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accession-icon GSE99996
A biobank of 30 molecularly characterized patient-derived xeongraft models of pediatric brain tumors
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A biobank of patient-derived pediatric brain tumor models.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE99961
A biobank of 30 molecularly characterized patient-derived xeongraft models of pediatric brain tumors [Affymetrix]
  • organism-icon Homo sapiens
  • sample-icon 55 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have generated and comprehensively characterized 30 patient-derived orthotopic xenograft (PDOX) models and 7 cell lines represeneting subgroups of medulloblastoma, high-grade glioma, atypical teratoid/rhabdoid tumor, ependymoma and pineoblastoma.

Publication Title

A biobank of patient-derived pediatric brain tumor models.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE14402
TNF-a-induced MEK/ERK-dependent regulation of Cartilage Matrix Genes
  • organism-icon Rattus norvegicus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

TNF-a is increased in the synovial fluid of patients with rheumatoid arthritis and osteoarthritis. TNF-a activates MEK/ERK in chondrocytes; however the overall functional relevance of MEK/ERK to TNF-a-regulated gene expression in chondrocytes is unknown. Chondrocytes were treated with TNF-a with or without the MEK1/2 inhibitor U0126 for 24 h. Microarray analysis was used to identify genes regulated by TNF-a in a MEK1/2-dependent fashion.

Publication Title

Egr-1 inhibits the expression of extracellular matrix genes in chondrocytes by TNFalpha-induced MEK/ERK signalling.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE58997
Expression data from livers from Sco1 liver-specific KO and WT adult mice
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Sco1 is a gene required for cytochrome c oxidase biogenesis and the regulation of copper homeostasis. We characterized the transcriptional changes that occur as a result of liver-specific deletion of Sco1 in mice at 27 days of age

Publication Title

The Mitochondrial Metallochaperone SCO1 Is Required to Sustain Expression of the High-Affinity Copper Transporter CTR1 and Preserve Copper Homeostasis.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE65069
5Z-7-Oxozeanol inhibits the effect of TGFB1 on human gingival fibroblasts
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Microarray analysis was used to show that in gingival fibroblasts essentially all TGFB1 responsive genes were blocked by TAK inhibition

Publication Title

5Z-7-Oxozeanol Inhibits the Effects of TGFβ1 on Human Gingival Fibroblasts.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE117855
Engineered FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Cholesterol is an essential cell membrane component and precursor in metabolic pathways. Control of cholesterol levels is essential to human health. The endocrine hormone FGF19 potently inhibits CYP7A1, which controls a key step in cholesterol catabolism. However, the molecular mechanisms that integrate FGF19 with other cholesterol metabolic pathways are incompletely understood. Here we show that FGF19 and analogue promote HDL biogenesis and cholesterol efflux from the liver by selectively modulating liver X receptor signaling without inducing hepatic steatosis. We further identify ATP-binding cassette transporter A1 and FGFR4 as mediators of this effect. In dyslipidemic Apoe-/- mice fed a Western diet, treatment with FGF19 analogue dramatically reduced atherosclerotic lesion area in aortas. In healthy human volunteers, FGF19 analogue caused a placebo-adjusted increase in HDL cholesterol levels of 26% in seven days. These findings outline a regulatory role for FGF19 in cholesterol metabolism and advance our understanding of the mechanisms that coordinate sterol homeostasis.

Publication Title

Therapeutic FGF19 promotes HDL biogenesis and transhepatic cholesterol efflux to prevent atherosclerosis.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE83610
Renal fibrosis mRNA classifier: validation in experimental lithium-induced interstitial fibrosis in the rat kidney
  • organism-icon Rattus norvegicus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 1.0 ST Array (ragene10st)

Description

Metzincins and related genes (MARGS) play important roles in ECM remodeling in fibrotic conditions.

Publication Title

Renal Fibrosis mRNA Classifier: Validation in Experimental Lithium-Induced Interstitial Fibrosis in the Rat Kidney.

Sample Metadata Fields

Sex, Specimen part

View Samples
accession-icon GSE42808
Expression data from human umbilical vein endothelial cells (HUVEC) treated with DMSO, telmisartan, or telmisartan and amlodipine
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Objective Telmisartan, an angiotensin II type 1 (AT1) receptor blocker, and amlodipine, a calcium channel blocker, are antihypertensive agents clinically used as monotherapy or in combination. They exert beneficial cardiovascular effects independently of blood pressure lowering and classic mechanisms of action. In this study, we investigate molecular mechanisms responsible for the off-target effects of telmisartan and telmisartan-amlodipine in endothelial cells (EC), using an unbiased approach.

Publication Title

Telmisartan exerts pleiotropic effects in endothelial cells and promotes endothelial cell quiescence and survival.

Sample Metadata Fields

Specimen part, Disease, Treatment

View Samples
accession-icon GSE45564
Expression data in the presence of miR-29a inhibition in human dermal fibroblast cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

miR-29 can target many gene transcripts encoding extracellular matrix proteins. To unravel novel targets, we used microarray analysis to detect global gene expression changes when inhibiting endogenous miR-29.

Publication Title

Ten-eleven translocation (Tet) and thymine DNA glycosylase (TDG), components of the demethylation pathway, are direct targets of miRNA-29a.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon SRP048701
Charaterization of genetic alterations and gene expression signatures found in BCR-ABL inhibitor-resistant KCL-22 subpopulations and single clones
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

KCL-22 is a chronic myeloid leukemia (CML) cell line derived from a patient in blast crisis phase and harbors the BCR-ABL translocation. The catalytic (ATP-competitive) BCR-ABL inhibitors imatinib and nilotinib have dramatically improved CML patient outcome, but the development of resistance remains a clinical challenge. The recent identification of allosteric BCR-ABL inhibitors, such as GNF-2, which target the enzyme by binding to the myristoyl pocket rather than catalytic site of ABL1, may provide a strategy to broadly overcome resistance to the class of ABL1 ATP competitive inhibitors. We therefore wanted to use the ClonTracer barcoding system to compare the clonal responses of KCL-22 to imatinib, nilotinib and GNF-2. RNA-seq was employed to characterize genetic alterations and gene expression signatures in the pooled cell populations resistant to BCR-ABL inhibitors as well as single clones showing differential response to the three inhibitors. Overall design: mRNA profiling of the subpopulations and single clones of human CML cell line KCL-22 that contribute to BCR-ABL inhibitor resistance

Publication Title

Studying clonal dynamics in response to cancer therapy using high-complexity barcoding.

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)

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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