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accession-icon GSE6743
1,25 (OH)2 vitamin D3 induces expression of CCR10 and other genes
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Human naive T cells from peripheral blood were cultured in 24 wells coated with anti-CD3 and anti-CD28 antibodies in the presence or absence of retinoid acid, IL-12, and 1,25 (OH)2 vitamin D3. The T cells were FACS-sorted based on expression of CD3, integrin alpha4beta7, cutaneous lymphocyte antigen (CLA) and chemokine receptor 10. This serie includes microarray data from stimulated T cells under indicated conditions.

Publication Title

DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE37196
Interference of PPAR gamma signaling in thoracic aorta
  • organism-icon Mus musculus
  • sample-icon 5 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

Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.

Sample Metadata Fields

Specimen part

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accession-icon GSE37194
Gene expression profiling during interference with PPAR gamma signaling in thoracic aorta
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Pharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in thoracic aorta from SP467L mice and their control littermates using the Affymetrix Mouse Genome 430 2.0 array.

Publication Title

Dominant negative PPARγ promotes atherosclerosis, vascular dysfunction, and hypertension through distinct effects in endothelium and vascular muscle.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP091503
Effect of PPAR Gamma Agonist Rosiglitazone on Carotid Artery Gene Expression after Knockout of Retinol Binding Protein 7 (RBP7)
  • organism-icon Mus musculus
  • sample-icon 28 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To examine the role of retinol binding protein 7 (RBP7) in PPAR gamma mediated regulation of target gene expression in the carotid artery, RNA-Seq was used to quantitate gene expression in carotid artery from both wild-type and RBP7 knockout mice after ligand-mediated activation of PPAR gamma with Rosiglitazone. Overall design: Carotid artery were removed from wild-type (WT) and RBP7 knockout (KO) mice and treated with either Rosliglitazone (ROSI, 10 uM) or vehicle DMSO (CONT) for 24 hrs.

Publication Title

Retinol-binding protein 7 is an endothelium-specific PPAR<b>γ</b> cofactor mediating an antioxidant response through adiponectin.

Sample Metadata Fields

Sex, Specimen part, Treatment, Subject

View Samples
accession-icon GSE11870
Gene expression changes in primary aortic endothelial cells during expression of dominant negative PPAR gamma (V290M).
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension. Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion. To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the global gene expression profile in primary aortic endothelial cells in response to endothelial cell specific expression of a dominant negative isoform of PPAR gamma (V290M).

Publication Title

Endothelium-specific interference with peroxisome proliferator activated receptor gamma causes cerebral vascular dysfunction in response to a high-fat diet.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE8949
Gene expression changes in mouse aorta during activation of or interference with PPAR gamma signaling.
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Ligand-mediated activation of the nuclear hormone receptor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. Two naturally occurring mutations (P467L, V290M) in the ligand binding domain of PPAR gamma have been described in humans that lead to severe insulin resistance and hypertension. Experimental evidence suggests that these mutant versions of PPAR gamma act in a dominant negative fashion. To better understand the molecular mechanisms underlying PPAR gamma action in the vasculature, we determined the gene expression patterns in mouse aorta in response to activation or interference with the PPAR gamma signaling pathway.

Publication Title

Bioinformatic analysis of gene sets regulated by ligand-activated and dominant-negative peroxisome proliferator-activated receptor gamma in mouse aorta.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE64613
CaMKII inhibition in smooth muscle cells controls Ang-II-induced gene transcription in the aorta
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

The Ca2+/calmodulin-dependent kinase II is expressed in smooth muscle and believed to mediate intracellular calcium handling and calcium-dependent gene transcription. CaMKII is activated by Angiotensin-II.

Publication Title

Calcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE67264
Differential gene expression in human THP-1 cell line undifferentiated, 3 days or 8 days differentiated with phorbol myristate acetate (PMA)
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We analysed the capacity of THP-1 cells (differentiated to macrophagoid cells) to recognize RNA sequences via pattern recognition receptors in vitro. Gene expression was analysed by RNA-Microarray. Cytokine production was analysed by ELISA assays.

Publication Title

Human TLR8 senses UR/URR motifs in bacterial and mitochondrial RNA.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon SRP061800
Mechanisms of Fibrotic Aortic Valve Stenosis
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

To examine molecular mechanisms of aortic valve stenosis in mice with hypertension and hypercholesterolemia, RNA-Seq was used during the developmental phase of stenosis to identify new gene targets. Overall design: Four groups of mice were studied: controls (CON), hypertensive (HT), hypercholesterolemic (HC), and HC/HT. Transgenic mice overexpressing human renin and human angiotensinogen served as the HT model and ApoE knockout mice served as the HC model. A sample size of N=4 was used for each of the four groups.

Publication Title

Fibrotic Aortic Valve Stenosis in Hypercholesterolemic/Hypertensive Mice.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP068859
Adipose Angiotensin AT2 Receptors Modulate Thermogenesis
  • organism-icon Mus musculus
  • sample-icon 133 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

The brain renin-angiotensin system (RAS) stimulates resting metabolic rate in part through a mechanism involving suppression of the circulating RAS. This effect appears to be mediated through a reduction in angiotensin AT2 receptor (AT2R) signaling within inguinal fat. To examine the molecular mechanisms underlying this effect, mice with hyperactivity of the brain RAS (“sRA” mice, expressing human renin via the synapsin promoter and human angiotensinogen via its own promoter) and littermate controls were chronically infused with vehicle or the AT2R specific agonist, CGP-42112a (CGP, 90 ng/hr, 8 wk, sc). To identify altered signaling pathways, total RNA was isolated from inguinal adipose tissue and transcript abundance was quantitated by RNA-Seq. Overall design: Four groups of mice were studied: controls receiving either a saline infusion (CON) or a specific angiotensin type 2 receptor agonist (CON_CGP), transgenic mice with specific activation of the brain renin-angiotensin receiving either a saline infusion (SRA) or a specific angiotensin type 2 receptor agonist (SRA_CGP). A sample size of N=3-4 was used for each of the four groups.

Publication Title

Suppression of Resting Metabolism by the Angiotensin AT2 Receptor.

Sample Metadata Fields

Sex, Specimen part, Cell line, 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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