This SuperSeries is composed of the SubSeries listed below.
Muscle Expression of SOD1(G93A) Modulates microRNA and mRNA Transcription Pattern Associated with the Myelination Process in the Spinal Cord of Transgenic Mice.
Age, Specimen part
View SamplesChlorine 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.
Inhibition of chlorine-induced airway fibrosis by budesonide.
Sex, Age, Specimen part, Treatment
View SamplesThis series includes the four major subtypes of pituitary adenomas and normal post-mortem pituitary tissue
Differential gene expression in pituitary adenomas by oligonucleotide array analysis.
No sample metadata fields
View SamplesNeuronal 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
Biallelic loss of human CTNNA2, encoding αN-catenin, leads to ARP2/3 complex overactivity and disordered cortical neuronal migration.
No sample metadata fields
View SamplesExpression Profiling of a Genetic Animal Model of Depression Reveals Novel Molecular Pathways Underlying Depressive-like Behaviours
Expression profiling of a genetic animal model of depression reveals novel molecular pathways underlying depressive-like behaviours.
No sample metadata fields
View SamplesAnalysis 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.
DUSP3 Genetic Deletion Confers M2-like Macrophage-Dependent Tolerance to Septic Shock.
Sex, Age, Specimen part
View SamplesWe 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.
Similar effects of high-fructose and high-glucose feeding in a Drosophila model of obesity and diabetes.
Sex, Specimen part, Cell line, Subject
View SamplesG 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.
BRD4-targeted therapy induces Myc-independent cytotoxicity in Gnaq/11-mutatant uveal melanoma cells.
Cell line, Treatment
View SamplesWe 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.
CoA protects against the deleterious effects of caloric overload in Drosophila.
Sex, Specimen part, Subject
View SamplesSystemic 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.
Expression profiling of skeletal muscle following acute and chronic beta2-adrenergic stimulation: implications for hypertrophy, metabolism and circadian rhythm.
Treatment
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