Transcriptional and epigenetic basis for restoration of G6PD enzymatic activity in human G6PD-deficient cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Valentina Caputo
PROVIDER: E-MTAB-2533 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Gene expression profiles of E14 embryonic stem cells (ESCs) before and after treatment with low levels of the histone deacetylase (HDAC) inhibitors valproic acid (VPA) and sodium butyrate (NaBu). E14 cells were treated with VPA or NaBu for 16 hrs in duplicates. Cells were harvested along with untreated control E14 cells. RNA was isolated from the cells and hybridized on Affymetrix chips.
2011-09-16 | E-GEOD-23956 | biostudies-arrayexpress
Project description:We wanted to compare gene expression from control (untreated) zebrafish larvae and 2 mM NaBu-treated larvae for 24 hours, in order to assess the effect of inhibition of the HDAC pathway in these animals
2017-08-23 | E-MTAB-5992 | biostudies-arrayexpress
Project description:Base-pair level resolution of DNase susceptibility of the native chromatin state. These maps represent and are dependent upon the nature and the specificity of interaction of the DNA with the regulatory/modulatory proteins binding at specific loci in the genome; thus they represent the native chromatin state of the genome under investigation. The deep sequencing approach has been used to define the footprint landscape of the genome by identifying DNA motifs that interact with known or novel DNA-binding proteins 2 replicates of the erythroid cells were generated and profiled by Dnase I.
2014-03-05 | E-GEOD-55579 | biostudies-arrayexpress
Project description:We wanted to analyze the differences in acetyl-H4 content related to inter-individual behavioral variability. We retrieved three groups of samples: The first one was composed by 4 different clusters of zebrafish composed each one by 5 zebrafish larvae. Within each cluster, the behavioral differences across the larvae were minimal, while between the clusters, there were high differences in the behavior. The second one was composed by 4 different clusters of sodium butyrate (NaBu)-treated zebrafish composed each one by 5 larvae. The selection choice was the same as in the first group, but due to their behavioral effect of NaBu, the differences between the clusters were significantly reduced compared to control. The third one was composed by 3 different clusters of 5 zebrafish each randomly selected from the behavioral space. This group is a control of variability not associated to behavior.
2017-09-01 | E-MTAB-5993 | biostudies-arrayexpress
Project description:Enhancers of transcription activate transcription via binding of sequence-specific transcription factors to their target sites in chromatin. In this report, we identify GATA1-bound enhancers genome-wide and find a global reorganization of the nucleosomes at these enhancers during differentiation of hematopoietic stem cells (HSCs) to erythrocytes. We show that the catalytic subunit BRG1 of BAF complexes localizes to these enhancers during differentiation and generates a longer nucleosome repeat length surrounding the GATA1 sites by shifting the flanking nucleosomes away. Intriguing, we find that the nucleosome shifting specifically facilitates binding of TAL1 but not GATA1, which subsequently activates transcription of target genes. Human hematopoietic stem cells (referred as CD34+ cells) were differentiated into erythroid lineage expressing the cell surface marker CD36 (referred as CD36+ cells). To study the function of ATP-dependent chromatin remodeling BAF complexes in the establishment of erythroid specific enhancers during differentiation, we mapped the genome-wide binding sites of GATA1 and TAL1, the key transcription regulators of erythroid differentiation, in CD36+ cells, then determined the genomic positions of the catalytic subunit BRG1 of the BAF complexes and the nucleosome landscapes, by ChIP-Seq and Mnase-Seq, respectively, for both HSCs and the differentiated cells. We compared changes in nucleosome landscapes with BRG1 binding at GATA1 and TAL1 binding sites and found that BRG1 binding is correlated with nucleosome shifting away from the binding sites, which is critical for TAL1 binding. To confirm that BRG1 is responsible for the nucleosome shift, we knocked down BRG1 in CD36+ cells and analyzed the nucleosome changes in the knockdown cells. The data indicated that inhibition of BRG1 caused a nucleosome shift towards the GATA1 or TAL1 sites, indicating that BRG1 is indeed responsible for the observed nucleosome shift.
2011-07-01 | E-GEOD-26501 | biostudies-arrayexpress
Project description:B19V NS1 is known to be cytotoxic and involved in the pathogenesis of B19V infection. Our previous data demonstrated that NS1 impaired the cell-cycle progression of the CD36+ EPCs by inducing a stable G2 arrest. Microarray analysis was used to identify genes whose expressions were associated with the NS1-induced G2 arrest. A total of 1045 genes displayed a more than 1.5-fold differential expression in the NS1-transduced cells. Out of 1045 differentially expressed genes, 177 were involved in cell-cycle regulation and 51 were involved in the regulation of cell differentiation. Keywords: RNA CD36+ EPCs were generated from CD34+ stem cells, and transduced with B19V NS1 or control-lentivirus for 12, 24,and 48 hours. Each sample has triplicates. There are 18 samples analyzed.
2010-11-03 | E-GEOD-18906 | biostudies-arrayexpress
Project description:Analysis of sodium butyrate（NaBu） on angiotensin II（Ang II-induced cardiac fibrosis at gene expression level. The hypothesis tested in the present study was that NaBu influence the balance of gene expression of Ang II-induce cardiac fibrosis. Results provide important information of the response of NaBu to cardiac fibrosis, such as specific genes, up- or down-regulated specific cardiac cellular functions.
2021-12-01 | GSE142436 | GEO
Project description:Knockdown of HSPA9 causes a dose-dependent decrease in erythroid maturation of CD34+ cells differentiated in culture. Due to differences in the degree of differentiation, a more homogeneous population was selected for using FACS and the gene expression profile of these cells was compared. We used a lentiviral vector (pLKO.1) expressing short hairpin RNAs targeting either luciferase (control shLUC) or HSPA9 (shHSPA9-433) to knock down expression of HSPA9. We isolated CD34+ cells from human cord blood (Day 0), transduced cells with a lentiviral vector (Day 1), selected for transduced cells with puromycin and differentiated them in erythroid culture media before FACS isolation of the CD34+/CD71- population (Day 5). Four independent CD34+ populations were isolated, differentiated and sorted for biologic replicates.
2016-02-23 | E-GEOD-78164 | biostudies-arrayexpress
Project description:Signaling through the AKT and ERK pathways controls cell proliferation. However, the integrated regulation of this multistep process, involving signal processing, cell growth and cell-cycle progression, is poorly understood. Here we study different murine hematopoietic cell types, in which AKT and ERK signaling is triggered by erythropoietin (Epo). Although these cell types share the molecular network topology for pro-proliferative Epo signaling, they exhibit distinct proliferative responses. Iterating quantitative experiments and mathematical modeling, we identify two molecular sources for cell-type-specific proliferation. First, cell-type-specific protein abundance patterns cause differential signal flow along the AKT and ERK pathways. Second, downstream regulators of both pathways have differential effects on proliferation, suggesting that protein synthesis is rate-limiting for faster-cycling cells while slower cell-cycles are controlled at the G1-S progression. The integrated mathematical model of Epo-driven proliferation explains cell-type-specific effects of targeted AKT and ERK inhibitors and faithfully predicts based on the protein abundance anti-proliferative effects of inhibitors in primary human erythroid progenitor cells. Our findings suggest that the effectiveness of targeted cancer therapy might become predictable from protein abundance patterns.
2017-01-30 | PXD004816 | Pride
Project description:Lipid accumulation associated with immune cell infiltration leading to hepatocellular ballooning and lobular inflammation are the cardinal features of NASH. With onset and development of multi-omics approaches in the last decade, we have been able to comprehend the existence and functionality of gut microbial ecology. Apart from the compositional variation (dysbiosis), functional alteration of the microbial population i.e., the impact of the crosstalk between gut microbiota-derived metabolites with host cells also remains elusive in terms of regulation of immunometabolic homeostasis and overall human health and disease. Sodium butyrate (NaBu), a short chain fatty acid derived metabolite is known to modulate the inflammatory status of NASH pathogenesis; however, its mechanism of action is not clearly deciphered. To unveil the immunomodulatory activity of NaBu, we found robust anti-inflammatory effect of NaBu in diet induced NASH model with reduced macrophage infiltration. Mechanistically, independent of p65 nuclear translocation, by maintaining the enhanced acetylation status of p65 along with differential p65 recruitment to the proinflammatory gene promoter, NaBu suppressed the inflammatory milieu and resulted in better prognosis. Along with transcriptional rewiring, NaBu also altered the metabolic status, modified the functional outcome and exhibited differential secretome which ultimately resulted skewing of macrophages towards a prohealing phenotype and induced autocrine as well as paracrine death of proinflammatory macrophages to abrogate inflammation in both isolated LMs and in vivo model.
2023-01-15 | GSE219093 | GEO