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Redox Biology

ISSN: 2213-2317

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Datasets associated with articles published in Redox Biology

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1970
2024
1970 2024
27 results
  • Data for: Reactive Species Generated by Heme Impair Alveolar Epithelial Sodium Channel Function in Acute Respiratory Distress Syndrome
    These are original western blot data used in the manuscript
    • Dataset
  • Data for: Development of an Enzyme-linked Immunosorbent Assay for Keap1-Nrf2 Interaction Inhibitors Identification
    Development a new ELISA format to identify KEAP1-NRF2 inihbitors
    • Dataset
  • Data for: C1q/TNF-Related Protein 5 contributes to Diabetic Vascular Endothelium Dysfunction Through promoting Nox-1 Signaling
    This supplemental database presented all the raw data for Figures.
    • Dataset
  • Data for: The nuclear transcription factor FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways
    Inflammation is a self-defense response to protect individuals from infection and tissue damage, but excessive or persistent inflammation can have adverse effects on cell survival. Many individuals become especially susceptible to chronic- inflammation-induced sensorineural hearing loss as they age, but the intrinsic molecular mechanism behind aging individuals' increased risk of hearing loss remains unclear. FoxG1 (forkhead box transcription factor G1) is a key transcription factor that plays important roles in hair cell survival through the regulation of mitochondrial function, but how the function of FoxG1 changes during aging and under inflammatory conditions is unknown. In this study, we first found that FoxG1 expression and autophagy both increased gradually in the low concentration lipopolysaccharide (LPS)-induced inflammation model, while after high concentration of LPS treatment both FoxG1 expression and autophagy levels decreased as the concentration of LPS increased. We then used siRNA to downregulate Foxg1 expression in hair cell-like OC-1 cells and found that cell death and apoptosis were significantly increased after LPS injury. Furthermore, we used D-galactose (D-gal) to create an aging model with hair cell-like OC-1 cells and cochlear explant cultures in vitro and found that the expression of Foxg1 and the level of autophagy were both decreased after D-gal and LPS co-treatment. Lastly, we knocked down the expression of Foxg1 under aged inflammation conditions and found increased numbers of dead and apoptotic cells. Together these results suggest that FoxG1 affects the sensitivity of mimetic aging hair cells to inflammation by regulating autophagy pathways.
    • Dataset
  • Data for: Impaired inflammasome activation and bacterial clearance in G6PD deficiency due to defective NOX/p38 MAPK/AP-1 redox signaling
    The attachment is the raw data of western blot.
    • Dataset
  • Data for: Activation leads to a significant shift in the intracellular redox homeostasis of neutrophil-like cells
    Figure supplement 1 to Figure 7 C – E of Xie et al. "Activation leads to a significant shift in the intracellular redox homeostasis of neutrophil-like cells".
    • Dataset
  • Data for: Ammonia Sensitive SLC4A11 Mitochondrial Uncoupling Reduces Glutamine Induced Oxidative Stress
    Unedited western blots
    • Dataset
  • Data for: Catalyst-free Click PEGylation reveals substantial mitochondrial ATP synthase sub-unit alpha oxidation before and after fertilisation
    The Excel files contains the raw data densitometry data for the experiments described in the manuscript. The percentage reversibly oxidised, reduced and S-glutathionylated have been calculated.
    • Dataset
  • Data for: Lung epithelial protein disulfide isomerase A3 (PDIA3) plays an important role in influenza infection, inflammation, and airway mechanics
    This file contains the raw data for all the figures.
    • Dataset
  • Data for: Nitric oxide contributes to protein homeostasis by S-nitrosylations of the chaperone HSPA8 and the ubiquitin ligase UBE2D
    DIB1: We generated nNOS+ SH-SY5Y cells that express nNOS at a level comparable to mouse brain, replicating the aging phenotype. nNOS+ and MOCK cells were exposed to proteostasis stress by treatment with rapamycin or serum-free starvation versus control. To analyze NO-mediated S-nitrosylations (SNO) and other reversible protein modifications including disulfides and sulfoxides we used complimentary proteomic approaches encompassing 2D-SNO-DIGE (differential gel electrophoresis), SNO-site identification (SNOSID), SNO Super-SILAC, SNO BIAM-Switch and Redox-BIAM switch. The redox proteomes were analyzed using hybrid liquid chromatography/mass spectrometry (LC/MS) on an LTQ Orbitrap XL (2D-SNO-DIGE, SNOSID, SNO-SILAC) or on a Thermo Scientific™ Q Exactive Plus (BIAM switch assays), the latter equipped with an ultra-high performance liquid chromatography unit and a Nanospray Flex Ion-Source. Full scan MS-data were acquired using Xcalibur, and raw mass spectra were analyzed using the proteomics software MaxQuant. The data are MaxQuant output files (Table 1 2D-SNO-DIGE, Table 2 SNOSID, Table 3 SNO-SILAC, Table 4 GO of SNO modified proteins, Table 5 SNO-BIAM switch, Table 6 Redox BIAM switch) providing essential information including peptide and protein identification, accession numbers, protein and gene names, sequence coverage and quantification values of each sample. Identifications from the reverse decoy database, identified by site only and known contaminants were excluded. The Excel file also contains Gene Ontology terms associated with the SNOed proteins (Table 4 and specified columns in Table 5 and 6). The GO overrepresentation analysis (Table 4) was performed with the Panther GO overrepresentation tool (http://www.pantherdb.org/). Excel Table 1: 2D-SNO DIGE Excel Table 2: SNOSID Excel Table 3: SNO-SILAC Excel Table 4: Gene ontology of redox modified proteins (pooled hits of 2D-DIGE, SNOSID and SNO-SILAC) Excel Table 5: SNO-BIAM switch Excel Table 6: Redox-BIAM switch DIB2 The data are MaxQuant output files (Table 1 SILAC, Table 3 LFQ proteome) of the Full Proteome including peptide and protein identification, accession numbers, protein and gene names, sequence coverage and SILAC or label free quantification (LFQ) values of each sample. Identifications from the reverse decoy database, identified by site only and known contaminants were excluded. The raw MS proteomics data of the Full Proteome have been deposited to the ProteomeXchange Consortium via the PRIDE [1] partner repository with the dataset identifier PXD010538. Reviewer account details: Username: reviewer95719@ebi.ac.uk; Password: UR0ZlqWo. Excel Table 1: MaxQuant data of normalized SILAC proteome (vehicle versus 6h rapamycin) Excel Table 2: Gene Ontology analysis of significantly regulated proteins (SILAC experiment) Excel Table 3: MaxQuant data of label-free deep proteome (conditions: full medium, 24h serum-free, 24h rapamycin)
    • Dataset
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