Review



nlrp3 inhibitor mcc950  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 99

    Structured Review

    MedChemExpress nlrp3 inhibitor mcc950
    8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and <t>NLRP3</t> in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.
    Nlrp3 Inhibitor Mcc950, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 636 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nlrp3+inhibitor+mcc950/MCC950/pmc13223851-69-6-13
    Average 99 stars, based on 636 article reviews
    nlrp3 inhibitor mcc950 - by Bioz Stars, 2026-09
    99/100 stars

    Images

    1) Product Images from "8-oxo-7,8-dihydroguanosine (8-oxo-Guo) drives pulmonary inflammatory pathways through pattern recognition receptors"

    Article Title: 8-oxo-7,8-dihydroguanosine (8-oxo-Guo) drives pulmonary inflammatory pathways through pattern recognition receptors

    Journal: Redox Biology

    doi: 10.1016/j.redox.2026.104211

    8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and NLRP3 in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.
    Figure Legend Snippet: 8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and NLRP3 in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Techniques Used: Protein-Protein interactions, Expressing

    Dose-dependent suppression of 8-oxo-Guo/polyU-induced inflammation upon NOD2, TLR2, and NLRP3 inhibition. (A-F) Protein expression changes in NLR, TLR, and downstream signaling pathways (left panels) and concentrations of TNF-α, MIP-2, IL-1β, and MCP-1 in the culture supernatant (right panels) of MH-S cells following 4-h co-stimulation with 8-oxo-Guo and polyU in the presence of GSK717 (A, B) , Cu-CPT22 (C, D) , or MCC950 (E, F) . ∗∗ p < 0.01, ∗∗∗ p < 0.001. (G, H) Protein expression profiles of relevant signaling pathways (G) and cytokine concentrations in the culture supernatant (H) of MH-S cells that were treated for 4 h with 8-oxo-Guo and polyU combined with GSK717, Cu-CPT22, or MCC950, either individually or combined. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.
    Figure Legend Snippet: Dose-dependent suppression of 8-oxo-Guo/polyU-induced inflammation upon NOD2, TLR2, and NLRP3 inhibition. (A-F) Protein expression changes in NLR, TLR, and downstream signaling pathways (left panels) and concentrations of TNF-α, MIP-2, IL-1β, and MCP-1 in the culture supernatant (right panels) of MH-S cells following 4-h co-stimulation with 8-oxo-Guo and polyU in the presence of GSK717 (A, B) , Cu-CPT22 (C, D) , or MCC950 (E, F) . ∗∗ p < 0.01, ∗∗∗ p < 0.001. (G, H) Protein expression profiles of relevant signaling pathways (G) and cytokine concentrations in the culture supernatant (H) of MH-S cells that were treated for 4 h with 8-oxo-Guo and polyU combined with GSK717, Cu-CPT22, or MCC950, either individually or combined. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Techniques Used: Inhibition, Expressing, Protein-Protein interactions

    Related Articles

    Infection:

    Article Title: Caspase-4/11-mediated non-canonical pyroptosis disrupts blood-brain barrier integrity via VEGFA/VEGFR2 signaling in Escherichia coli meningitis.
    Article Snippet: Bacterial meningitis is a severe inflammatory disease of the central nervous system (CNS) that involves bloodbrain barrier (BBB) disruption.. However, the underlying mechanisms remain incompletely understood.. We previously reported that meningitis-associated extraintestinal pathogenic Escherichia coli (ExPEC) induces BBB dysfunction through endothelial pyroptosis and tight junction degradation, but the role of caspase-4/11 in these processes remains unclear.

    Incubation:

    Article Title: Dachaihu decoction alleviates septic liver injury by modulating the intestinal barrier dysfunction and suppressing the NF-κB/NLRP3/Caspase-1 signaling pathway
    Article Snippet: .. To determine the contribution of the TLR4/NF-κB/NLRP3/Caspase-1 signaling pathway to DCHD-mediated anti-inflammatory effects in ImKCs, cells were incubated for 2 h with either the TLR4 inhibitor TAK-242 (resatorvid, 10 μM) (HY-11109; MedChemExpress, USA) [ , ] or the NLRP3 inhibitor MCC950 (10 μM) (HY-12815; MedChemExpress, USA) [ ] and then exposed to either LPS alone or in combination with 10% DCHD-DS. ..

    Control:

    Article Title: sEH inhibition attenuates mtROS-mediated NLRP3 inflammasome activation by promoting mitophagy in tubular epithelial cells in diabetic kidney disease
    Article Snippet: Cells were maintained in DMEM/F-12 medium (Gibco, USA) supplemented with 10% fetal bovine serum (PAN, Germany), 1000 U/L penicillin, and 100 μg/mL streptomycin at 37 °C in a 5% CO 2 atmosphere. .. For glucose treatments, cells were exposed to low glucose (LG, 5.5 mM D-glucose), high glucose (HG, 30 mM D-glucose), or an osmotic control (5.5 mM glucose + 24.5 mM D-mannitol) for 24 h. In pharmacological experiments, HK-2 cells were treated under various conditions with the sEH inhibitor trans -4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB, 10 μM, ApexBio, USA), the NLRP3 inhibitor MCC950 (10 μM, MedChemExpress), the autophagy inducer rapamycin (Rapa, 10 μM, Selleck, S1039), the mitochondrial antioxidant MitoTEMPO (100 μM, MedChemExpress), or the autophagy inhibitor 3-methyladenine (3-MA, 5 nM, Selleck, S2767). ..

    other:

    Article Title: Betulinic acid alleviates the inflammatory injury of osteoblasts in osteoporosis by augmenting autophagy via the AMPK-mTOR signaling pathway
    Article Snippet: BA, 3-Methyladenin (3-MA), ROS scavenger N-acetyl-L-cysteine (NAC), NLRP3 inhibitor MCC950 and Dorsomorphin (synonyms: Compound c, CC) were purchased from MedChemExpress, and Essential Medium α (α-MEM) and fetal bovine serum (FBS) were purchased from Gibco, Thermo Fisher Scientific, Inc.

    Positive Control:

    Article Title: Chikusetsu saponin IVa mitigates septic cardiac injury by targeting DRP1 to suppress mitochondrial damage and NLRP3 inflammasome activation.
    Article Snippet: Aims: Sepsis-induced myocardial injury represents a serious complication with limited treatment options.. Chikusetsu saponin IVa (CHS), a triterpenoid saponin derived from Rhizoma Panacis japonica, exhibits potent antiinflammatory and cardioprotective properties, positioning it as a promising candidate.. Materials and methods: To elucidate the therapeutic potential and mechanism of CHS in septic cardiac dysfunction, the effects of CHS administration on lipopolysaccharide (LPS, 40 mg/kg, i.p.) and cecal ligation and puncture (CLP)-induced septic murine models were evaluated through echocardiography and histological analyses.

    In Vitro:

    Article Title: Chikusetsu saponin IVa mitigates septic cardiac injury by targeting DRP1 to suppress mitochondrial damage and NLRP3 inflammasome activation.
    Article Snippet: Aims: Sepsis-induced myocardial injury represents a serious complication with limited treatment options.. Chikusetsu saponin IVa (CHS), a triterpenoid saponin derived from Rhizoma Panacis japonica, exhibits potent antiinflammatory and cardioprotective properties, positioning it as a promising candidate.. Materials and methods: To elucidate the therapeutic potential and mechanism of CHS in septic cardiac dysfunction, the effects of CHS administration on lipopolysaccharide (LPS, 40 mg/kg, i.p.) and cecal ligation and puncture (CLP)-induced septic murine models were evaluated through echocardiography and histological analyses.



    Similar Products

    99
    MedChemExpress nlrp3 inhibitor mcc950
    8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and <t>NLRP3</t> in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.
    Nlrp3 Inhibitor Mcc950, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nlrp3+inhibitor+mcc950/MCC950/pmc13223851-69-6-13
    Average 99 stars, based on 1 article reviews
    nlrp3 inhibitor mcc950 - by Bioz Stars, 2026-09
    99/100 stars
      Buy from Supplier

    96
    InvivoGen nlrp3 inhibitor mcc950
    The impact of SYK inhibition on <t>NLRP3</t> activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor <t>MCC950</t> was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Nlrp3 Inhibitor Mcc950, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nlrp3+inhibitor+mcc950/MCC950/pmc13139746-43-5-14
    Average 96 stars, based on 1 article reviews
    nlrp3 inhibitor mcc950 - by Bioz Stars, 2026-09
    96/100 stars
      Buy from Supplier

    99
    MedChemExpress nlrp3 specific inhibitor mcc950
    The impact of SYK inhibition on <t>NLRP3</t> activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor <t>MCC950</t> was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Nlrp3 Specific Inhibitor Mcc950, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nlrp3+inhibitor+mcc950/MCC950/pm42431105-111-37-42
    Average 99 stars, based on 1 article reviews
    nlrp3 specific inhibitor mcc950 - by Bioz Stars, 2026-09
    99/100 stars
      Buy from Supplier

    99
    MedChemExpress nlrp3 inflammasome inhibitor mcc950
    The impact of SYK inhibition on <t>NLRP3</t> activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor <t>MCC950</t> was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Nlrp3 Inflammasome Inhibitor Mcc950, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nlrp3+inhibitor+mcc950/MCC950/pm42378757-79-12-18
    Average 99 stars, based on 1 article reviews
    nlrp3 inflammasome inhibitor mcc950 - by Bioz Stars, 2026-09
    99/100 stars
      Buy from Supplier

    Image Search Results


    8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and NLRP3 in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Redox Biology

    Article Title: 8-oxo-7,8-dihydroguanosine (8-oxo-Guo) drives pulmonary inflammatory pathways through pattern recognition receptors

    doi: 10.1016/j.redox.2026.104211

    Figure Lengend Snippet: 8-oxo-Guo and polyU stimulate inflammation via NLR and TLR signaling pathways. (A, B) Transcriptome analysis of MH-S cells following 2-h stimulation with 8-oxo-Guo and/or polyU. (A) KEGG pathway enrichment analysis. (B) GSEA. (C) Relative mRNA expression levels of NOD2 , TLR2 , and NLRP3 in cells after 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. (D) Protein expression changes and grayscale quantification of key components of NLR, TLR, MAPK, JAK-STAT, and NF-κB signaling pathways following 2-h stimulation with 8-oxo-Guo and/or polyU. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: The NOD2 inhibitor GSK717 (HY-136555) and NLRP3 inhibitor MCC950 (HY-12815A) were obtained from MedChemExpress (MCE), and the TLR2 inhibitor Cu-CPT22 (S8677) was obtained from Selleck.

    Techniques: Protein-Protein interactions, Expressing

    Dose-dependent suppression of 8-oxo-Guo/polyU-induced inflammation upon NOD2, TLR2, and NLRP3 inhibition. (A-F) Protein expression changes in NLR, TLR, and downstream signaling pathways (left panels) and concentrations of TNF-α, MIP-2, IL-1β, and MCP-1 in the culture supernatant (right panels) of MH-S cells following 4-h co-stimulation with 8-oxo-Guo and polyU in the presence of GSK717 (A, B) , Cu-CPT22 (C, D) , or MCC950 (E, F) . ∗∗ p < 0.01, ∗∗∗ p < 0.001. (G, H) Protein expression profiles of relevant signaling pathways (G) and cytokine concentrations in the culture supernatant (H) of MH-S cells that were treated for 4 h with 8-oxo-Guo and polyU combined with GSK717, Cu-CPT22, or MCC950, either individually or combined. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Journal: Redox Biology

    Article Title: 8-oxo-7,8-dihydroguanosine (8-oxo-Guo) drives pulmonary inflammatory pathways through pattern recognition receptors

    doi: 10.1016/j.redox.2026.104211

    Figure Lengend Snippet: Dose-dependent suppression of 8-oxo-Guo/polyU-induced inflammation upon NOD2, TLR2, and NLRP3 inhibition. (A-F) Protein expression changes in NLR, TLR, and downstream signaling pathways (left panels) and concentrations of TNF-α, MIP-2, IL-1β, and MCP-1 in the culture supernatant (right panels) of MH-S cells following 4-h co-stimulation with 8-oxo-Guo and polyU in the presence of GSK717 (A, B) , Cu-CPT22 (C, D) , or MCC950 (E, F) . ∗∗ p < 0.01, ∗∗∗ p < 0.001. (G, H) Protein expression profiles of relevant signaling pathways (G) and cytokine concentrations in the culture supernatant (H) of MH-S cells that were treated for 4 h with 8-oxo-Guo and polyU combined with GSK717, Cu-CPT22, or MCC950, either individually or combined. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

    Article Snippet: The NOD2 inhibitor GSK717 (HY-136555) and NLRP3 inhibitor MCC950 (HY-12815A) were obtained from MedChemExpress (MCE), and the TLR2 inhibitor Cu-CPT22 (S8677) was obtained from Selleck.

    Techniques: Inhibition, Expressing, Protein-Protein interactions

    The impact of SYK inhibition on NLRP3 activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor MCC950 was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: European Journal of Immunology

    Article Title: SYK Signalling in NLRP3 Inflammasome‐Mediated Response of Murine Microglia Activated by Immune Complexes Formed of Viral Proteins and Specific IgG

    doi: 10.1002/eji.70199

    Figure Lengend Snippet: The impact of SYK inhibition on NLRP3 activation. Cells were treated with VLPs (20 µg/mL) and mAbs (7.5 µg/mL) for 24 h, and 1 µM of SYK inhibitor R406 or NLRP3 inhibitor MCC950 was added 1 h before treatment. (A) Western blot data show the expression of the indicated protein in microglia lysates, and the images are representative of five to six experiments. (B) Quantification of NLRP3 expression from Western blot data, normalised to a loading control, N = 5–6. (C) Quantification of ASC speck formation in primary microglia, N = 6. (D, E) IL‐1β secretion and (F) TNF‐α secretion were tested by ELISA in microglia supernatants, (D) N = 4, (E) N = 4–6, (F) N = 8–9. (G) Fluorescent microscopy images of the immunostained NLRP3 (cyan) and ASC specks (yellow), NLRP3 was stained with primary Ab anti‐NLRP and secondary Ab—AlexaFluor 488, ASC specks were stained with primary Ab anti‐ASC‐PE. Representative images are shown. The scale bars indicate 50 µm in large images and 20 µm in magnified images. In (B–F), data are represented using a box plot with dots showing the number of individual experiments. Significance was established using one‐way ANOVA followed by Tukey's test * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: SYK kinase inhibitor R406 (#inh‐r406), NLRP3 inhibitor MCC950 (#inh‐mcc), and Zymosan (#tlrl‐zyn) were from Invivogen.

    Techniques: Inhibition, Activation Assay, Western Blot, Expressing, Control, Enzyme-linked Immunosorbent Assay, Microscopy, Staining