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accession-icon GSE59949
Expression data from human dental follicle cells
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.1 ST Array (hugene11st)

Description

We analysed the genexpression of dental follicle cells (DFCs) after 3 days osteogenic differentiation with BMP2 after transfection with a DLX3 plasmid (pDLX3) and after transfection with an empty plasmid (pEV)

Publication Title

A protein kinase A (PKA)/β-catenin pathway sustains the BMP2/DLX3-induced osteogenic differentiation in dental follicle cells (DFCs).

Sample Metadata Fields

Specimen part

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accession-icon SRP083919
Effect of SWELL1 gene deletion on gene expression in adipocytes
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

We used RNA-Seq to detail the global expression changes induced when SWELL1 is genetically deleted from adipocytes. Overall design: We generated isogenic SWELL1 KO adipocyte cell lines from 3T3-F442A cells. CRISR/Cas9 was used to knockout the SWELL1 gene in the parental 3T3-F442A line. These cell lines were grown in culture and RNA was extracted for sequencing. RNA was sequenced on an Illumina Hi-Seq at the University of Iowa Core Facility.

Publication Title

SWELL1 is a regulator of adipocyte size, insulin signalling and glucose homeostasis.

Sample Metadata Fields

Specimen part, Cell line, Subject

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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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accession-icon GSE17539
Expression profile of grafted human engineered skin substitutes compared with intact human
  • organism-icon Homo sapiens
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The goal of the experiment: To characterize the dynamic gene expression profile of engineered human skin in vitro and after grafting, and compare with expression profile of uninjured human skin.

Publication Title

Engineered human skin substitutes undergo large-scale genomic reprogramming and normal skin-like maturation after transplantation to athymic mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE50820
Expression data from MCF7 and BT474 cell lines after long term estrogen deprivation culture
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

MCF7 and BT474 cell lines were exposed to LTED culture for 0 and 2 days, 6 weeks and 10 months and monitored for changes in gene expression

Publication Title

Clinical instability of breast cancer markers is reflected in long-term in vitro estrogen deprivation studies.

Sample Metadata Fields

Cell line, Treatment, Time

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accession-icon GSE8050
A cryptic VEGF T-cell epitope: Identification and characterization by mass spectrometry and T-cell assays.
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The vascular endothelial growth factor A (VEGF) is involved in various physiological processes such as angiogenesis or wound healing but is also crucial in pathological events such as tumor growth. Thus, clinical anti-VEGF treatments have been developed which could already prove to have enormous beneficial effects for cancer patients. In this article we describe the first VEGF-derived CD8+ T-cell epitope. The natural HLA ligand SRFGGAVVR was identified by differential mass spectrometry in two primary renal cell carcinomas (RCC) and was significantly over-presented on both tumor tissues. SRFGGAVVR is derived from a cryptic translated region of VEGF presumably by initiation of translation at the non-classical start codon CUG499. SRFGGAVVR specific T-cells were generated in vitro using peptide loaded dendritic cells or artificial antigen presenting cells. They were identified by HLA tetramer analysis after in vitro stimulation. SRFGGAVVR specific CD8+ T-cells were fully functional T-effector cells, which were able to secrete IFN-gamma upon stimulation and killed tumor cells in vitro. Additionally, we have quantitatively analyzed VEGF mRNA and protein levels in RCC tumor and normal tissue samples by gene chip analysis, qRT-PCR, in situ hybridization, and bead based immuno assay. In the future, T-cells directed against VEGF as a tumor associated antigen may represent a possible way of combining peptide-based anti-VEGF immunotherapy with already existent anti-VEGF cancer therapies.

Publication Title

A cryptic vascular endothelial growth factor T-cell epitope: identification and characterization by mass spectrometry and T-cell assays.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE93611
Time-course expression data from HEK293RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF and labelled with 4SU
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

An immediate-late gene expression module decodes ERK signal duration.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE72919
Time-course expression data from HEK293RAF1:ER cells stimulated with 4OHT, U0126, CYHX, ActD, EGF, FGF, or IGF
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We integrate experimental data and mathematical modelling to unveil how ERK signal duration is relayed to mRNA dynamics.

Publication Title

An immediate-late gene expression module decodes ERK signal duration.

Sample Metadata Fields

Cell line

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accession-icon GSE17800
Myocardial gene expression profiles and cardiodepressant autoantibodies predict response of patients with dilated cardiomyopathy to immunoadsorption therapy
  • organism-icon Homo sapiens
  • sample-icon 46 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Background: Immunoadsorption with subsequent IgG substitution (IA/IgG) represents a novel therapeutic approach in treatment of dilated cardiomyopathy (DCM) which leads to improvement of left ventricular ejection fraction (LVEF). However, response to this therapeutic intervention shows wide inter-individual variability. In this pilot study, we tested the value of clinical, biochemical and molecular parameters for prediction of the response of patients with DCM to IA/IgG.

Publication Title

Myocardial gene expression profiles and cardiodepressant autoantibodies predict response of patients with dilated cardiomyopathy to immunoadsorption therapy.

Sample Metadata Fields

Sex, Age, Disease

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accession-icon GSE98757
Dysregulated Signalling leads to altered cell migration: an oncogenic basis for the development of CCSK
  • organism-icon Homo sapiens
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 2.1 ST Array (hugene21st)

Description

The oncogenic mechanisms and tumour biology underpinning Clear Cell Sarcoma of Kidney (CCSK), the second commonest paediatric renal malignancy, are poorly understood and currently therapy depends heavily on Doxorubicin with cardiotoxic side-effects. Previously, we characterised the balanced t(10;17)(q22;p13) chromosomal translocation, identified at that time as the only recurrent genetic aberration in CCSK. This translocation results in an in-frame fusion of the YWHAE (encoding 14-3-3e) and NUTM2 genes, with a somatic incidence of 12%. Clinico-pathological features of that cohort suggested that this aberration might be associated with higher stage and grade disease. Since no primary CCSK cell line exists, we generated various stably transfected cell lines containing doxycycline-inducible HA-tagged-YWHAE-NUTM2, in order to study the effect of expressing this transcript. 14-3-3e-NUTM2-expressing cells exhibited significantly greater cell migration compared to mock-treated controls. Gene and protein expression studies conducted in parallel on this model system suggested dysregulation of signalling pathways as a basis to the migration changes. Importantly, by blocking these signalling pathways using anti-EGFR, anti-IGF1R and anti-PDGFa neutralising antibodies, the migratory advantage conferred by transcript expression was abrogated. These results support 14-3-3e-NUTM2 expression as a contributor to CCSK tumorigenesis and provide avenues for the exploration of novel therapeutic approaches in CCSK.

Publication Title

Dysregulated mitogen-activated protein kinase signalling as an oncogenic basis for clear cell sarcoma of the kidney.

Sample Metadata Fields

Disease, Cell line

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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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