Expression profile for hemocytes from hml-Gal4, UAS-2xEGFP larvae were compared to hemocytes from hml-Gal4, UAS-2xEGFP; UAS-Idh-R195H larvae
Genetic dissection of leukemia-associated IDH1 and IDH2 mutants and D-2-hydroxyglutarate in Drosophila.
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View SamplesDifferential gene expression of cerebral cortex might be responsible for distinct neurovascular developments between different mouse strains
A novel genetic locus modulates infarct volume independently of the extent of collateral circulation.
Sex, Specimen part
View SamplesThe rat pancreatic cell line AR42J is relatively undifferentiated under normal culture conditions. When the glucocorticoid dexamethasone is added to the medium the cells display a dramatic decrease in proliferative rate and are induced to a more exocrine phenotype that includes increased expression of exocrine pancreas products (digestive enzymes) and more developed regulated secretion. We used microarray to determine changes in gene expression comparing control (without dexamethasone) vs induced (plus dexamethasone).
No associated publication
Specimen part, Cell line
View SamplesTotal RNA was prepared using TRIzol reagent from the pancreata of eight week old male mice. The genotypes were Control: gastrin+/-, CFTR+/+; and CF: gastrin+/-, CFTR-/-. All mice were on 95% black6, 5% 129Sv background. Mice were fed Peptamen from age 10 days to prevent intestinal obstruction.
Acidic duodenal pH alters gene expression in the cystic fibrosis mouse pancreas.
No sample metadata fields
View SamplesTotal RNA was prepared from the entire small intestines of 40 day old Control and CFTR null mice (2 males and 1 female of each genotype), congenic on the black6 background, using TRIzol reagent. Mice were fed Peptamen from age 10 days to prevent intestinal obstruction.
No associated publication
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View SamplesBackground: Cystic fibrosis (CF) is caused by mutations in the CFTR gene that impair function of this cAMP-regulated Cl- channel. In the small intestine, loss of CFTR function creates a dehydrated, acidic luminal environment which is believed to cause an accumulation of mucus, a phenotype characteristic of CF. CF mice have an innate immune response and impaired intestinal transit as well. We investigated whether lubiprostone, which activates the CLC2 Cl- channel, would improve the CF intestinal phenotype.
Lubiprostone ameliorates the cystic fibrosis mouse intestinal phenotype.
Specimen part, Treatment
View SamplesWe used microarrays to detail the global program of gene expression changes in wild type and Fbln5-/- adult mice. Estrogen status was controlled
No associated publication
Sex, Age, Specimen part
View SamplesGentamicin is a highly efficacious antibiotic against gram-negative bacteria. However, its usefulness in treating infection is compromised by its poorly understood renal toxicity. This toxic effect is seen in a variety of organisms. While the yeast Saccharomyces cerevisiae is relatively insensitive to gentamicin, mutations in any one of 20 or so genes causes a dramatic increase in sensitivity. Many of these genes encode proteins important for translation termination or specific protein trafficking complexes. Here, we demonstrate by microarray analysis that gentamicin treatment leads to dramatic decreases in genes under the control of the MADS box protein Mcm1, including genes encoding products involved in mating, nitrogen utilization, and ribosome biogenesis. Furthermore, microarray analysis also demonstrates an increase in a Rlm1-dependent set of genes involved in maintaining the structure of the cell wall that are also induced by the antifungal agents caspofungin and calcofluor white. Subsequent inspection of the physical and genetic interactions of the remaining gentamicin sensitive mutants revealed a network centered around chitin synthase and the Arf Pathway. Furthermore, conditional arf1 mutants are hypersensitive to gentamicin even under permissive conditions. These results suggest that gentamicin may act as a cell wall stress, possibly by disrupting Arf-dependent trafficking of proteins involved in forming the cell wall.
No associated publication
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View SamplesThe transcription factor MEF2C is specifically induced by VEGF in endothelial cells. To delineate target genes of MEF2C in endothelial cells, which might be important during angiogenesis also, MEF2C was overexpressed adenovirally in human umbilical vein endothelial cells (HUVECs) over a period of 8 to 32 hours.
The transcription factor MEF2C negatively controls angiogenic sprouting of endothelial cells depending on oxygen.
Specimen part, Treatment
View SamplesWnt9b is expressed in the ureteric bud of the kidney at all stages of development. In Wnt9b mutants, the ureteric bud forms but the metanephric mesenchyme is never induced to undergo differentiation.
Myc cooperates with β-catenin to drive gene expression in nephron progenitor cells.
Specimen part
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