Reactive gliosis is a complex process that involves profound changes in gene expression. We used microarray to indentify differentially expressed genes and to investigate the molecular mechanisms of reactive gliosis in optic nerve head in response to optic nerve crush injury.
The Time Course of Gene Expression during Reactive Gliosis in the Optic Nerve.
Sex, Specimen part
View SamplesReactive astrocytes are typically studied in models that cause irreversible mechanical damage to axons, neuronal cell bodies, and glia. We evaluated the response of astrocytes in the optic nerve head to a subtle injury induced by a brief, mild elevation of the intraocular pressure. Astrocytes demonstrated reactive remodeling showing hypertrophy, process retraction and simplification of their shape.
Reversible reactivity by optic nerve astrocytes.
Sex
View SamplesS. aureus SA564 and SA564-codY-mutant were grown in bovine aqueous humor, bovine vitreous humor and a chemically defined medium. Samples were extracted in midlog phase and affymetrix microarray processing was performed.
No associated publication
No sample metadata fields
View SamplesComparative global gene expression analysis was caried out using pupal head tissue of otd-uvi an eye specific mutant allele of Otd and wild type control Canton S., in order to delineate the function of homeobox transcription factor Otd in Drosophila photoreceptor development and function.
No associated publication
No sample metadata fields
View SamplesThis data set is intended as a public resource documenting the identity of roughly 10,000 genes that are abundantly expressed in the mouse cochlea. The data have many uses, including for making comparisons with proteomics studies, and for comparisons of expression profiles with other mouse strains and with other species. The CBA/CaJ strain was chosen because of its lack of known vulnerabilities to premature cochlear degeneration or to extreme reactions to cochlear stresses. It may therefore be considered a normal mouse. No experimental manipulations were done on the mice of this study. Contamination of the results by genes expressed in the surrounding petrous bone and from those in blood cells was minimized.
Immunocytochemical traits of type IV fibrocytes and their possible relations to cochlear function and pathology.
No sample metadata fields
View SamplesWe used microarrays to assess transcriptional changes in regulatory T cells upon deletion of PTEN.
No associated publication
Sex, Age
View SamplesThe goal of this experiment was to explore the extent of KIN10 (At3g01090) transcriptional regulation and identify its early target genes in Arabidopsis mesophyll protoplasts. Results suggest that KIN10 targets a remarkably broad array of genes that orchestrate transcription networks, promote catabolism and autophagy, and suppress anabolism and ribosome biogenesis. The transient expression condition ruled out secondary or long-term effects of metabolism and growth, and circumvented experimental limitations caused by redundancy and embryonic lethality observed in mammals and plants.
A central integrator of transcription networks in plant stress and energy signalling.
No sample metadata fields
View SamplesThe goal of this experiment was to investigate the early transcript changes (6h) induced by hypoxia treatment in mesophyll protoplasts. A single pair (control & hypoxia) of GeneChips was used to confirm that hypoxia treatment altered the expression of an overlapping set of genes controlled by KIN10 (At3g01090) in Arabidopsis mesophyll protoplasts.
A central integrator of transcription networks in plant stress and energy signalling.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
An epigenetic mechanism of resistance to targeted therapy in T cell acute lymphoblastic leukemia.
Specimen part, Cell line
View SamplesHere we modeled T-ALL resistance to Notch inhibition, identifying persister cells that readily expand in the presence of gamma secretase inhibitor (GSI) and the absence of Notch signaling. Rare persister cells are already present in nave T-ALL populations, and the reversibility of the phenotype is suggestive of an epigenetic mechanism. Relative to GSI-sensitive cells, persisters activate distinct signaling and gene expression programs, and exhibit global chromatin compaction. A shRNA screen identified chromatin regulators whose depletion preferentially impairs persister cell viability, including BRD4, an acetyl-histone reader. BRD4 is up-regulated in the persisters and binds enhancers near genes with critical functions in T-ALL, including MYC and BCL2. Treatment of persisters with the BRD4 inhibitor JQ1 down-regulates these targets and induces growth arrest and apoptosis, at doses well tolerated by GSI-sensitive cells. Prompted by these findings, we examined and established the efficacy of GSI JQ1 combination therapy against primary human leukemias in vivo. Our findings establish a role for epigenetic heterogeneity in leukemia drug resistance and suggest the potential of combination therapies that include epigenetic modulators to prevent and treat resistant disease.
An epigenetic mechanism of resistance to targeted therapy in T cell acute lymphoblastic leukemia.
Specimen part, Cell line
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