP040584
Chemical Inhibition of the ROR?t-dependent Transcriptional Network in Th17 cells [RNA-Seq 2]
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

ROR?t is a transcription factor required for T helper 17 (Th17) cell development. We identified three ROR?t-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized ROR?t binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and ROR?t-deficient cells. ROR?t is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced ROR?t from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. Overall design: Transcriptional profiling of Th17 cells under chemical perturbations of ROR?t, DMSO, and knockout of ROR?t. It includes repeats for all the data in GSE56018, plus one additional condition.

Publication Title

Small-molecule RORγt antagonists inhibit T helper 17 cell transcriptional network by divergent mechanisms.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP040294
Chemical Inhibition of the ROR?t-dependent Transcriptional Network in Th17 cells [RNA-Seq]
  • organism-icon Mus musculus
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer II

Description

ROR?t is a transcription factor required for T helper 17 (Th17) cell development. We identified three ROR?t-specific inhibitors that suppress Th17 cell responses including Th17 cell-mediated autoimmune disease. We systemically characterized ROR?t binding data in the presence and absence of drug with corresponding whole-transcriptome sequencing for wild-type and ROR?t-deficient cells. ROR?t is central in a densely interconnected regulatory network, acting both as a direct activator of genes important for Th17 cell differentiation and as a direct repressor of genes from other T-cell lineages. The three inhibitors identified here reversed both of these modes of action, but to varying extents and through distinct mechanisms. Whereas one inhibitor displaced ROR?t from its target-loci, the two more potent inhibitors affected transcription predominantly without removing DNA-binding. Our work illustrates the power of a system-scale analysis of transcriptional regulation to characterize potential therapeutic compounds that inhibit pathogenic Th17 cells and suppress autoimmunity. Overall design: Transcriptional profiling of Th17 cells under chemical perturbations of ROR?t, DMSO, and knockout of ROR?t

Publication Title

Small-molecule RORγt antagonists inhibit T helper 17 cell transcriptional network by divergent mechanisms.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP042228
Core Ileal Transcriptome in Pediatric Crohn Disease
  • organism-icon Homo sapiens
  • sample-icon 322 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

We report the global pattern of ileal gene expression in a cohort of 359 treatment-naïve pediatric Crohn Disease, Ulcerative Colitis patients and controls. We focus on genes with consistent altered expression in inflamed and unaffected ileum of CD [ileal-involved CD (iCD) and non-invloved ileal CD (cCD)], but not in the ileum of ulcerative colitis or control. Overall design: Ileal biopsies were obtained during diagnostic colonoscopies of children and adolescents aged less than 17 years, who presented with IBD-like symptoms. All patients underwent baseline colonoscopy and histological characterization; non-IBD controls were those with suspected IBD, but with no microscopic or macroscopic inflammation and normal radiographic, endoscopic, and histologic findings. Biopsies were stored at -80 degrees.

Publication Title

Defining the Celiac Disease Transcriptome using Clinical Pathology Specimens Reveals Biologic Pathways and Supports Diagnosis.

Sample Metadata Fields

No sample metadata fields

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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