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GSE22385
Homo sapiens
6 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Transcriptome analysis was performed from human U87 glioblastoma cell clones: U87 IRE1.NCK DN (U87dn, IRE1 dominant negative) and U87 control (U87ctrl, empty plasmid). Cells were grown in DMEM supplemented with 10% FBS and glutamine for 16 hours in culture prior mRNA isolation and analyses
Publication Title
Inositol-requiring enzyme 1alpha is a key regulator of angiogenesis and invasion in malignant glioma.
Sample Metadata Fields
Cell line
View Samples- Danio rerio
- 1 Downloadable Sample
IlluminaHiSeq2000
Description
Gene expression profiling of several wildtype strains of zebrafish embryos. The samples were pooled from several developmental stages ranging from 2 to 7 days post fertilization. This breadth of sampling gives a broad idea of genes expressed during early development and SNPs associated with wildtype strains.
Publication Title
RNA-seq-based mapping and candidate identification of mutations from forward genetic screens.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 12 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Pbx homeodomain proteins have been implicated in the regulation of gene expression during muscle development. Whether Pbx proteins are required broadly for the regulation of muscle gene expression or are required for the expression of a specific subset of muscle gene expression is not known. We employed microarrays to determine the requirements for Pbx proteins during zebrafish development.
Publication Title
Pbx homeodomain proteins direct Myod activity to promote fast-muscle differentiation.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- NextSeq 500
Description
After inactivation of Hoxa5 at postnatal days (P)1-P4, we established RNA-seq profiling with RNA extracted from P21 brainstem of tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2+/- (Hoxa5 cKO) pups and tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2-/-(Hoxa5 control) pups Overall design: To explore HOXA5 downstream target genes in the postnatal brainstem, we carried out transcriptomic analyses by RNA-Seq using a model of postnatal Hoxa5 loss-of-function. We induced Hoxa5 inactivation after birth (P1 to P4) using the tamoxifen-inducible CMV-CreERT2 mice and conditional Hoxa5 floxed allele mice (Hoxa5flox). RNA was extracted from the brainstem of P21 tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2+/- pups and from tamoxifen-treated Hoxa5flox/flox;CMV-CreERT2-/- littermates (see extract protocol).
Publication Title
Conditional Loss of <i>Hoxa5</i> Function Early after Birth Impacts on Expression of Genes with Synaptic Function.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Danio rerio
- 2 Downloadable Samples
- IlluminaHiSeq2500
Description
A zebrafish forward genetic screen for determinants of susceptibility to Mycobacterium marinum identified a hypersusceptible mutant deficient in the lysosomal hydrolase Cathepsin L that manifests the hallmarks of human lysosomal storage diseases. In uninfected mutants, macrophages progressively accumulate undigested material in their lysosomes, leading to impaired migration and the accumulation of unengulfed cell debris. During mycobacterial infection, these vacuolated macrophages cannot migrate to phagocytose infected macrophages undergoing apoptosis in the tuberculous granuloma. Consequently, unengulfed apoptotic macrophages undergo secondary necrosis causing granuloma breakdown and increased mycobacterial growth. Macrophage lysosomal accumulations similarly impair migration to newly infecting mycobacteria. We find that important aspects of this phenotype are recapitulated in human smokers, who are at increased risk for tuberculosis. A majority of alveolar macrophages from smokers exhibit lysosomal accumulations and do not migrate to Mycobacterium tuberculosis. This incapacitation of highly microbicidal first-responding macrophages may contribute to smokers' susceptibility to tuberculosis. Overall design: A forward genetic screen for zebrafish larvae that are hypersusceptible to Mycobacterium marinum infection identified a mutation in the transcription factor snapc1b at 13: 37996163 (T->C). Individuals of wild type (T/T) and mutant (C/C) were genotyped and pooled respectively for RNA isolation and transcriptome analysis.
Publication Title
Lysosomal Disorders Drive Susceptibility to Tuberculosis by Compromising Macrophage Migration.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
Background: Clinical trial and epidemiological data support that the cardiovascular effects of estrogen are complex, including a mixture of both potentially beneficial and harmful effects. In animal models, estrogen protects females from vascular injury and inhibits atherosclerosis. These effects are mediated by estrogen receptors (ERs), which when bound to estrogen can bind to DNA to directly regulate transcription. ERs can also activate several cellular kinases by inducing a rapid non-nuclear signaling cascade. However, the biologic significance of this rapid signaling pathway has been unclear.
Publication Title
Rapid estrogen receptor signaling is essential for the protective effects of estrogen against vascular injury.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 7 Downloadable Samples
- IlluminaGenomeAnalyzerII
Description
RNA libraries from immunoprecipitates of Tdrd1, Ziwi and Zili, total testis RNA, total RNA from 3 week old wild-type and tdrd1 mutant gonads. Overall design: Both size selected and non-size selected libraries were made. Sequencing was performed using Illumina platform.
Publication Title
Tdrd1 acts as a molecular scaffold for Piwi proteins and piRNA targets in zebrafish.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 44 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Swiss-Webster female mice (Charles River Laboratories, Wilmington, MA) 5-6 weeks of age were infected intranasally with 5 LD50 of either WT or lpp mutant of Y. pestis CO92. Uninfected mice were used as controls. At either 12 or 48 h post infection (p.i.), 3 mice per group were euthanized and the lungs, livers, and spleens were harvested and homogenized in 1 ml of RNALater (Ambion/Applied Biosystems, Austin, TX) using 50-ml tissue homogenizers (Kendell, Mansfield, MA). RNA was isolated from the tissue homogenates and purified using RNAqueous (Ambion). After an overnight precipitation, the RNA was resuspended in 20 ul of diethylpyrocarbonate (DEPC)-treated water and hybridized to Affymetrix GeneChip Mouse Genome 430 2.0 arrays, performed by the Molecular Genomics Core at UTMB Galveston, Texas, per manufacture protocols. The arrays had 45,000 probe sets representing more than 39,000 transcripts derived from ~34,000 well-substantiated mouse genes. The experiments were performed in triplicate (biological replicates), generating a total of 45 arrays.
Publication Title
Comparative Analyses of Transcriptional Profiles in Mouse Organs Using a Pneumonic Plague Model after Infection with Wild-Type Yersinia pestis CO92 and Its Braun Lipoprotein Mutant.
Sample Metadata Fields
Sex, Specimen part, Time
View Samples- Mus musculus, Homo sapiens
- 23 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.
Publication Title
VEGF-B signaling impairs endothelial glucose transcytosis by decreasing membrane cholesterol content.
Sample Metadata Fields
Specimen part, Cell line, Treatment
View Samples