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 |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Introduction: Ischemia/reperfusion injury (IRI) is a common damage due to the restoration of blood flow after an ischemic insult. The pathogenesis of IRI is mainly linked to the production of ROS which sustain cell damage and ultimately promote cell death. The tardigrade damage suppressor protein (Dsup) is a DNA-binding protein that enables tardigrades to tolerate stress conditions including oxidative stress. Aim: We aim to investigate the ability of the tardigrade-derived Damage Suppressor (Dsup) protein to protect human cells from IRI, using an in vitro model of hypoxia and reoxygenation. Methods: The protective role of the tardigrade Dsup protein against ischemia-reperfusion injury was studied in transfected HEK293T cells. We analyzed cell viability, oxidative stress, and the expression of antioxidant proteins using functional assays, proteomics, and Western Blotting. Results: Dsup expression significantly enhanced cell survival following hypoxia-reoxygenation and markedly reduced intracellular ROS levels. Proteomic and Western Blot analyses revealed a significant upregulation of antioxidant enzymes in Dsup-expressing cells. Furthermore, Dsup modulated autophagy and key stress-related pathways, including the MAPK cascade. Dsup remained cytoplasmic under all conditions, and its expression was notably increased by hypoxic stimulus. Conclusion: This study demonstrate that Dsup protects human cells from ischemia-reperfusion injury by reducing oxidative stress and modulating key cytoprotective pathways. Our results establish Dsup as a promising candidate for future therapeutic applications against IRI, meriting further exploration in in vivo models.
2025-11-24 | PXD067125 | Pride
Project description:Success of phage therapies is limited by bacterial defenses against phages. While a variety of anti-phage defense mechanisms has been characterized, how expression of these systems is distributed across individual cells and how their combined activities translate into protection from phages has not been studied. Using bacterial single-cell RNA sequencing, we profiled the transcriptomes of ~50,000 cells from cultures of a human pathobiont, Bacteroides fragilis, infected with a lytic bacteriophage. We quantified the asynchronous progression of phage infection in single bacterial cells and reconstructed the infection timeline, characterizing both host and phage transcriptomic changes as infection unfolded. We discovered subpopulations of bacteria that remained uninfected and heterogeneously expressed protective factors. Each cell’s vulnerability to phage infection was defined by combinatorial expression of multiple genetic loci, including phase-variable capsular polysaccharide (CPS) biosynthesis pathways, restriction-modification systems (RM), and a novel operon predicted to encode fimbrial genes. Acting in concert, these heterogeneously expressed anti-phage defense mechanisms create a phenotypic landscape where distinct protective combinations enable the survival and re-growth of bacteria expressing these phenotypes without acquiring additional mutations. The emerging model of complementary action of multiple protective mechanisms heterogeneously expressed across an isogenic bacterial population showcases the potent role of phase variation and stochasticity in bacterial anti-phage defenses.
2026-02-09 | GSE318809 | 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 sod1Δ cells before and after treatment with H2O2.
2014-03-18 | GSE55081 | GEO
Project description:Tissue damage activates immediate responses to restrict further harm and initiate repair. How injury sensing is coupled to regeneration is still not well understood. Here, we studied regenerative responses in the adult Drosophila brain, where proliferation is normally strongly restricted. We show that localized brain damage triggers oxidative stress and diverse brain protective programs. We find that ROS generation by the NADPH Oxidase Duox on glial cells is responsible for injury-induced oxidative stress. Both genetic and chemical suppression of ROS in injured brains lead to impaired regeneration. In particular, selective knock-down of calcium-sensitive duox in glia, which show elevated calcium after injury, strongly reduces injury-induced proliferation. We further provide evidence that diffusing ROS can sustain the activity of pro-regenerative signaling, which is required to stimulate cell divisions. Although oxidative stress is generally considered as harmful in the brain, we uncover here an unanticipated beneficial role of transient ROS release by glia to promote brain repair.
2026-02-09 | GSE309567 | 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: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: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: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