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mcc950  (MedChemExpress)


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    Structured Review

    MedChemExpress mcc950
    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/mcc950/MCC950/pmc13489862-49-5-9
    Average 99 stars, based on 636 article reviews
    mcc950 - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Negative Control:

    Article Title: Agomir-223 treatment after lung blast injury reduces the inflammatory response by regulating the NLRP3 inflammasome to inhibit M1 macrophage function.
    Article Snippet: Blast lung injury (BLI) is a significant cause of death in military conflicts and terrorist attacks.. At present, the specific pathogenesis is not clear, and clinical treatment still relies mainly on symptomatic support.. In this study, we aimed to explore the mechanisms of microRNAs in shock wave-induced lung blast injury.

    Injection:

    Article Title: Agomir-223 treatment after lung blast injury reduces the inflammatory response by regulating the NLRP3 inflammasome to inhibit M1 macrophage function.
    Article Snippet: Blast lung injury (BLI) is a significant cause of death in military conflicts and terrorist attacks.. At present, the specific pathogenesis is not clear, and clinical treatment still relies mainly on symptomatic support.. In this study, we aimed to explore the mechanisms of microRNAs in shock wave-induced lung blast injury.

    Concentration Assay:

    Article Title: Agomir-223 treatment after lung blast injury reduces the inflammatory response by regulating the NLRP3 inflammasome to inhibit M1 macrophage function.
    Article Snippet: Blast lung injury (BLI) is a significant cause of death in military conflicts and terrorist attacks.. At present, the specific pathogenesis is not clear, and clinical treatment still relies mainly on symptomatic support.. In this study, we aimed to explore the mechanisms of microRNAs in shock wave-induced lung blast injury.

    Positive Control:

    Article Title: Agomir-223 treatment after lung blast injury reduces the inflammatory response by regulating the NLRP3 inflammasome to inhibit M1 macrophage function.
    Article Snippet: Blast lung injury (BLI) is a significant cause of death in military conflicts and terrorist attacks.. At present, the specific pathogenesis is not clear, and clinical treatment still relies mainly on symptomatic support.. In this study, we aimed to explore the mechanisms of microRNAs in shock wave-induced lung blast injury.



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    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.
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    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.
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    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