Carrying out both RNA-seq and Smad1/5 genome-wide chromatin immunoprecipitation and sequencing (ChIP-seq) analyses of mESCs in the naïve or primed states, we revisit the roles of BMP signaling in mESCs. Overall design: RNA-seq analysis in 2 cell types; mESCs and ES-derived EpiSC (ESD-EpiSCs).
BMP Sustains Embryonic Stem Cell Self-Renewal through Distinct Functions of Different Krüppel-like Factors.
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Ras and TGF-β signaling enhance cancer progression by promoting the ΔNp63 transcriptional program.
Specimen part, Cell line
View SamplesWe demonstrate that activation of Ras and TGF- pathways strengthens the binding of p63 to its genomic sites and modulates the expression of p63 target genes.
Ras and TGF-β signaling enhance cancer progression by promoting the ΔNp63 transcriptional program.
Cell line
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 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 SamplesInflammatory activation of endothelial cells enables leukocyte recruitment to tissues. We here investigate how Notch1 signaling affects the transcriptional profile of inflammatory activated human umbilical vein cells.
Inhibition of Endothelial NOTCH1 Signaling Attenuates Inflammation by Reducing Cytokine-Mediated Histone Acetylation at Inflammatory Enhancers.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide analysis reveals conserved transcriptional responses downstream of resting potential change in Xenopus embryos, axolotl regeneration, and human mesenchymal cell differentiation.
Sex, Specimen part
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