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accession-icon GSE71194
Muscle expression of SOD1G93A modulates microRNA and mRNA expression pattern associated with the myelination process in the spinal cord of transgenic mice.
  • organism-icon Mus musculus
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.

Sample Metadata Fields

Age, Specimen part

View Samples
accession-icon GSE109365
Gene expression in developing fibrotic lesions in tracheas of chlorine-exposed mice
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Chlorine is a widely used industrial chemical that is also considered a chemical threat agent. Inhalation of chlorine gas can cause acute injury to the respiratory tract, including the death of airway epithelial cells. Failure to efficiently repair the epithelial damage is associated with long-term respiratory abnormalities, including airway fibrosis. We previously developed a model of airway injury in which mice exposed to chlorine gas exhibit epithelial damage and develop fibrosis in large airways.

Publication Title

Inhibition of chlorine-induced airway fibrosis by budesonide.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE2175
Differential gene expression in pituitary adenomas by oligonucleotide array analysis
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This series includes the four major subtypes of pituitary adenomas and normal post-mortem pituitary tissue

Publication Title

Differential gene expression in pituitary adenomas by oligonucleotide array analysis.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP063669
Human stem cell based models of neuronal migration provide insight into neurological disease pathogenesis and potential treatment
  • organism-icon Homo sapiens
  • sample-icon 7 Downloadable Samples
  • Technology Badge IconIlluminaHiSeq2000

Description

Neuronal migration defects (NMDs) are among the most common and severe brain abnormalities in humans. Lack of disease models in mice or in human cells has hampered the identification of underlying mechanisms. From patients with severe NMDs we generated iPSCs then differentiated neural progenitor cells (NPCs). On artificial extracellular matrix, patient-derived neuronal cells showed defective migration and impaired neurite outgrowth. From a cohort of 107 families with NMDs, sequencing identified two homozygous C-terminal truncating mutations in CTNNA2, encoding aN-catenin, one of three paralogues of the a-catenin family, involved in epithelial integrity and cell polarity. Patient-derived or CRISPR-targeted CTNNA2- mutant neuronal cells showed defective migration and neurite stability. Recombinant aN-catenin was sufficient to bundle purified actin and to suppress the actin-branching activity of ARP2/3. Small molecule inhibitors of ARP2/3 rescued the CTNNA2 neurite defect. Thus, disease modeling in human cells could be used to understand NMD pathogenesis and develop treatments for associated disorders. Overall design: 2 biological replicates per individual (2 iPSC clone differentiations), excluding 1263A, which has one sample

Publication Title

Biallelic loss of human CTNNA2, encoding αN-catenin, leads to ARP2/3 complex overactivity and disordered cortical neuronal migration.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE20388
Expression Profiling of a Genetic Animal Model of Depression
  • organism-icon Rattus norvegicus
  • sample-icon 78 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Expression Profiling of a Genetic Animal Model of Depression Reveals Novel Molecular Pathways Underlying Depressive-like Behaviours

Publication Title

Expression profiling of a genetic animal model of depression reveals novel molecular pathways underlying depressive-like behaviours.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE66782
Genome-wide analysis of LPS or PBS challenged DUSP3-KO and WT female mice peritoneal macrophages gene expression
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina MouseWG-6 v2.0 expression beadchip

Description

Analysis of gene expression profile in peritoneal macrophage extracted from LPS or PBS challenged DUSP3-/- and WT mice. DUSP3 deletion protects mice from sepsis and endotoxemia. We performed a microarray analysis to get insights into the differentially regulated pathways between WT and KO under inflammatory conditions.

Publication Title

DUSP3 Genetic Deletion Confers M2-like Macrophage-Dependent Tolerance to Septic Shock.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon SRP164900
Effects of high fructose and high glucose on third instar larval fat body gene expression in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We characterized monosaccharide-dependent gene expression in the Drosophila fat body using fructose and glucose. Control and high-sugar diets were compared and RNA-seq was used to identify potential target genes. Overall design: Drosophila were reared on control (0.3 M fructose or glucose) or high sugar (1.7 M fructose or glucose) diets until the wandering third instar stage. Fat bodies were isolated and RNA was extracted to determine the effects of each sugar at different concentrations on gene expression using Illumina RNA-seq.

Publication Title

Similar effects of high-fructose and high-glucose feeding in a Drosophila model of obesity and diabetes.

Sample Metadata Fields

Sex, Specimen part, Cell line, Subject

View Samples
accession-icon GSE66048
Whole-transcript expression data of BRD4 inhibition in uveal melanoma
  • organism-icon Homo sapiens
  • sample-icon 48 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

G protein alpha q and 11 are mutated in 80% of uveal melanoma. We observed that treatment with the BRD4 inhibitor JQ1 resulted in different phenotypic responses in G-protein mutant uveal melanoma cell lines and wild type uveal melanoma cell lines.

Publication Title

BRD4-targeted therapy induces Myc-independent cytotoxicity in Gnaq/11-mutatant uveal melanoma cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon SRP067643
Effect of high-sugar feeding on wandering third instar larval fat body gene expression in Drosophila melanogaster
  • organism-icon Drosophila melanogaster
  • sample-icon 26 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We compared gene expression in the Drosophila fat body on control and high-sugar diets in order to gain insight into the role of this organ during caloric overload. Differential expression analysis revealed changes in gene expression suggestive of a role for CoA metabolism in the ability to tolerate high-sugar feeding. This led us to perform biochemical and mutant studies supporting a model where CoA is limiting in the face of caloric overload. Overall design: Wild-type Drosophila were reared on control (0.15M sucrose) and high-sugar (0.7M sucrose) diets until the wandering stage. Fat bodies were isolated and RNA extracted to determine the effects of diet on gene expression using Illumina RNA-seq.

Publication Title

CoA protects against the deleterious effects of caloric overload in Drosophila.

Sample Metadata Fields

Sex, Specimen part, Subject

View Samples
accession-icon GSE15793
Expression profiling of skeletal muscle following acute 2-adrenergic stimulation
  • organism-icon Mus musculus
  • sample-icon 16 Downloadable Samples
  • Technology Badge IconIllumina Mouse Ref-6 V1

Description

Systemic administration of -adrenoceptor (-AR) agonists has been found to induce skeletal muscle hypertrophy and significant metabolic changes. In the context of energy homeostasis, the importance of -AR signaling has been highlighted by the inability of 13-AR-deficient mice to regulate energy expenditure and susceptibility to diet induced obesity. However, the molecular pathways and gene expression changes that initiate and maintain these phenotypic modulations are poorly understood. Therefore, the aim of this study was to identify differential changes in gene expression in murine skeletal muscle associated with systemic acute administration of the 2-AR agonist formoterol. Skeletal muscle gene expression (from murine tibialis anterior) was profiled at both 1 and 4 hours following systemic administration of the 2-AR agonist formoterol, using 46K Illumina(R) Sentrix BeadArrays. Illumina expression profiling revealed significant expression changes in genes associated with skeletal muscle hypertrophy, myoblast differentiation, metabolism, circadian rhythm, transcription, histones, and oxidative stress.

Publication Title

Expression profiling of skeletal muscle following acute and chronic beta2-adrenergic stimulation: implications for hypertrophy, metabolism and circadian rhythm.

Sample Metadata Fields

Treatment

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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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