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235 results for “Inflammasome”
Post-injury immunosuppression and secondary infections are caused by an AIM2 inflammasome-driven signaling cascade
<p>RAW FCS files for the manuscript:</p> <p>"Post-injury immunosuppression and secondary infections are caused by an AIM2 inflammasome-driven signaling cascade"</p> <p> </p>
Portimine A toxin causes skin pathology through ZAKα-dependent NLRP1 inflammasome activation: LC-MS/MS raw data for Figure 1. C
<p>This dataset pertains to the LC-MS/MS analyses conducted as part of a study on microalgal toxins present in samples from Senegal, published in the paper entitled <em>"Portimine A toxin causes skin pathology through ZAK</em><em>α</em><em>-dependent NLRP1 inflammasome activation."</em> The data correspond to the quantification results of environmental samples presented in Figure 1C.</p> <p>The raw data were acquired using Analyst software (Applied Biosystems proprietary software). The materials and methods used to generate these data are detailed in the associated publication in <em>EMBO Molecular Medicine</em> (ISSN: 1757-4676, 2024).</p>
Exprimental Data:Caspase-11 non-canonical inflammasome mediates the expression of proinflammatory cytokines in murine macrophages infected with leptospira interrogans.
<p>This is the exprimental data of manuscripts submitted in ALL LIFE magazine. The title is Caspase-11 non-canonical inflammasome mediates the expression of proinflammatory cytokines in murine macrophages infected with leptospira interrogans.)</p>
Raw Data for the article: Cigarette smoke promotes inflammasome-independent activation of caspase-1 and -4 leading to gasdermin D cleavage in human macrophages
<p>Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investigated whether other ASC-dependent inflammasomes could be involved in caspase activation by CSE and whether caspase activation led to GSDMD cleavage and other downstream effects. Presented results demonstrate that CSE promoted ASC-independent activation of caspase-1 leading to GSDMD cleavage and increased cell permeability, in the absence of cell death. GSDMD cleavage was strongly enhanced upon stimulation with LPS+CSE, suggesting a synergistic effect between the two stimuli. Noteworthy, CSE promoted LPS internalization leading to caspase-4 activation, thus contributing to increased GSDMD cleavage. Caspase-dependent GSDMD cleavage was associated with mitochondrial superoxide generation. Increased cleaved GSDMD was found in lung macrophages of smokers compared to ex-smokers and non-smoking controls. Our findings revealed that ASC-independent activation of caspase-1, -4, and -8 and GSDMD cleavage upon exposure to CS may contribute to macrophage dysfunction and feed the chronic inflammation observed in the smokers' lung.</p>
Human STING is a proton channel (HEK293T Inflammasome Experiment)
<p>HEK293T cells transduced to express NLRP3-mNeonGreen and STING-HA were plated in 24-well glass-bottom plates (Greiner Bio-One) and, after 24 hours, stimulated with 2 µM nigericin or 1 µM diABZI with or without the addition of 10 µM C53 for 1 hour. Cells were then fixed with 2% Paraformaldehyde (Electron Microscopy Sciences) in PHEM buffer (Electron Microscopy Sciences) for 30 minutes at 37°C, washed three times with PBS and quenched with freshly prepared 0.1M Glycine for 10 minutes. Cells were permeabilized in 100% methanol for 30 minutes and stained with anti-HA (Millipore, #11867423001) and anti p-STING (Cell Signaling Technology cat. #19781s) for 1 hour at room temperature in 3% BSA, washed 5 times, and then stained with Alexa 647 anti-rat IgG (H+L) (Thermo, A-21247) and Alexa 555 plus anti-rabbit (Thermo, A32732) in 3% BSA for 1 hour. After five washes, cells were incubated in 2X SSC with 200 ng/mL DAPI (Thermo Fisher) and imaged using the Nikon microscope used for organelle pH images. Images were acquired using a 60X 1.40 NA Plan Apo λ oil immersion objective (Nikon MRD01605) with Nikon type F immersion oil with the following lasers and filters: DAPI (405 nm laser, Chroma <a href="https://www.chroma.com/products/parts/et455-50m">ET455/50</a>), NLRP3 mNeonGreen (488nm laser, Chroma ET525/36) pSTING (561 nm laser, Chroma ET605/52), and STING-HA (640 nm laser, Chroma ET705/72), assaying five z planes per field of view with 0.625 µm spacing. Fields of view were selected using NIS Elements software coordinates without manual preselection.</p> <p>Images are maximum projections of multiple z-stacks. Channels are: DAPI, NLRP3 mNeonGreen, pSTING, and STING.</p>
The Association of Resistance Exercise With the Inflammasome Activation in Obesity Subjects
ClinicalTrials.gov study NCT05482178. IPD Sharing: NO. Countries: 1. Publications: 7.
TLR priming licenses NAIP inflammasome activation by immunoevasive ligands
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Data from: RAC2 gain of function variants causing inborn error of immunity drive NLRP3 inflammasome activation
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Data from: CARD8 inflammasome activation during HIV-1 cell-to-cell transmission
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Test and Train data for the retrieval experiment in "A molecule generation-oriented lead compound optimization architecture: discovery of potent, selective, oral NLRP3 inflammasome inhibitors"
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Combined immune checkpoint blockade increases myocardial secretion of H-FABP, NT-Pro-BNP, NLRP-3 inflammasome, Interleukin-1β and Interleukin-6: biochemical implications in cardio-immuno-oncology
<p>Background: Immune checkpoint inhibitors have transformed the treatment of several cancers by releasing restrained antitumor immune responses. Ipilimumab, an anti–cytotoxic T-lymphocyte–associated antigen 4 (CTLA-4) antibody, and nivolumab, an anti–programmed death-1 (PD-1) antibody, have individually improved survival in patients with melanoma, and their combination further enhances antitumor activity and survival. More recently, an anti-LAG3 human monoclonal antibody, Relatlimab, has been approved by FDA for combinatorial treatment with Nivolumab for metastatic melanoma and an anti-PD-L1 mAb,Atezolizumab, is undergoing clinical trials evaluation in combination with Ipilimumab for metastatic lung cancer.However,adverse events associated with these agents include dermatitis, endocrinopathies, colitis, hepatitis, and pneumonitis, which are all thought to arise from aberrant activation of autoreactive T cells. These toxic effects are more frequent and severe when immunomodulatory mAbs are used in combination. </p> <p>Methods: human cardiomyocytes co-cultured with hPBMC were exposed to monotherapy and combinatorial ICIs (PD-L1 and CTLA-4 or PD-1 and LAG-3 blocking agents, at 200 nM) for 48 h. After treatments, cardiac cell lysis and secretion of biomarkers of cardiotoxicity (H-FABP, NT-Pro-BNP), NLRP3-inflammasome and Interleukin 1 and 6 were determined through colorimetric and enzymatic assays. <strong>Results:</strong>Both Combinations of immune checkpoint inhibitors exertmore potent cardiotoxic side effects compared to monotherapies against human cardiac cells co-cultured with human lymphocytes. LDH release from cardiac cells was 43% higher in PDL-1/CTLA-4 blocking agents, and 35.7% higher in PD-1/LAG-3 blocking agents compared to monotherapies. Biomarkers of cardiotoxicity, such as H-FABP and NT-Pro-BNP were also strongly increased in combination therapy than monotherapies. NLRP3 inflammasome, IL-1β and IL-6 levels were also increased by PDL-1/CTLA-4 and PD-1/LAG-3 combined blocking agents compared to untreated cells and monotherapies. </p> <p><strong>Conclusions:</strong>Data of the present study, although in vitro, indicate that combinatorial immune checkpoint blockade on co-cultures of hPBMCs and cardiac cells, including for the first time the anti LAG-3 monoclonal antibody, induce a pro- inflammatory phenotype, thus indicating that these therapies should be closely monitored by the multidisciplinary team consisting of oncologists, cardiologists and immunologists.</p>
Fig. 6 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 6. The inhibitory effects of 4 on the production of IL-1β and ROS in HepG2-IR cells. The expression levels of IL-1β were measured by ELISA analysis (A), Fluorescence intensity of ROS was recorded by a multimode microplate reader (B). ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 5 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 5. The glucose consumption assay of compounds 4–6, 10 and 11 in different concentrations. The concentrations of these compounds were from 1.56 to 50 μM, ROSI was the positive control. *p <0.05, **p <0.01, compared to the PA treatment group. ##p <0.01, compared to the control (CON) group.
Fig. 7 in Germacranolide- and guaianolide-type sesquiterpenoids from Achillea alpina L. reduce insulin resistance in palmitic acid-treated HepG2 cells via inhibition of the NLRP3 inflammasome pathway
Fig. 7. Inhibitory effects of 4 on the expression of proteins related to NLRP3 inflammasome in PA-induced HepG2-IR cells. Representative protein bands of Western blot (A and B). Densitometric analysis of the Western blot analysis results (C). Glibenclamide (1 μM, Gliben) was a positive control. ##P <0.01 vs CON group, *P <0.05, **P <0.01 vs PA treatment group.
Fig. 12 in Toonaones A I, limonoids with NLRP3 inflammasome inhibitory activity from Toona ciliata M. Roem
Fig. 12. In vitro bioactivity of compounds 3–14. (A) Primary screening of compounds from Toona ciliata against LDH release (n = 2). MCC950 (1 μM) was used as a positive control. Compounds with LDH release level lower than 50% were marked by arrows. (B) IC50 values of potent compounds in an LDH release assay (n = 2). These compounds were low cytotoxic with CC50 values above 20 μM. (C) Inhibition of LDH and IL-1β release (n = 2). (D) PI (propidium iodide) uptake by fluorescent microscopy (n = 1). (E–G) Western blot assays of GSDMD, Casp- 1, and IL-1β (n = 1). Compared to LPS + Nig group, *P <0.05, **P <0.01. LPS, lipopolysaccharide. Nig, Nigericin. FL, full length. NT, N-terminal.
Fig. 4. Correlations between experimental and calculated 13C in Toonaones A I, limonoids with NLRP3 inflammasome inhibitory activity from Toona ciliata M. Roem
Fig. 4. Correlations between experimental and calculated 13C NMR chemical shifts of (21S)-2 (left) and (21R)-2 (right).
Fig. 7. Correlations between experimental and calculated 13C in Toonaones A I, limonoids with NLRP3 inflammasome inhibitory activity from Toona ciliata M. Roem
Fig. 7. Correlations between experimental and calculated 13C NMR chemical shifts of (23S)-5 (left) and (23R)-5 (right).
Role NLRP3 Inflammasome in Weight Loss Following Sleeve Gastrectomy in Morbidly Obese Patients
ClinicalTrials.gov study NCT04814147. IPD Sharing: NO. Countries: 1. Publications: 5.
Effect of Fasting on the NLRP3 Inflammasome
ClinicalTrials.gov study NCT02122575. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Role of Inflammasome in Platelet Activation in Sickle Cell Disease Patient
ClinicalTrials.gov study NCT06986837. IPD Sharing: NO. Countries: 1. Publications: 1.
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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.