Whole transcriptome microarray of U87 Gliblastoma cells transfected with mir-93 or negative Control and stimulated with IL1b
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ABSTRACT: We inended to investigate the regulatory impact of miR-93 on Glioblastoma cells during an inflammatory Stimulus with a special focus on pro-inflammatory pathways and cytokines.
Project description:Response of Cupriavidus metallidurans AE104(delta zupT) mutant to Zn/EDTA stress In this study 2 different treatments were performed to acquire expression profiles of the total genome of Cupriavidus metallidurans
Project description:Response of Cupriavidus metallidurans CH34 to cisplatin, Pt(IV)chloride and Au-NP In this study 7 different treatments were performed (first 2 as 3 replicates) to acquire expression profiles of the total genome of Cupriavidus metallidurans
Project description:Response of Cupriavidus metallidurans CH34, AE104 and delta zupT mutant to Zn/EDTA stress In this study 3 different treatments were performed to acquire expression profiles of the total genome of Cupriavidus metallidurans
Project description:Response of Cupriavidus metallidurans CH34 to NaAuCl4, Au(I)-thiomalate, Au(I)-thiosulfate, KAuCN, (KCN as control) In this study 10 different treatments were performed (first 7 as 3 replicates) to acquire expression profiles of the total genome of Cupriavidus metallidurans
Project description:Feather pecking is a major welfare problem in egg production. It may be caused by genetic, physiological and environmental factors. The main aim of this study was to uncover variability in gene expression between individuals from high (HFP) and for low feather pecking (LFP) line using Chicken Gene Expression Microarrays (Agilent Technologies). Samples were assorted to two groups, each containing 9 biological replicates from high feather pecking (HFP) and low feather pecking (LFP) line.
Project description:Livers for tissue preparation and HSC isolation were derived from 2 and 22 months old male Wistar rats from Janvier Labs (France). Samples from three different lobes (median lobe, left lateral lobe, right lateral lobe) of each liver were collected and pooled for tissue analysis by gene expression. To isolate HSC, the livers were digested with enzyme solutions and HSC were enriched by density gradient centrifugation. HSC were purified by fluorescence-activated cell sorting using their typical retinoid fluorescence emitted after UV-light excitation. The sorted HSC were collected in IMDM supplemented with 10% FCS and 1 % antibiotic-antimycotic solution and cultured for 24 hours. Total RNA of HSC and whole liver tissue from 3 young and 3 old rats was extracted using the Qiagen RNeasy Mini Kit. RNA samples obtained from cultured HSC and whole liver tissues were sent to IMGM Laboratories (Martinsried, Germany) for gene expression analyses by microarrays (Affymetrix, GeneChip Rat Gene 2.0 ST Array, Thermo Fisher Scientific) in triplicates for each age group. The array data were processed by the Transcriptome Analysis Console 3.0 (Thermo Fisher Scientific).
Project description:We have developed a new method to study DNA-protein interaction in vivo called DamIP, which is based on fusing a protein of interest to a mutant form of DNA adenine methylatransferase (Dam) from E. coli. We showed previously that DamIP can efficiently identify in vivo binding sites of Dam-tethered human estrogen receptor alpha (hERα). In current study, we present the cistrome of hERα determined by DamIP and high throughput sequencing (DamIP-seq). The DamIP-seq defined hERα cistrome overlaps significantly with those determined by ChIP-chip or ChIP-seq, but identifies many new binding regions. As shown by conventional ChIP assay, many DamIP-seq unique hERα binding regions show relatively stable hERα binding, whereas DamIP-seq misses some regions with very transient hERα binding. The methyl-adenine modifications introduced by Dam are stable and do not decrease over 12 days. In summary, the current study provides both an alternate view of the hERα cistrome to further understand the mechanism of hERα mediated transcription, and a new tool to explore other transcriptional factors and cofactors. MCF7 cells were transfected with DamK9A or DamK9A-hERalpha. DamIP were performed from each sample and subjected to solexa sequencing
Project description:Effective anti-viral immunity depends on the ability of infected cells or cells triggered with virus-derived nucleic acids to produce type I interferon (IFN), which activates transcription of numerous antiviral genes. However, disproportionately strong or chronic IFN expression is a common cause of inflammatory and autoimmune diseases. Here we describe an epigenetic mechanism that determines cell-type specific differences in IFN and IFN-stimulated gene expression in response to exogenous signals. We identify di-methylation of histone H3 at lysine 9 (H3K9me2) as a suppressor of IFN and IFN-inducible antiviral gene expression. We show that levels of H3K9me2 at IFN and IFN stimulated genes (ISG) correlate inversely with the scope and amplitude of IFN and ISG expression in fibroblasts and dendritic cells. Accordingly, genetic ablation or pharmacological inactivation of lysine methyltransferase G9a, which is essential for the generation of H3K9me2, resulted in phenotypic conversion of fibroblasts into highly potent IFN-producing cells and rendered these cells resistant to pathogenic RNA viruses. In summary, our studies implicate H3K9me2 and enzymes controlling its abundance as key regulators of innate antiviral immunity. Examination of epigenetic modifications in WT and G9a deficient MEFs and splenic DCs
Project description:This SuperSeries is composed of the following subset Series: GSE22102: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (sequencing) GSE24774: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient DCs) GSE24776: Histone H3 lysine 9 di-methylation as an epigenetic signature of the interferon response (WT and G9a deficient MEFs) Refer to individual Series