Ontology highlight
ABSTRACT:
PROVIDER: PRJNA849620 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19664635_1.fastq.gz | Fastqsanger.gz | |||
| SRR19664635_2.fastq.gz | Fastqsanger.gz | |||
| SRR19664650_1.fastq.gz | Fastqsanger.gz | |||
| SRR19664650_2.fastq.gz | Fastqsanger.gz | |||
| SRR19664651_1.fastq.gz | Fastqsanger.gz |
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Project description:An important cellular defense mechanism against oxidative stress is the induction of genes involved in ROS resistance and DNA damage repair. Under normal conditions, Sod1 is localized mainly in the cytosol. However, we found that Sod1 translocates into the nucleus after oxidative stress. To address the physiological role of Sod1, we performed DNA microarray analysis of global gene expression in wild type (WT) and sod1Δ cells before and after treatment with H2O2.
2014-03-18 | GSE55081 | GEO
Project description:Overexpression of p21 in NEMOΔhepa animals protects against DNA damage, acceleration of hepatocarcinogenesis and cholestasis. As strengthened by our LPS stimulation experiments, we identified a novel protective role of p21 against DNA damage.
2015-03-01 | GSE61100 | GEO
Project description:Overexpression of p21 in NEMOM-NM-^Thepa animals protects against DNA damage, acceleration of hepatocarcinogenesis and cholestasis. As strengthened by our LPS stimulation experiments, we identified a novel protective role of p21 against DNA damage. Expression profiling of livers from wild type, NEMO, and NEMO-P21 null mice.
2015-03-01 | E-GEOD-61100 | biostudies-arrayexpress
Project description:Reactive oxygen species (ROS) generated as by-products of metabolism can induce stochastic damage to cellular components including DNA. A localised oxidative damage may arise during transcriptional activation at promoters of protein coding genes. ROS are generated during oxidative demethylation of histones and 5-methyl cytosine in promoter CpG clusters. ROS induced oxidation of DNA bases, mainly 7,8-dihydro-8-oxoguanine (8-oxoG) is normally resolved through a well characterised repair pathway where the oxidised base is first removed by components of base excision repair (BER) pathway, and the resulting breaks in the DNA backbone are subsequently repaired by the single-strand repair (SSBR) machinery that includes TDP1 and XRCC1. In this project we have identified the role of a putative mitotic assembly protein, TDIF in ROS induced single strand break repair. Using semi-quantitative LC-MS/MS and biochemical assays we show that the long isoform of TDIF specifically interacts with SSBR machinery after oxidative damage.
2022-10-12 | PXD018002 | Pride
Project description:Tardigrades are remarkable in their ability to survive extreme environments. The damage suppressor (Dsup) protein is thought responsible for their extreme resistance to reactive oxygen species (ROS) generated by irradiation. Here we show that expression of Ramazzottius varieornatus Dsup in Saccharomyces cerevisiae reduces oxidative DNA damage and extends the lifespan of budding yeast with chronic oxidative damage. This protection from ROS requires either the Dsup HMGN-like domain or sequences C-terminal to same. Dsup associates with no apparent bias across the yeast genome, using multiple modes of nucleosome binding; the HMGN-like region interacts with both the H2A/H2B acidic patch and H3/H4 histone tails, while the C-terminal region binds DNA. These findings give precedent for engineering an organism by physically shielding its genome to promote survival and longevity in the face of oxidative damage.
2024-01-14 | GSE237436 | GEO
Project description:An important cellular defense mechanism against oxidative stress is the induction of genes involved in ROS resistance and DNA damage repair. Under normal conditions, Sod1 is localized mainly in the cytosol. However, we found that Sod1 translocates into the nucleus after oxidative stress. To address the physiological role of Sod1, we performed DNA microarray analysis of global gene expression in wild type (WT) and sod1M-NM-^T cells before and after treatment with H2O2. Early log phase WT and sod1M-NM-^T cells were treated with or without H2O2 for 20 min and RNA samples were extracted and subjected to hybridization on Affymetrix microarrays. We then compared the dataset of WT +/- H2O2 with SOD1 deleted cells +/- H2O2 to identify the H2O2-responsive genes whose induction was attenuated in sod1M-NM-^T cells by more than 50%.
2014-03-18 | E-GEOD-55081 | biostudies-arrayexpress
Project description:Reactive oxygen species (ROS) are extensively assessed in physiological and pathological studies; however, the genes and mechanisms involved in antioxidant reactions are elusive. To address this knowledge gap, we used a forward genetic approach with mouse haploid embryonic stem cells (haESCs) to generate high-throughput mutant libraries, from which numerous oxidative stress-targeting genes were screened out. We performed proof-of-concept experiments to validate the potential inserted genes. Slc25a43 (one of the candidates) knockout (KO) ESCs presented reduced damage caused by ROS and higher cell viability when exposed to H2O2. Subsequently, ROS production and mitochondrial function analysis also confirmed that Slc25a43 was a main target gene of oxidative toxicity. In addition, we identified that KO of Slc25a43 activated mitochondria-related genes including Nlrx1 to protect ESCs from oxidative damage. Overall, our findings facilitated revealing target genes of oxidative stress and shed lights on the mechanism underlying oxidative death.
2022-03-16 | GSE198548 | GEO
Project description:Background: Pseudomonas aeruginosa, a pathogen infecting those with cystic fibrosis, encounters toxicity from phagocyte-derived reactive oxidants including hydrogen peroxide during active infection. P. aeruginosa responds with adaptive and protective strategies against these toxic species to effectively infect humans. Despite advances in our understanding of the responses to oxidative stress in many specific cases, the connectivity between targeted protective genes and the rest of cell metabolism remains obscure. Results: Herein, we performed a genome-wide transcriptome analysis of the cellular responses to hydrogen peroxide in order to determine a more complete picture of how oxidative stress-induced genes are related and regulated. Our data reinforce the previous conclusion that DNA repair proteins and catalases may be among the most vital antioxidant defense systems of P. aeruginosa. Our results also suggest that sublethal oxidative damage reduces active and/or facilitated transport and that intracellular iron might be a key factor for a relationship between oxidative stress and iron regulation. Perhaps most intriguingly, we revealed that the transcription of all F-, R-, and S-type pyocins was upregulated by oxidative stress and at the same time, a cell immunity protein (pyocin S2 immunity protein) was downregulated, possibly leading to self-killing activity. Conclusions: This finding proposes that pyocin production might be another novel defensive scheme against oxidative attack by host cells. Experiment Overall Design: We conducted four and five independent microarray experiments with biological replicates in the absence (control) and the presence (experimental) of hydrogen peroxide, respectively.
2007-07-19 | E-GEOD-3090 | biostudies-arrayexpress
Project description:Oxidative modifications can disrupt protein folds and functions, and are strongly associated with human aging and diseases. Conventional oxidation pathways typically involve the free diffusion of reactive oxygen species (ROS), which primarily attack the protein surface. Yet, it remains unclear whether and how internal protein folds capable of trapping oxygen (O2) contribute to oxidative damage. Here, we report a novel pathway of protein damage, which we refer to asO2-confined photooxidation. In this process, O2 is captured in protein cavities and subsequently converted into multiple ROS, primarily mediated by tryptophan residues under blue light irradiation. The generated ROS then attack the protein interior through constrained diffusion, causing protein damage. The effects of this photooxidative reaction appear to be extensive, impacting a wide range of cellular proteins,as supported by whole-cell proteomic analysis. This photooxidative mechanism may represent a latent oxidationpathway in human tissuesdirectly exposed to visible light, such as skin and eyes.
2024-11-27 | PXD056895 | JPOST Repository
Project description:Ionizing radiation-induced changes to the redox balance does not only represent a risk for the cellular homeostasis, but can also induce a drastic modulation in the overall signalling system of cells. In the current study, effects of chronic exposure to ionizing gamma radiation were assessed in the radioresistant nematode Caenorhabditis elegans in order to understand whether antioxidant defences (AODs) could ameliorate radical formation, or if increased ROS levels would cause oxidative damage. This analysis was accompanied by phenotypical as well as molecular investigations, via assessment of reproductive capacity and somatic growth and differential gene expression through RNA sequencing. The use of a fluorescent reporter strain (sod1::gfp) and two ratiometric biosensors (Hyper and Grx1-roGFP2) demonstrated increased ROS production (H2O2) and activation of AODs (SOD1 and GPx) in vivo. The data indicate that at dose-rates ≤10 mGy/h defence mechanisms were able to prevent the manifestation of oxidative stress. In contrast, at dose-rates ≥40 mGy/h the constant formation of radicals induced a redox shift, which lead to oxidative damage responses, including changes in mitochondrial metabolism and functions, protein degradation, lipid metabolism, collagen synthesis and modulation of transcription. Moreover, genotoxic effects were among the most over-represented functions affected by chronic gamma irradiation, as indicated by differential regulation of genes involved in DNA damage, DNA repair, cell-cycle checkpoints, chromosome segregation and chromatin remodelling. Ultimately, the exposure to gamma radiation caused reprotoxic effects, with >20% reduction in the number of offspring per adult hermaphrodite at dose-rates ≥40 mGy/h, accompanied by the down-regulation of more than 300 genes related to reproductive system, meiotic functions and gamete development and fertilization.
2019-10-17 | E-MTAB-8284 | biostudies-arrayexpress