This SuperSeries is composed of the SubSeries listed below.
Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.
Specimen part, Cell line, Time
View SamplesGenome-wide analysis of gene expression in response to bortezomib treatment (33 nM) in cell lines before and after selection for resistance.
Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.
Specimen part, Cell line, Time
View SamplesGenome-wide analysis of gene expression in response to bortezomib treatment(33 nM) in cell lines before and after selection for resistance.
Profiling bortezomib resistance identifies secondary therapies in a mouse myeloma model.
Specimen part, Cell line, Time
View SamplesThe goal was to identify genes that are differentially expressed between the bone marrow-derived CD11b+ myeloid cells infiltrating intracranial tumors and the peripheral myeloid cells (e.g. infiltrating the spleen and bone marrow).
Hematopoietic Stem Cell Gene Therapy for Brain Metastases Using Myeloid Cell-Specific Gene Promoters.
Age, Specimen part
View SamplesProtein and mRNA levels for several selenoproteins, such as glutathione peroxidase-1 (Gpx1), are down-regulated dramatically by selenium (Se) deficiency.
Selenium toxicity but not deficient or super-nutritional selenium status vastly alters the transcriptome in rodents.
Specimen part, Treatment
View SamplesWe report RNAseq analysis of the transcriptome of 3 biological replicates of bovine retina Overall design: Examine retinal transcriptome of 3 biological replicates with tissue collected between 7:00 - 10:00AM
Argonaute high-throughput sequencing of RNAs isolated by cross-linking immunoprecipitation reveals a snapshot of miRNA gene regulation in the mammalian retina.
Specimen part, Cell line, Subject
View SamplesGenome-wide expression analysis in C. Elegans grown in axenic media with low to toxic selenium concentrations
Toxic-selenium and low-selenium transcriptomes in Caenorhabditis elegans: toxic selenium up-regulates oxidoreductase and down-regulates cuticle-associated genes.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View SamplesNotch1 is a key regulator of endothelial cell behaviour. This experiment was designed to identify genes regulated by Notch1 signaling in inflammatory activated mouse endothelial cells.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View SamplesProinflammatory activation of endothelial cells leads to recruitment of leukocytes by upregulation of adhesion molecules and presentation of chemoattractants. In response to such activation there is also a strong shift in the endothelial expression of Notch ligands, with downregulation of Dll4 and a upregulation of JAG1. To assess whether Jagged1 would affect the endothelial activation profile, we suppressed JAG1 expression during IL-1-induced activation by means of siRNA and performed a genome-wide transcriptome analysis. Our results show for the first time that Jagged1 modulates the transcription profile of activated endothelial cells and describe data that imply a role for Jagged1 in sharpening the inflammatory profile of the vasculature, giving it an edge towards leukocyte recruitment. These findings imply that Jagged1 might be a potential therapeutic target to attenuate inflammation and reduce tissue damage in inflammatory diseases.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View Samples