E-GEOD-39690
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA171484
PROVIDER: E-GEOD-39690 | ExpressionAtlas | 2016-01-08
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Transcriptome analysis of ire1 mutants after treatment with or without tunicamycin in the presence of actinomycin D
| PRJNA171484 | ENA
Project description:Ribosome profiling (RiboSeq) analysis of murine 17 clone 1 (17Cl-1) cells with and without Tunicamycin treatment. Tunicamycin is known to induce the unfolded protein response, and the objective of this work was to assess the impact of Tunicamycin on cellular translation. Additionally, we sought to assess the impact of differing library preparation methods by using three separate approaches: flash freezing, 1X Cycloheximide, and 100X Cycloheximide.
2021-11-09 | E-MTAB-5391 | biostudies-arrayexpress
Project description:Methicillin resistance in Staphylococcus aureus depends on the production of mecA, which encodes penicillin-binding protein 2A (PBP2A), an acquired peptidoglycan transpeptidase with reduced susceptibility to beta-lactam antibiotics. Here, we show that preventing the expression of wall teichoic acids (WTAs) genetically or with a TarO inhibitor sensitizes MRSA strains to beta-lactams although PBP2A is still expressed. Using S. aureus microarrays and array data analysis protocols (NIAID's Pathogen Functional Genomics Resource Center) we have characterized the transcriptomes of S. aureus COL. in order to further understand the sensitization of strain COL to methicillin by tunicamycin we determined the tunicamycin and methicillin transcriptomes alone and in combination. Methicillin treatment of COL at 500 µg/mL had almost no effect on cell growth rate and, remarkably, the only gene in the transcriptome that showed a more than two-fold change in expression was lytM, which was downregulated. The tunicamycin transcriptome of COL, acquired at 0.4 µg/mL, shows modest changes compared to the untreated control both in terms of the total numbers of affected genes and in the degree of up- or downregulation. Several of the genes upregulated upon tunicamycin treatment are part of the cell wall stress stimulon.COL was grown with methicillin to an OD600 ~0.4, and challenged with tunicamycin for 2 hrs whereas the control culture contained methicillin alone. transcriptome for COL growing in the presence of both agents showed extensive changes in gene expression. , the cell wall stress stimulon, which was not induced by methicillin when tunicamycin was absent, was clearly induced in its presence and the changes were far more dramatic than observed with tunicamycin alone. ). vraS and vraR, which encode a two component signaling system dedicated to the cell wall regulon, were upregulated 3.8 and 3.7 fold, respectively. Other upregulated cell wall stress stimulon genes include pbp2, fmtA, mvaD (mevalonate diphosphate decarboxylase), crtN (dehydrosqualene desaturase) mvak1 (mevalonate kinase), recU, SAV1424 (methionine sulfoxide reductase A), prsA (peptidyl-prolyl cis/trans isomerase), tcaA (Tca protein) and cwrA. A considerable number of genes were also downregulated upon challenge of COL with the combination of tunicamycin and methicillin. These included sspB, lrgA, dltA, capL, SAS0988, sspA, pflB, and spa. Several of these genes have been found to be downregulated in previous studies of cell wall-active antibiotic challenge of S. aureus.
2010-10-20 | GSE24439 | GEO
Project description:To obtain a better understanding of molecular mechanisms underlying the DNA damage response in Δckb1 and Δckb2 mutants, transcriptome analyses were performed between WT, Δckb1, and Δckb2 strains. Comparative transcriptome analysis of Δckb1 and Δckb2 mutants showed similar transcriptional profiles in the presence and absence of MMS. The data also indicated that compared with WT, about 200 genes were up or downregulated in Δckb1 and Δckb2 strains with or without treatment with 0.01% MMS. GO analysis highlighted that the differentially expressed genes in Δckb1 and Δckb2 were significantly enriched in the processes related to the programmed formation of DNA double-strand breaks (DSBs), recombination, and DNA repair coordination of the meiotic cell cycle.
2023-10-11 | GSE232439 | GEO
Project description:To investigate the gene expression upon mitochondrial stress, oligomycin A or ER stress, tunicamycin treatment, we established HCT116 cell lines after 24h treatment of oligomycin A or tunicamycin.
2023-05-03 | GSE226549 | GEO
Project description:Transcriptomics analysis of wild type and osm-3(dh441)IV under vehicle and tunicamycin treatment for 6 hours
2020-02-04 | GSE144675 | GEO
Project description:Purpose: Evaluate transcriptional changes in glioma derived stem cells, U251, and normal human astrocytes following treatment with NH125, Tunicamycin, or 0.1% DMSO Methods: Glioma derived stem cells, U251 and Normal Human Astrocytes were plated in individual dishes and treated with either 2.5 micromolar NH125, 1.0 mcg/mL Tunicamycin, or 0.1% DMSO (vehicle) for twenty-four hours followed by total RNA extraction, library preparation and next generation sequencing Results: Using our analysis pipeline we mapped our sequence reads to the reference genome GRCh38. Following read count normalization and differential expression of NH125 and tunicamycin treated samples to vehicle treated controls we found that NH125 and tunicamycin treatment lead to activation of similar signalling pathways Conclusions: We present an optimized workflow for analysis of transcriptional changes in drug treated glioma derived stem cells, glioblastoma cells and normal human astrocytes
2018-03-02 | GSE102505 | GEO
Project description:Accumulation of aggregated and misfolded proteins, leading to endoplasmic reticulum stress and activation of the unfolded protein response, is a hallmark of several neurodegenerative disorders, including Alzheimer’s and Parkinson’s disease. Genetic screens are powerful tools that are proving invaluable in identifying novel modulators of disease associated processes. Here, we performed a loss-of-function genetic screen using a human druggable genome library, followed by an arrayed-screen validation, in human iPSC-derived cortical neurons. We identified 13 genes, whose knockout was neuroprotective against Tunicamycin, a glycoprotein synthesis inhibitor widely used to induce endoplasmic reticulum stress. We also demonstrated that pharmacological inhibition of KAT2B, a lysine acetyltransferase identified by our genetic screens, by L-Moses, attenuates Tunicamycin-mediated neuronal cell death and activation of CHOP, a key pro-apoptotic member of the unfolded protein response in both cortical and dopaminergic neurons. Follow-up transcriptional analysis suggested that L-Moses provided neuroprotection by partly reversing the transcriptional changes caused by Tunicamycin. Finally, L-Moses treatment attenuated the total protein levels affected by Tunicamycin, without affecting their acetylation profile. In summary, using an unbiased approach, we identified KAT2B and its inhibitor, L-Moses, as potential therapeutic targets for neurodegenerative diseases.
2023-03-10 | PXD038395 | Pride
Project description:Microarray analysis was performed to evaluate the changes in gene expression that are associated with manf-1 deficiency with and without exposure to tunicamycin. RNA was isolated from four groups, (wildtype (N2) and manf-1 mutant (tm3603) L1 stage larve with and without 5 hours exposure to tunicmycin (5microgram/milliliter)) for transcriptomic profiles analysis
2019-06-26 | GSE118294 | GEO
Project description:GPT inhibitor Tunicamycin develops ER stress causing anti-angiogenic response in breast tumor microvasculature due to unfolded protein response-mediated apoptosis. cDNA microarray identified 123 and 454 differentially regulated genes with 10 genes overlapping between 3h and 32 h of Tunicamycin treatment. Alg-2 expression is inconsistent but not the Dpms. Evidences support that Tunicamycin completely destroys DPMS activity in capillary endothelial cells without affecting its protein or the mRNA levels but by knocking down the phosphorylation. DPMS’ contribution to developing upr during ER stress has therefore been evaluated because of its inherent regulatory property of GPT. FTIR spectroscopy confirmed protein denaturation. Restablishing the phosphorylation status helps the DPMS regaining its activity. As a result, ER stress is reduced reversing apoptosis and bringing more cells into cycling with normal cellular morphology. Furthermore, differential expression of DPMS in breast tumor microvasculature during Tunicamycin therapy raises its potential as a tumor prognostic marker in the clinic.
2017-11-15 | GSE33729 | GEO