E-GEOD-44343
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA189508PRJNA189507PRJNA189506
PROVIDER: E-GEOD-44343 | ExpressionAtlas | 2015-12-02
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-44343-analysis-methods.tsv | Tabular | |||
| E-GEOD-44343-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-44343-configuration.xml | Xml | |||
| E-GEOD-44343-percentile-ranks.tsv | Tabular | |||
| E-GEOD-44343.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 50 |
Similar Datasets
Project description:Effect of NDRG3 overexpression on cell response to hypoxia
| PRJNA238940 | ENA
Project description:Effect of AtHRE1 and AtHRE2 overexpression in normoxia and hypoxia
| PRJNA117819 | ENA
Project description:The effect of the overexpression of Plant Cysteine Oxidase (PDCO1) on the transcriptome of Arabidopsis resettes was investigated with plants subjected to a 4h hypoxia (5% O2 v/v in air). For this purpose, 4-week old rosette of wild-type and 35S:FLAG:CDO1 plants were compared. Samples were composed of pools of 5 plants. In total, 6 samples were analyzes, subdivided in 2 thesis with 3 replicates each. 35S:PCO1 plants (treated with hypoxia) were compared to wild-type plants (treated with hypoxia).
2014-02-07 | E-GEOD-44343 | biostudies-arrayexpress
Project description:Hypoxia is known to regulate tumor-initiating cells and to have an effect on miRNA expression. We were interested in studying the role of hypoxia-induced miR-210 in colorectal cancer patient-derived sphere cultures. Downregulated genes after overexpression of miR-210 were retained as potential miR-210 target genes for further validation sudies.
2016-10-27 | GSE80236 | GEO
Project description:Rapidly proliferating tumors are exposed to a hypoxic microenvironment due to their density, high metabolic consumption, and interruptions in blood flow due to immature angiogenesis. Cellular responses to hypoxia promote highly malignant and metastatic behavior, as well as a chemotherapy-resistant state. In order to better understand the complex relationships between hypoxic adaptations and cancer progression, we studied the dynamic proteome responses of glioblastoma cells exposed to hypoxia via an innovative approach: quantification of newly synthesized proteins using heavy stable-isotope arginine labeling combined with accurate assessment of cell replication by quantification of the light/heavy arginine ratio of peptides in histone H4. We found that hypoxia affects cancer cells in multiple intertwined ways: inflammation, typically with over-expressed glucose transporter (GLUT1), DUSP4/ MKP2, and RelA proteins; a metabolic adaptation with overexpression of all glycolytic pathway enzymes for pyruvate/lactate synthesis; and the EMT (epithelial-mesenchymal transition) and cancer stem cell (CSC) renewal with characteristic morphological changes and mesenchymal/CSC protein expression profiles. For the first time, we identified the vitamin B12 transporter protein TCN2, which is essential for one-carbon metabolism, as being significantly downregulated. Further, we found, by knockdown and overexpression experiments, that TCN2 plays an important role in controlling cancer cell transformation towards the highly aggressive mesenchymal/CSC stage; low expression of TCN2 has an effect similar to hypoxia, while high expression of TCN2 can reverse it. We conclude that hypoxia induces sequential metabolic responses of one-carbon metabolism in tumor cells.
2017-09-07 | PXD007280 | Pride
Project description:Hypoxia stress (<1% oxygen) followed by reoxygenation, is accompanied by formation of reactive oxygen species (ROS) and nitric oxide (NO), which act as signaling molecules, but also cause nitro-oxidative stress. The NO concentration is regulated by phytoglobins (formerly hemoglobins) in the NO cycle. To understand how changes in phytoglobin expression affect plant metabolism under hypoxia, we studied the proteome and metabolome of barley (Hordeum vulgare L., cv. Golden Promise) plants without (WT) or with (HO) overexpression of phytoglobins. WT plants were more susceptible to hypoxia than HO. The chlorophyll a+b content was lowered by 50% and biomass by 30% in WT24, compared to WT, while HO plants were unaffected. We observe increase in ROS production during hypoxia treatment in WT seedlings had that was not observed in HO seedlings. But most importantly we identified and quantified 9694 proteins out of which 1107 changed significantly in abundance in at least one of the four comparisons – HO/WT andHO24/WT24) (giving genotype differences), WT24/WT and HO24/HO giving treatment differences. The main proteome changes between genotypes shown that many proteins were downregulated in HO24/HO but not in WT24/WT, such as ion transporters, Ca2+ signal transduction, and proteins related to protein degradation. We also identified and quantified 1470 metabolites, and the abundance of >500 changed significantly. Hypoxia had a much larger overall effect on the metabolome than overexpression of phytoglobin. The metabolites that have the biggest influence on the differences between treatments were selected for further analysis, among them many amino acids, putrescine and metabolites taking part in glycolysis.
2020-03-02 | PXD017103 | Pride
Project description:Hypoxia inducible factor-2 alpha (HIF-2α) overexpression effect on primary mouse articular chondrocytes
| PRJNA413831 | ENA
Project description:The effect of the overexpression of Plant Cysteine Oxidase (PDCO1) on the transcriptome of Arabidopsis resettes was investigated with plants subjected to a 4h hypoxia (5% O2 v/v in air). For this purpose, 4-week old rosette of wild-type and 35S:FLAG:CDO1 plants were compared. Samples were composed of pools of 5 plants.
2014-02-07 | GSE44343 | GEO
Project description:Cellular senescence is a stress response mechanism maintaining tissue homeostasis by changing physiological state and inducing irreversible proliferative arrest. It has been reported that hypoxia can bypass senescence and extend lifespan of naïve primary cells, mainly, by the decrease in oxidative damage. However, it is unclear how hypoxia can promote the evasion of senescence and promote cell immortalization prior to malignant transformation. We observed that the lifespan of MEFs is increased when they are cultured in hypoxia, reducing the expression of p16INK4a, p15INK4b and p21Cip1. In transcriptional genetic screenings, we found that proliferating naïve MEFs in hypoxia overexpress Tfcp2l1, which is a main regulator of pluripotency and self-renewal in embryonic stem cells, ESCs, as well as stemness-associated genes like Oct3/4, Sox2, Nanog. Tfcp2l1 expression is lost during culture in normoxia. The expression of Tfcp2l1 in hypoxia seems to be regulated by Hif1α and only when it is overexpressed at similar levels to those induced physiologically by hypoxia it increases lifespan of MEFs and promotes overexpression of stemness-associated genes. In Chip-seq experiments, we found that Tfcp2l1 binds and activate the expression of genes which regulate proliferation, which in many cases, are also related to stem cell properties, such as Sox2, Sox9 and Tgfa. Additionally, Tfcp2l1 can replicate the effect of hypoxia increasing cellular reprogramming and its expression correlates positively with the expression of Nanog and negatively with p21Cip1 and p16INK4a. Altogether, our data suggests that the activation of Tfcp2l1 by hypoxia could be relevant in the immortalization prior to malignant transformation, facilitating tumorigenesis and dedifferentiation of cells.
2024-02-22 | GSE173648 | GEO