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accession-icon GSE62868
Expression of cytokine-sensitive genes in islets from diabetes-prone mice
  • organism-icon Mus musculus
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Genome-wide association studies in human type 2 diabetes (T2D) have renewed interest in the pancreatic islet as a major site of T2D risk. In this study, microarray data collected from mouse islets were used to identify genes that are regulated by cytokines at levels consistent with the chronic low-grade inflammation observed in T2D. The most cytokine-sensitive genes were then examined for association of single nucleotide polymorphisms (SNPs) with acute insulin response to glucose (AIRg) measured in the Genetics UndeRlying DIAbetes in HispaNics (GUARDIAN) study. In GUARDIAN, there was evidence of association of AIRg with SNPs in ARAP3 (5q31.3), F13A1 (6p25.3), KLHL6 (3q27.1), NID1 (1q42.3), PAMR1 (11p13), RIPK2 (8q21.3), and STEAP4 (7q21.12). These data support the mouse islet microarray data in detection of seven novel genes with potential importance to islet dysfunction in T2D. To further assess each gene, murine islets were exposed for 48-hrs to the following stressors representing models of beta-cell failure: 20nM rotenone (oxidative stress), 100nM thapsigargin (ER stress), 10pg/ml IL-1B + 20pg/ml IL-6 (cytokines/low-grade inflammation), 28mM glucose (hyperglycemia), or 50uM palmitate + 100uM oleate + 50uM linoleate (lipotoxicity). RT-PCR revealed that F13a1 was downregulated 3.3-fold by cytokines (P<0.05) and 2.6-fold by rotenone (P<0.05), Klhl6 was upregulated 4.3-fold by thapsigargin (P<0.01), Ripk2 was mildly (1.5-3-fold) but significantly upregulated by all stressors (P<0.05), and STEAP4 was profoundly cytokine-sensitive (167-fold upregulation, P<0.01). These findings reveal promising leads in elucidating islet dysfunction during the development of T2D.

Publication Title

An Islet-Targeted Genome-Wide Association Scan Identifies Novel Genes Implicated in Cytokine-Mediated Islet Stress in Type 2 Diabetes.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE15822
High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice
  • organism-icon Mus musculus
  • sample-icon 96 Downloadable Samples
  • Technology Badge IconIllumina mouse-6 v1.1 expression beadchip

Description

Analysis of tissues of DBA/2 mice fed a standard breeding diet (SBD) and high fat diet (HFD) revealed tissue specific roles in inflammation and disease, and altered communication between tissues. The tissues surveyed incuded adipose tissues (brown, inguinal, mesenteric, retro-peritoneal, subcutaneious and gonadal), muscle and liver.

Publication Title

High-fat diet leads to tissue-specific changes reflecting risk factors for diseases in DBA/2J mice.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE44037
Expression data from airway epithelial cells from patients with asthma, rhinitis, and helathy controls
  • organism-icon Homo sapiens
  • sample-icon 34 Downloadable Samples
  • Technology Badge Icon Affymetrix HT HG-U133+ PM Array Plate (hthgu133pluspm)

Description

The link between upper and lower airways in patients with both asthma and allergic rhinitis is still poorly understood. As the biological complexity of these disorders can be captured by gene expression profiling we hypothesized that the clinical expression of rhinitis and/or asthma is related to differential gene expression between upper and lower airways epithelium.

Publication Title

The impact of allergic rhinitis and asthma on human nasal and bronchial epithelial gene expression.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE51021
DKK1 expression is down-regulated in the lymph node pre-metastatic niche in esophageal cancer
  • organism-icon Homo sapiens
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Lymph node metastasis is a poor prognosis indicator in esophageal cancer. Although tumor spreading currently forms the main basis for therapy selection, the molecular mechanisms underlying the metastatic pathway remain insufficiently understood. Several studies aimed to investigate these mechanisms but focused mainly on regulatory patterns in the tumors themselves and/or the invaded lymph nodes. To date no study has yet investigated the potential changes on transcription level, which take place within the yet non-invaded niche. Here we provide a comprehensive description of these regulations in patients. In this study the transcriptomic profiles of regional lymph nodes were determined for two patient groups: patients classified as pN1 (metastasis) or pN0 (no metastasis) respectively. All investigated lymph nodes, also those from pN1 patients, were still free of metastasis. The gene expression data was obtained via microarray analysis. Top candidates were validated via PCR and immunohistochemistry. The results show that regional lymph nodes of pN1 patients differ decisively from those of pN0 patients even before metastasis has taken place. In the pN0 group distinct immune response patterns were observed. In contrast, lymph nodes of the pN1 group exhibited a clear profile of reduced immune response and reduced proliferation, but increased apoptosis, enhanced hypoplasia and morphological conversion processes. DKK1 was the most significant gene associated with the molecular mechanisms taking place in lymph nodes of patients suffering from metastasis (pN1). We assume that the two molecular profiles observed constitute two different stages of a progressive disease. Finally we suggest that DKK1 might play an important role within the mechanisms leading to lymph node metastasis.

Publication Title

Molecular changes in pre-metastatic lymph nodes of esophageal cancer patients.

Sample Metadata Fields

Specimen part, Subject

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accession-icon GSE47900
Differential gene expression analysis in motor and sensory cortex as a result of experimental autoimmune encephalomyelitis (EAE), a neuroinflammatory model for Multiple sclerosis.
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

We performed micrarrays to investigate neuronal gene expression changes during acute inflammatory CNS axon injury using the murine myelin oligodendrocyte glycoprotein 35-55 (MOG35-55)-induced experimental autoimmune encephalomyelitis (EAE) model. The present study was assigned to assess the direct and indirect endogenous neuronal response to spinal axonal injury in the motor and sensory cortex.

Publication Title

Axonally derived matrilin-2 induces proinflammatory responses that exacerbate autoimmune neuroinflammation.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE31212
Mammary carcinomas in WAP-SV40 transgenic mice
  • organism-icon Mus musculus
  • sample-icon 34 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

Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.

Sample Metadata Fields

Specimen part, Disease stage, Time

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accession-icon GSE29117
Mammary carcinomas in WAP-SV40 transgenic mice [gene expression]
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis.

Publication Title

Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.

Sample Metadata Fields

Specimen part, Disease stage

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accession-icon GSE33038
Involuted normal mammary gland in WAP-SV40 transgenic mice [gene expression]
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Transgenic expression in mice of two synergistically acting SV40 early region encoded proteins, large (LT) and small (sT) tumor antigens, in the mammary epithelium recapitulates loss of p53 and Rb function and deregulation of PP2A-controlled mitogenic pathways in human breast cancer. In primiparous mice, WAP-promoter driven expression of SV40 proteins induces well and poorly differentiated mammary adenocarcinomas. We performed a correlative aCGH and gene expression analysis of 25 monofocal tumors, representing four histopathological grades, to explore the molecular traits of SV40-induced mammary tumors and to emphasize the relevance of this tumor model for human breast tumorigenesis.

Publication Title

Low-grade and high-grade mammary carcinomas in WAP-T transgenic mice are independent entities distinguished by Met expression.

Sample Metadata Fields

Specimen part, Time

View Samples
accession-icon SRP189743
scRNA sequencing of 2 leukemia patients in remission after T cell therapy
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

peripheral blood samples of two leukemia patients in remission were profiled by single cell RNA sequencing approximately 1 year after receiving WT1 specific transgenic T cell therapy, at a time when patients were in clinical remission Overall design: single cell RNA sequencing of peripheral blood mononuclear cells

Publication Title

T cell receptor gene therapy targeting WT1 prevents acute myeloid leukemia relapse post-transplant.

Sample Metadata Fields

Specimen part, Disease, Subject

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accession-icon SRP075541
Unique Transcriptional Programs Identify Subtypes of AKI
  • organism-icon Mus musculus
  • sample-icon 53 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Two metrics, a rise in serum creatinine concentration and a decrease in urine output, are considered tantamount to the injury of the kidney tubule and the epithelial cells thereof (AKI).Yet neither criterion emphasizes the etiology or the pathogenetic heterogeneity of acute decreases in kidney excretory function. In fact, whether decreased excretory function due to contraction of the extracellular fluid volume (vAKI) or due to intrinsic kidney injury (iAKI) actually share pathogenesis and should be aggregated in the same diagnostic group remains an open question. To examine this possibility, we created mouse models of iAKI and vAKI that induced a similar increase in serum creatinine concentration. Using laser microdissection to isolate specific domains of the kidney, followed by RNA sequencing, we found that thousands of genes responded specifically to iAKI or to vAKI, but very few responded to both stimuli. In fact, the activated gene sets comprised different, functionally unrelated signal transduction pathways and were expressed in different regions of the kidney. Moreover, we identified distinctive gene expression patterns in human urine as potential biomarkers of either iAKI or vAKI, but not both. Hence, iAKI and vAKI are biologically unrelated, suggesting that molecular analysis should clarify our current definitions of acute changes in kidney excretory function. Overall design: Examining transcriptional profiles of two models of "acute kidney injury" (iAKI and pAKI), compared to controls, in different microanatomic regions of the kidney using laser capture microdissection

Publication Title

Unique Transcriptional Programs Identify Subtypes of AKI.

Sample Metadata Fields

Subject

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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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