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984 results for “Cell stress”
Data from: Response to persistent er stress in plants: a multiphasic process that transitions cells from prosurvival activities to cell death
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Spermatozoa RRBS data: Post-Bismark aligned files extracted for the methylation call for every single C in the CpG context of sperm cells of Murrah buffalo bulls under heat stress
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Data from: Effect of mitochondrial oxidative stress on regulatory T cell manufacturing for clinical application in transplantation: Results from a pilot study
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prg-1 longevity germline nucleoli: Piwi mutant germ cells transmit a form of heritable stress that promotes longevity
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Supporting Information of the article "mesenchymal stem cell-derived exosomes protect trabecular meshwork from oxidative stress"
<p>Supporting Information of the article "mesenchymal stem cell-derived exosomes protect trabecular meshwork from oxidative stress". </p>
Decoding the Brain Mosaic: Region and Cell Type-Specific Dysregulation Patterns in Stress and Psychiatric Disorders
<p>Supplementary Online Tables for the doctoral thesis "Decoding the Brain Mosaic: Region and Cell Type-Specific Dysregulation Patterns in Stress and Psychiatric Disorders" by Nathalie Gerstner. </p> <p>This repository includes complete lists of differentially expressed and differential hub genes, alongside the results of enrichment analysis for 8 brain regions examined in a mouse model for transcriptomic alterations following glucocorticoid stimulation (Online Tables 1-30). Additionally, the repository encompasses the complete results of differential expression and chromatin accessibility analyses across various cell types examined in postmortem brain tissue of the orbitofrontal cortex (Online Tables 31-37). These findings delineate the transcriptomic and epigenomic changes between psychiatric cases and controls, as well as between donors with high and low genetic risk for psychiatric disorders.</p> <p>The lists of all genes tested in the respective studies, not just the significant ones, can be found in the "GRactivation_MouseBrain_tables.zip" and the "SingleNuc_PostmortemBrain_Tables.zip" archives.</p> <p> </p>
Endogenous plasma resuspension of peripheral blood mononuclear cells prevents preparative-associated stress that modifies polyA-enriched RNA responses to subsequent acute stressors
<p>This dataset is for a 2024 manuscript by Dongyang Li<sup>1,2</sup>, Karina Al-Dahleh<sup>1</sup>, Daniel A. Murphy<sup>3</sup>, Sonya Georgieva<sup>1</sup><em>,</em> Nik Matthews<sup>4</sup>, and Claire L. Shovlin<sup>1,2,5*</sup><strong> </strong>from the <sup>1</sup>National Heart and Lung Institute, Imperial College London, UK; <sup>2 </sup>National Institute for Health Research (NIHR) Imperial Biomedical Research Centre, London, W2 1NY UK; <sup>3</sup>Pharmacy, Imperial College Healthcare NHS Trust; London, W12 OHS, UK ; <sup>4</sup> NIHR Genomic Facility, Faculty of Medicine, Imperial College London; <sup>5</sup> Specialist Medicine, Imperial College Healthcare NHS Trust; London, W12 OHS, UK. </p>
DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C
<p>DNA damage and reticular stress in cytotoxicity and oncotic cell death of MCF-7 cells treated with fluopsin C</p>
Novel insight into the effects of CPXR on Salmonella enteritidis cells during the chlorhexidine treatment and non-stressful growing conditions
<p>The emergence and spread of antimicrobial resistance is a significant global challenge. To solve this emerging problem, the discovery of novel bacterial cellular targets and the critical pathways associated with antimicrobial resistance is urgently needed. In this study, we investigated the role of the two most critical extracytoplasmic stress response regulators, RpoE and CpxR, on the physiology and susceptibility of growing <i>Salmonella</i> <i>enterica</i> serovar Enteritidis cells using the polycationic antimicrobial agent, chlorhexidine (CHX). We showed that deletion of the <i>cpxR</i> gene significantly increased the susceptibility of this organism, whereas deletion of the <i>rpoE</i> gene had no effect on the pathogen's susceptibility to the drug. It has been shown that a lack of the CpxR regulator induces multifaceted stress responses not only in the envelope but also in the cytosol, further affecting the key biomolecules, including DNA, RNA, and proteins. We showed that alterations in cellular trafficking and most of the stress responses are associated with a dysfunctional CpxR regulator during non-stressful (exponential growth phase) conditions, indicating that these physiological changes are intrinsically associated with the lack of the CpxR regulator. In contrast, induction of type II toxin-antitoxin systems and decrease of abundances of enzymes and proteins associated with the recycling of muropeptides and resistance to polymixin and cationic antimicrobial peptides were specific responses of the ∆<i>cpxR</i> mutant to the CHX treatment. Overall, our study provides insight into the effects of CpxR on the physiology of S. Enteritidis cells during the exponential growth phase and drug treatment, which may point to potential cellular targets for the development of an effective antimicrobial agent. </p>
Fig. 12 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 12. Effects of vernicivanol A (9) on MAPKs pathway. (A) Immunoblot analysis of the indicated molecules in SH-SY5Y cells. (B) Grey intensity analysis of p-p38 and p-ERK. Data are presented as the mean SD of three independent experiments. *p <0.05 and ***p <0.001 compared with indicated control. &p <0.05 and ± &&&p <0.001 compared with the H O -treated group.
Fig. 8 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 8. Effects of verniciflavanol A (9) on apoptosis-related proteins. (A) Immunoblot analysis of the apoptosis-related molecules in SH-SY5Y cells. (B) Grey intensity analysis of Bax/Bcl-2, Cl-PARP, and p53. Data are presented as the mean ± SD of three independent experiments. *p <0.05 and **p <0.01 compared with indicated control. &&p <0.01 and &&&p <0.001 compared with the H O -treated group.
Fig. 7 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 7. Effects of verniciflavanol A (9) on cell apoptosis of H2O2 treated SH-SY5Y cells. (A–B) The apoptosis rate was determined by flow cytometry in SH-SY5Y cells. Data are presented as the mean SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&p <0.01 compared with the ± H2O2-treated group.
Fig. 10 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 10. Effects of verniciflavanol A (9) on PI3K/Akt/mTOR pathway. (A) The protein levels of PI3K/Akt/mTOR pathway in SH-SY5Y cells are analyzed by Western Blot. (B) Grey intensity analysis of p-PI3K, p-Akt, p-mTOR. Data are presented as the mean ± SD of three independent experiments. *p <0.05 and ***p <0.001 compared with indicated control. &p <0.05, &&p <0.01, and &&&p <0.001 compared with the H O -treated group.
Fig. 4 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 4. Effects of compounds 9–12 against H2O2-induced oxidative damage in SH-SY5Y cells using MTT assay. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05, &&p <0.01, and &&&p <0.001 compared with the H O -treated group.
Fig. 6 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 6. Effects of verniciflavanol A (9) on mitochondrial membrane potential of H2O2 treated SH-SY5Y cells. (A) Immunofluorescence staining and (B–C) flow cytometry was employed to test mitochondrial membrane potential in SH-SY5Y cells according to kit instructions. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&&p <0.001 compared with the H O -treated group.
Fig. 9 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 9. Effects of verniciflavanol A (9) on Nrf2/HO-1 signaling. (A) Proteins in SH-SY5Y cells are analyzed by Western Blot. (B) Grey intensity analysis of HO-1 and Nrf2. **p <0.01 and ***p <0.001 compared with indicated control. &&p <0.01 and &&&p <0.001 compared with the H O -treated group.
Fig. 5 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 5. Effects of verniciflavanol A (9) on intracellular ROS production of H2O2 treated SH-SY5Y cells. (A) Immunofluorescence staining and (B–C) flow cytometry was employed to test the ROS production caused by H2O2 in SH-SY5Y cells. Data are presented as the mean ± SD of three independent experiments. ***p <0.001 compared with indicated control. &p <0.05 and &&p <0.01 compared with the H O -treated group.
Fig. 8. Compounds 1–3 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress
Fig. 8. Compounds 1–3 reduced mitochondrial dysfunction in H2O2-induced SH-SY5Y cells. Cells were pretreated with 1, 2, 3 (50 μM), then treated with H2O2 (200 μM) for 4h. The loss of ΔΨm was determined by JC-1 staining and measured by flow cytometric analysis. ##P <0.01 compared with the control group, **P <0.01, *P <0.05 compared with the H2O2 group.
Fig. 6 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress
Fig. 6. Effects of compounds 1–3 to attenuate apoptosis of H2O2-treated SH-SY5Y cells. Cells were pretreated with 1, 2, 3 (50 μM), then treated with H2O2 (200 μM) for 4 h. Flow cytometry was used to determine the apoptotic ratio after Annexin V-FITC/PI staining. Data were shown as mean ± SD from three separate experiments. ##P <0.01 compared with the control group, *P <0.05, **P <0.01 compared with the H O group.
Fig. 5 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress
Fig. 5. Neuroprotective effects of compounds 1–18 on H2O2-damaged SH-SY5Y cells using MTT assay. Data are presented as means ± S.D. (n = 3). *p <0.05, **p <0.01, ***p <0.001 as compared to model.
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.