E-MEXP-1957
Ontology highlight
ABSTRACT:
PROVIDER: E-MEXP-1957 | ExpressionAtlas | 2015-10-22
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MEXP-1957-analysis-methods.tsv | Tabular | |||
| E-MEXP-1957-atlasExperimentSummary.Rdata | Rdata | |||
| E-MEXP-1957-configuration.xml | Xml | |||
| E-MEXP-1957-configuration.xml.auto.old | Xml | |||
| E-MEXP-1957-percentile-ranks.tsv | Tabular |
Items per page: 5 1 - 5 of 203 |
Similar Datasets
Project description:Oxidative stress is induced by various natural abiotic factors including irradiation among many microorganisms and has been demonstrated that it significantly improved growth rate and lipid production of R. glutinis. However, the specific mechanisms of how irradiation influence the metabolism of R. glutinis remains still unavailable. To investigate and better understand the mechanisms involved in irradiation-induced stress resistance in R. glutinis, a multi-omics metabolism analysis was implemented. The results confirmed that irradiation indeed not only improve cell biomass but also accelerate carotenoids and lipid production, especially neutral lipid. Compared with the control, metabolome profiling in the group exposed to irradiation exhibited obvious difference in the activation of TCA cycle and transition of glucose utilization pattern from glycolysis to pentose phosphate pathway. The results of proteome showed that 423 proteins were changed significantly and proteins associated with protein folding and transport, the Hsp40 and Sec12, were obviously up-regulated, indicating that cells responded to irradiation by accelerating the protein folding and transport of correctly folded proteins as well as enhanced the degradation of misfolded proteins. A significant up-regulation of carotenoids biosynthetic pathway was observed which revealed that increased carotenoids is a cellular defense mechanism against oxidative stress generated by irradiation. Therefore, the results of comprehensive omics analysis provide new insights on the response and tolerance mechanism of R. glutinis to irradiation-induced oxidative stress resistance and could be helpful in the further investigation of R. glutinis as model microorganism for biofuel production.
2018-10-25 | PXD009678 | Pride
Project description:Purpose: to explore the function and mechanism of skin damage induced by ultraviolet irradiation. The mouse model of UVB irradiation was established. Using miRNA Sequence analysis, the miRNA expression profile of the mouse skin model exposed to UVB radiation and the normal skin mice. GO and Pathway analysis were employed for the prediction of miRNA targets. Results:Compared with normal skin, a total of 23 miRNAs were screened for significantly different expressions. Among them, 7 miRNAs were up-regulated and 16 were down-regulated in the skin wound tissue of mice exposed to UVB irradiation. The differential expression of miRNA is related to a variety of signal transduction pathways, among which mmu-miR-195a-5p and mitogen-activated protein kinase (MAPK) signal pathway is worthy of attention. Conclusion: There was significant difference expression of miRNA in the skin tissue of normal mice and the skin injury induced by UVB irradiation. Differential expression of miRNA can be used in the diagnosis and treatment of UVB-induced acute skin injury.
2024-08-08 | GSE181657 | GEO
Project description:Arabidopsis plants (Col-0) were exposed to heat stress (40oC) or microwave irradiation (23W) for 1h. Shoots were sampled and transcripts significantly up- or down-regulated by heat stress or microwave irradiation were investigated.
2025-04-30 | GSE241899 | GEO
Project description:Primary term human trophoblasts exposed to ionizing irradiation
| PRJNA215352 | ENA
Project description:human hepatoma Hep3B cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-10-20 | GSE65678 | GEO
Project description:human hepatoma Hep3B cells were treated with 40 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with Hep3B_UV_40J-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in Hep3B_UV_40J-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in Hep3B_UV_40J-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of Hep3B_UV_40J-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in Hep3B_UV_40J-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-02-06 | GSE65676 | GEO
Project description:LAP-35 and SK-N_MC cells were treated with 10 J/m2 UV light versus untreated Alternative pre-mRNA processing plays a key role in the response to DNA damage as well as in neoplastic transformation. We found that two Ewing Sarcoma (ES) cell lines exhibit different sensitivity to UV light irradiation, with SK-N-MC cells being more sensitive than LAP-35 cells. RNA profiling during the response to low doses of UV light irradiation revealed genes differentially regulated between the two cell lines. In particular, UV light irradiation induced a novel isoform of the RNA helicase DHX9 which is targeted to nonsense-mediated decay (NMD) and therefore causes down-regulation of DHX9 in SK-N-MC cells, but not in LAP-35 cells. DHX9 protein forms a complex with RNA polymerase II (RNAPII) and EWS-FLI1 to enhance transcription, and we found that down-regulation of DHX9 by UV light irradiation in SK-N-MC cells impairs the recruitment of EWS-FLI1 to target genes and increases sensitivity to DNA damage. Notably, sensitivity of SK-N-MC cells to irradiation correlated with enhanced phosphorylation and decreased processivity of RNAPII upon irradiation, which in turn causes inclusion of the novel DHX9 exon in SK-N-MC cells exposed to UV light, an observation that could be recapitulated in LAP35 cells by pharmacological reduction of RNAPII processivity. Our data suggest that EWS-FLI1 oncogene activity could be targeted by modulation of DHX9 gene expression.
2015-10-20 | GSE59889 | GEO
Project description:Abstract Background: Faithful transcription of DNA is constantly threatened by different endogenous and environmental genotoxic effects. Transcription coupled repair has been described to quickly remove DNA lesions from the transcribed strand of active genes, permitting rapid resumption of blocked transcription. This repair mechanism has been well characterized in the past using individual target genes. However, the precise mechanism by which RNA polymerase II (Pol II) transcription is affected following UV irradiation during the repair processes genome-wide is not well understood. Results: We investigated the effect of a non-lethal dose of UVB on global DNA-bound Pol II distribution in human cells. We find that about 90% of the promoters of expressed genes show reduced Pol II occupancy 2-4 hours following UVB irradiation, and that the presence of Pol II is restored to “normal”, or higher, levels 5-6 hours after irradiation. We also identified a smaller set of genes, where the presence of Pol II at the promoter regions does not decrease after UVB irradiation, but often increases throughout the entire transcription units. Interestingly, at promoters, where Pol II promoter clearance occurs, TFIIH but not TBP follows the behavior of Pol II suggesting that at these genes TFIIH may be sequestered for DNA repair upon UVB treatment. Conclusions: Thus, our study reveals a global negative regulatory mechanism that targets Pol II transcription initiation on the large majority of transcribed genes following sublethal UVB irradiation, and a small subset of genes (including regulators of repair, cell growth and survival), where Pol II escapes this negative regulation. Following genome-wide RNA Polymerase II redistribution over time upon UVB irradiation
2014-07-25 | E-GEOD-52789 | biostudies-arrayexpress
Project description:Total lung RNA from 3 mouse strains after 18Gy thoracic irradiation. Thoracic cavity radiotherapy is limited by the development of alveolitis and fibrosis in susceptible patients. To define the response to 18 Gy pulmonary irradiation in mice, at the expression level, and to identify pathways which may influence the alveolitis and fibrosis phenotypes expression profiling was completed. Male mice of three strains, A/J (late alveolitis response), C3H/HeJ (C3H, early alveolitis response) and C57BL/6J (B6, fibrosis response) were exposed to thoracic radiation, euthanised when moribund and lung tissue gene expression was assessed with microarrays.
2009-09-11 | GSE2250 | GEO
Project description:Transcription profiling of wild type and DNA repair-deficient cells upon exposure to ultraviolet irradiation.
2009-04-01 | E-MEXP-1968 | biostudies-arrayexpress