Project description:This SuperSeries is composed of the following subset Series: GSE32923: The NIH Human Pluripotent Stem Cell Database (Agilent, mRNA) GSE33789: The NIH Human Pluripotent Stem Cell Database (Affymetrix, mRNA) GSE34199: The NIH Human Pluripotent Stem Cell Database (Agilent, miRNA) GSE34869: The NIH Human Pluripotent Stem Cell Database (Illumina, methylation) GSE35157: The NIH Human Pluripotent Stem Cell Database (Illumina, snp) GSE35735: The NIH Human Pluripotent Stem Cell Database (Agilent, cgh) Refer to individual Series

2012-10-31 | E-GEOD-34200 | biostudies-arrayexpress

dynamic SILAC NIH/3T3 treated with DMSO/CHX

Project description:NIH/3T3 cells were cultured at least 2 weeks in light medium: DMEM for SILAC (Thermo scientific) supplemented with PS, dialyzed FBS (Thermo scientific), (light) L-Lysine-2HCl (0.666 mM), (light) L-Arginine-HCl (0.399 mM)44, and L-Proline (200 mg/L). Before switching from light to heavy medium, cells were treated with 0.05 µg/mL CHX or equivalent dilution of DMSO in 6-well plates. At timepoint 0 h, we replaced light medium with pre-warmed heavy medium: DMEM for SILAC (Thermo scientific) supplemented with PS, dialyzed FBS (Thermo scientific), (heavy) 13C6 15N2 L-Lysine-2HCl (0.666 mM), (heavy) 13C6 15N4 L-Arginine-HCl (0.399 mM), and L-Proline (200 mg/L) for NIH/3T3.

2025-10-07 | PXD061384 | Pride

Cigarette smoking induces changes in airway epithelial expression of genes associated with monogenic lung disorders

Project description:Smoking-induced lung disease is one of the most prevalent forms of lung disease but also one of the more diverse. Based on the phenotypic diversity caused by the same environmental stress, we hypothesized that smoking may induce changes in lung cell expression of genes that, with specific variants, are causative of monogenic lung disease, i.e., not that smoking induces a phenocopy of a genetic disease, but smoking may subtly modify the expression of genes known to be associated with genetic disorders with distinct lung disease phenotypes. To assess this hypothesis, and based on the knowledge that most smoking-related disease phenotypes start in the small airway epithelium, we asked: are the genes associated with the monogenic lung disorders expressed in the small airway epithelium, and if so, does smoking alter the expression of these genes? To accomplish this, we examined small airway epithelium expression of 92 genes known to be associated with 17 monogenic lung disorders in 230 samples of small airway epithelium (SAE) obtained from healthy nonsmokers and healthy smokers without any clinical evidence of disease. Of the 86 monogenic disorder-related genes we found expressed in the SAE, strikingly, 37 were significantly differentially expressed in normal smokers compared to normal nonsmokers (p<0.05, Benjamini-Hochberg correction for multiple comparisons). The data demonstrates that the effect of smoking on the transcriptome of small airway epithelium includes significantly altered regulation of the genes responsible for known monogenic disorders.

2017-08-30 | GSE63127 | GEO

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