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accession-icon GSE86298
Effect of hyperglycemia on the transcriptional profile of primary human macrophages
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Hyperglycemia is an essential factor leading to micro- and macrovascular diabetic complications. Macrophages are key innate immune regulators of inflammation that undergo 2 major directions of functional polarization: classically (M1) and alternatively (M2) activated macrophages. The aim of the study was to examine the effect of hyperglycemia on transcriptional activation of M0, M1 and M2 human macrophages.

Publication Title

Hyperglycemia induces mixed M1/M2 cytokine profile in primary human monocyte-derived macrophages.

Sample Metadata Fields

Specimen part, Treatment, Subject

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accession-icon GSE79521
Expression data from RAW-264.7 cells transfected with empty vector and mouse FoxQ1 expression construct
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transcription factor FoxQ1 belongs to family of Fox transcription factors containing forkhead box (winged helix) domain. This family of proteins plays an important role in cell growth, proliferation, and differentiation. Expression of FoxQ1 was found in cancer cells and was associated with increased migration and invasion. Recently, elevated FoxQ1 expression was found in IL4 stimulated macrophages.

Publication Title

IL-4 driven transcription factor FoxQ1 is expressed by monocytes in atopic dermatitis and stimulates monocyte migration.

Sample Metadata Fields

Cell line

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accession-icon GSE1956
Mouse neuroblastoma Tcof1
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Genomewide analysis of gene expression associated with Tcof1 in mouse neuroblastoma. NB N1E-115 cells with wildtype, overexpression, knockdown of Tcof1.

Publication Title

Genomewide analysis of gene expression associated with Tcof1 in mouse neuroblastoma.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE55092
Viral Expression and Molecular Profiling in Liver Tissue versus Microdissected Hepatocytes in Hepatitis B Virus - Associated Hepatocellular Carcinoma
  • organism-icon Homo sapiens
  • sample-icon 135 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The molecular mechanisms whereby hepatitis B virus (HBV) induces hepatocellular carcinoma (HCC) remain elusive. We used genomic and molecular techniques to investigate host-virus interactions by mapping the entire liver of patients with HCC. We compared the gene signature of whole liver tissue (WLT) versus laser capture-microdissected (LCM) hepatocytes with intrahepatic expression of HBV. Gene expression profiling was performed on up to 17 WLT specimens obtained at various distances from the tumor center in individual livers of 11 patients with HCC and on selected LCM samples. HBV biomarkers were determined by real-time PCR and confocal immunofluorescence. Analysis of 5 areas of the liver showed a sharp change in gene expression between the immediate perilesional area and tumor periphery that correlated with a significant decrease in the intrahepatic expression of HBsAg. The tumor was characterized by a large preponderance of down-regulated genes, mostly involved in the metabolism of lipid and fatty acid, glucose, amino acids and drugs, with down-regulation of pathways involved in the activation of PXR/RXR and PPARa/RXRa nuclear receptors, comprising PGC1 and FOXO1, two key regulators of the hepatic metabolic functions and HBV transcription. These findings were confirmed by gene expression of microdissected hepatocytes. However, LCM of malignant hepatocytes also revealed up-regulation of unique genes associated with cancer and signaling pathways, including two novel HCC-associated cancer testis antigen (CTA) genes, NUF2 and TTK. HCC-associated with HBV is characterized by a metabolism switch-off and by a significant reduction in HBsAg. LCM proved to be a critical tool to validate gene signatures associated with HCC and to identify genes that may play a role in hepatocarcinogenesis opening new perspectives for the discovery of novel diagnostic markers and therapeutic targets.

Publication Title

Viral expression and molecular profiling in liver tissue versus microdissected hepatocytes in hepatitis B virus-associated hepatocellular carcinoma.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon GSE84008
Genome-wide analysis of ex vivo gene expression of tumour pericytes and tumour endothelial cells obtained from 67NR mouse primary tumors
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Pericytes are integral components of the tissue vasculature and have essential functions in tumour angiogenesis. Endosialin (CD248) is a type I transmembrane glycoprotein highly expressed on pericytes in the tumour vasculature of most solid tumours, however it is low or negligibly expressed on normal tissue pericytes. Experiments using wild-type and endosialin-knockout mice has revealed that stromal endosialin expression facilitates intravasation of tumor cells from the primary tumor into the circulation, thereby promoting metastatic dissemination.

Publication Title

Endosialin-Expressing Pericytes Promote Metastatic Dissemination.

Sample Metadata Fields

Sex, Specimen part, Disease

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accession-icon SRP065507
SynapTRAP on SNAP25 TRAP Cortex
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

SynapTRAP. Identification of Synaptic mRNA of neurons of the cortex. Technique combines sucrose percoll fractionation of a synaptically rich sample (SN) and TRAP tagged ribosome IP (PreIP and PostIP). This experiment uses pan neuronal SNAP25 mice and a cortical dissection. Overall design: Three replicates of four samples.

Publication Title

Transcriptomic Analysis of Ribosome-Bound mRNA in Cortical Neurites <i>In Vivo</i>.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE61927
CMV-Specific CD8+ Memory T Cells Re-Emerge After Viral Challenge And Recapitulate CMV Immunity Under Various Adoptive Transfer Conditions
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Reconstitution of cytomegalovirus (CMV)-specific immunity following transplant remains a primary clinical objective to prevent CMV disease, and adoptive immunotherapy of CMV-specific T cells can be an effective therapeutic approach. Due to the persistence of CMV, most CMV-specific CD8+ T cells become terminally differentiated effector cells (TEFF). However, a minor subset retains a memory phenotype (TM). Interestingly, recent studies suggest that CMV-specific CD8+ T cells with different phenotypes may have different abilities to reconstitute sustained immunity following transfer. The immunology of human CMV (HCMV) infections is reflected in the mouse model of MCMV infection. We found that HCMV- and MCMV-specific T cells displayed shared genetic programs, validating the MCMV model for studies of CMV-specific T cells in vivo. After transfer, the proliferative capacity of MCMV-specific TM cells was vastly superior to TEFF cells. Strikingly, TM cells expanded and established sustained and diverse T cell populations even after multiple challenges. Although both TEFF and TM cells could protect Rag-/- mice, only TM cells could consistently survive after transfer into immune replete, latently infected recipients and respond if recipient immunity was lost. These data show that CMV-specific TM cells retain memory function during persistent infection and can re-establish CMV immunity when necessary.

Publication Title

Memory T cells specific for murine cytomegalovirus re-emerge after multiple challenges and recapitulate immunity in various adoptive transfer scenarios.

Sample Metadata Fields

Specimen part

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accession-icon GSE40540
IP of 5-hydroxymethylcytosine (5-hmC) and 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers
  • organism-icon Mus musculus
  • sample-icon 49 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

Dynamic changes in 5-hydroxymethylation signatures underpin early and late events in drug exposed liver.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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accession-icon GSE45465
Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure [Replicated control vs. pb treated study]
  • organism-icon Mus musculus
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Dynamic changes in the mouse liver DNA methylome associated with short (1 day) and prolonged (7, 28 and 91 days) exposure to the rodent liver non-genotoxic carcinogen (NGC), phenobarbital (PB).

Publication Title

Dynamic changes in 5-hydroxymethylation signatures underpin early and late events in drug exposed liver.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE40773
Dynamic changes in liver 5-hydroxymethylcytosine profiles upon non-genotoxic carcinogen exposure
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

29-32 days old male mice where either treated with Phenobarbital or untreated

Publication Title

Dynamic changes in 5-hydroxymethylation signatures underpin early and late events in drug exposed liver.

Sample Metadata Fields

Sex, Specimen part, Treatment, Time

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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