Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation.
Project description:TruCulture human whole blood ex vivo stimulation was performed on 17 healthy individuals and 17 post-onset type 1 diabetics, then gene expression was analyzed using Nanostring to characterize stimulated innate immune responses. Ex vivo whole blood stimulation revealed higher induced IFN-1 responses in type 1 diabetes as compared to healthy controls.
Project description:Human neuronal differentiation alters responsiveness to innate immune stimuli and virus infections. We used microarrays to examine the transcriptional responses of the human BE(2)-C neuroblastoma cell line to retinoic acid-induced differentiation and type I IFN stimulation. Experiment Overall Design: Cultured BE(2)-C cells were differentiated with 10 uM all-trans retinoic acid (RA) for 3 weeks, incubated with universal type I IFN (IFNa-A/D) for 6 or 12 h, and Affymetrix Human Genome Array U133 Plus 2.0 chips were used to analyze transcript levels.
Project description:This SuperSeries is composed of the following subset Series:; GSE16450: Human BE(2)-C neuronal responses to type I IFN stimulation; GSE16451: Human BE(2)-C neuronal responses to WEEV infection Experiment Overall Design: Refer to individual Series
Project description:BRD9 was identified in a genome-wide screen for genes regulating the response to interferon (IFN) in a A549 based reporter cell line. Subsequent experiments determined an involvement of BRD9 in the transcriptional regulation of Interferon-stimulated genes (ISGs) expression following stimulation with IFN-a2. The aim of this proximity-labelling experiments was to gain a more mechanistic understanding of BRD9 recruitment during the IFN signal transduction using A549 cells stably transduced with BRD9-TurboID and mCherry-TurboID fusion proteins. The BRD9 interactome in the absence of IFN- a2 was determined. We found that following IFN-a2 treatment, STAT2 significantly associates with BRD9-TurboID.