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accession-icon GSE42658
Expression profiles for paediatric brain tumours
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.

Sample Metadata Fields

Sex, Age, Specimen part, Disease stage

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accession-icon GSE42656
Gene expression profiles for paediatric brain tumours
  • organism-icon Homo sapiens
  • sample-icon 73 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

In this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles

Publication Title

Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.

Sample Metadata Fields

Sex, Age, Specimen part, Disease stage

View Samples
accession-icon GSE38205
Expression data for inbred mouse brains
  • organism-icon Mus musculus
  • sample-icon 25 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Prion diseases are fatal neurodegenerative disorders that include bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob disease (CJD) in humans. They are characterized by long incubation periods, variation in which is determined by many factors including genetic background. In some cases it is possible that incubation time may be directly correlated to the level of gene expression. In order to test this hypothesis we combined incubation time data from five different inbred lines of mice with quantitative gene expression profiling in normal brains and identified five genes with expression levels that correlate with incubation time. One of these genes, Hspa13 (Stch), is a member of the Hsp70 family of ATPase heat shock proteins which have been previously implicated in prion propagation. To test whether Hspa13 plays a causal role in determining the incubation period we tested two over-expressing mouse models. The Tc1 human chromosome 21 (Hsa21) transchromosomic mouse model of Down syndrome is trisomic for many Hsa21 genes including Hspa13 and following Chandler/RML prion inoculation shows a 4% reduction in incubation time. Furthermore, a transgenic model with eight fold over-expression of mouse Hspa13 exhibited highly significant reductions in incubation time of 16%, 15% and 7% following infection with Chandler/RML, ME7 and MRC2 prion strains respectively. These data further implicate Hsp70-like molecular chaperones in protein misfolding disorders such as prion disease.

Publication Title

Overexpression of the Hspa13 (Stch) gene reduces prion disease incubation time in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE42641
A Top-down Systems Analysis Identifies an Innate Feed-forward Inflammatory Circuit Leading to Lethal Influenza Infection
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE42639
Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Transcriptomic comparison of 5 cell types during lethal and non-lethal influenza infection and further use of these signatures in a top-down systems analysis investigating the relative pathogenic contributions of direct viral damage to lung epithelium vs. dysregulated immunity during lethal influenza infection.

Publication Title

A systems analysis identifies a feedforward inflammatory circuit leading to lethal influenza infection.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE28750
Development and Validation of a Novel Molecular Biomarker Diagnostic Test for the Early Detection of Sepsis
  • organism-icon Homo sapiens
  • sample-icon 41 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Introduction: Sepsis is a complex immunological response to infection characterized by early hyperinflammation followed by severe and protracted immunosuppression, suggesting that a multi-marker approach has the greatest clinical utility for early detection, within a clinical environment focused on SIRS differentiation. Pre-clinical research using an equine sepsis model identified a panel of gene expression biomarkers that define the early aberrant immune activation. Thus, the primary objective was to apply these gene expression biomarkers to distinguish patients with sepsis from those who had undergone major open surgery and had clinical outcomes consistent with systemic inflammation due to physical trauma and wound healing.

Publication Title

Development and validation of a novel molecular biomarker diagnostic test for the early detection of sepsis.

Sample Metadata Fields

Specimen part

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accession-icon GSE70216
Differential gene expression to VEGF in aorta from wild-type and C17S PKARI knock-in mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Angiogenesis is essential for tissue development, wound healing and tissue perfusion, with its dysregulation linked-to tumorigenesis, rheumatoid arthritis and heart disease. Here we show pro-angiogenic stimuli couple to NADPH oxidase-dependent generation of oxidants that catalyse an activating intermolecular-disulphide between regulatory-RI subunits of protein kinase A (PKA), which stimulates PKA-dependent ERK signalling. This is crucial to blood vessel growth as 'redox-dead' Cys17Ser RI knock-in mice fully resistant to PKA disulphide-activation have deficient angiogenesis in models of hind limb ischaemia and tumour-implant growth. Disulphide-activation of PKA represents a new therapeutic target in diseases with aberrant angiogenesis.

Publication Title

Deficient angiogenesis in redox-dead Cys17Ser PKARIα knock-in mice.

Sample Metadata Fields

Specimen part

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accession-icon GSE55170
Infection of Myeloid Angiogenic Cells (MACs) with Bartonella henselae (B.h.) induces a chord formation phenotype in vitro.
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Myeloid Angiogenic Cells (MACs) were infected with the intracellular, bacterial pathogen Bartonella henselae (B.h.). Infected cells were seeded onto Matrigel coated plates. While uninfected cells showed no phenotypic changes and died over time, infected cells showed strong phenotypic changes and developed into complex 2D chord networks over the course of long term culture (eg 49d). To examine the changes in gene expression associated with the development of the B.h.dependent chord formation phenotype, RNA was isolated from MACs shortly after isolation (d4) and from cells of the chord structures (+B.h. Matrigel). As primary endothelial cells are also know to form chord networks when cultured on Matrigel, a sample of human umbilical vein endothelial cells (HUVECs) cultured on Matrigel for 12hr was also included in the analysis as a control.

Publication Title

Reprogramming of myeloid angiogenic cells by Bartonella henselae leads to microenvironmental regulation of pathological angiogenesis.

Sample Metadata Fields

Specimen part, Subject, Time

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accession-icon SRP074887
Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.
  • organism-icon Mus musculus
  • sample-icon 77 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Huntington's disease (HD) is an inherited neurodegenerative disorder of which skeletal muscle atrophy is a common feature, and multiple lines of evidence support a muscle-based pathophysiology in HD mouse models. Inhibition of myostatin signaling increases muscle mass, and therapeutic approaches based on this are in clinical development. We have used a soluble ActRIIB decoy receptor (ACVR2B/Fc) to test the effects of myostatin/activin A inhibition in the R6/2 mouse model of HD. Transcriptional profiling of muscle in treated and untreated wild-type and R6/2 mice was performed to analyze the effect of the ActRIIB decoy on genes and pathways involved in maintaining normal muscle physiology as well as those dysregulated due to the mutant HTT gene mutation. Overall design: RNAseq was performed on tibialis muscle from wild-type, wildtype + decoy, R6/2 and R6/2 + decoy; N = 10 per group. RNAseq was done on an Illumina Hi-seq 2000. Paired-end sequencing was obtained, 4-plexed across lanes for a minimum of 38 million 50mer paired reads per sample

Publication Title

Myostatin inhibition prevents skeletal muscle pathophysiology in Huntington's disease mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Treatment, Subject

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accession-icon SRP071739
Changes in RNA expression in human oral cavity carcinoma cells as a result of LDB1 reduction
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2500

Description

The study was designed to identify differential expressed genes between human oral cavity carcinoma cell lines with and without LDBI knockout Overall design: Three parental human oral cavity carcinoma cell lines were used as control, LDB1 was knocked out in the three parent cell lines to create KO cell lines.

Publication Title

LIM-Only Protein 4 (LMO4) and LIM Domain Binding Protein 1 (LDB1) Promote Growth and Metastasis of Human Head and Neck Cancer (LMO4 and LDB1 in Head and Neck Cancer).

Sample Metadata Fields

No sample metadata fields

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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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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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