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myd88 inhibitor st 2825  (MedChemExpress)


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    Structured Review

    MedChemExpress myd88 inhibitor st 2825
    Myd88 Inhibitor St 2825, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 85 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/myd88+inhibitor+st+2825/ST+2825/pm41986877-40-22-26
    Average 95 stars, based on 85 article reviews
    myd88 inhibitor st 2825 - by Bioz Stars, 2026-10
    95/100 stars

    Images

    Related Articles

    Recombinant:

    Article Title: Peroxiredoxin 2 activates microglia by interacting with Toll-like receptor 4 after subarachnoid hemorrhage
    Article Snippet: .. The treatment groups were prepared with OxyHb-exposed neuron-microglia co-culture systems respectively adding 1, 5, and 10 μg/mL recombinant Prx2 (Abcam) for 24 h. MyD88 inhibitor ST-2825 (MCE) was premixed with culture medium at a concentration of 10 and 100 μmol/L, and the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) was premixed with microglial culture medium at a concentration of 80 μmol/L 24 h before the in vitro SAH model was induced respectively. .. The Cytotoxicity Detection Kit (LDH) (Roche) was used to measure neural cell viability as per the manufacturer’s instruction.

    Concentration Assay:

    Article Title: Peroxiredoxin 2 activates microglia by interacting with Toll-like receptor 4 after subarachnoid hemorrhage
    Article Snippet: .. The treatment groups were prepared with OxyHb-exposed neuron-microglia co-culture systems respectively adding 1, 5, and 10 μg/mL recombinant Prx2 (Abcam) for 24 h. MyD88 inhibitor ST-2825 (MCE) was premixed with culture medium at a concentration of 10 and 100 μmol/L, and the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) was premixed with microglial culture medium at a concentration of 80 μmol/L 24 h before the in vitro SAH model was induced respectively. .. The Cytotoxicity Detection Kit (LDH) (Roche) was used to measure neural cell viability as per the manufacturer’s instruction.

    In Vitro:

    Article Title: Peroxiredoxin 2 activates microglia by interacting with Toll-like receptor 4 after subarachnoid hemorrhage
    Article Snippet: .. The treatment groups were prepared with OxyHb-exposed neuron-microglia co-culture systems respectively adding 1, 5, and 10 μg/mL recombinant Prx2 (Abcam) for 24 h. MyD88 inhibitor ST-2825 (MCE) was premixed with culture medium at a concentration of 10 and 100 μmol/L, and the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) was premixed with microglial culture medium at a concentration of 80 μmol/L 24 h before the in vitro SAH model was induced respectively. .. The Cytotoxicity Detection Kit (LDH) (Roche) was used to measure neural cell viability as per the manufacturer’s instruction.

    other:

    Article Title: Interferon regulatory factor 1 eliminates mycobacteria by suppressing p70 S6 kinase via mechanistic target of rapamycin signaling.
    Article Snippet: Please cite this article as: Xinying Zhou , Jiahui Yang , Zelin Zhang , Lijie Zhang , Linmiao Lie , Bo Zhu , Lei Xu , Yuchi Gao , Xialin Du , Yingqi Huang , Ruining Wang , Honglin Liu , Yanfen Li , Shengfeng Hu , Chaoying Zhou , Qian Wen , Qiuwei Pan , Li Ma , Interferon regulatory factor 1 eliminates mycobacteria by suppressing p70 S6 kinase via mechanistic target of rapamycin signaling, Journal of Infection (2019), doi: https://doi.org/10.1016/j.jinf.2019.06.007



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    MedChemExpress inhibitor st2825 myd88
    a Schematic representation of TLR4 signaling, ligands used and contact point of the <t>MyD88</t> inhibitor <t>ST2825.</t> HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) ( b ) or S. minnesota (100 ng/ml) or preincubated with 10 µM of the MyD88 inhibitor ST2825. c Immunofluorescence microscopy for localization experiments of MyD88 (green) in transfected HEK293 KO-MyD88 cells before and after stimulation with LPS E. coli and LPS S. minnesota (100 ng/ml) for 5 min, 15 min or 45 min. Cells are transfected with 500 ng MyD88-Venus construct and counterstained with the nuclear probe Hoechst (blue). Scale bars, 5 µm. Images are representative of three biologically independent experiments. d HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) or S. minnesota (100 ng/ml). Baseline-corrected DMR recordings are mean + SEM and representative of three biologically independent experiments. Source data are provided as a Source Data file. ( a ) was created in BioRender. Weindl, G. (2024) BioRender.com/x63i940.
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    RABV inducing the activation of the <t>Myd88</t> pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).
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    RABV inducing the activation of the <t>Myd88</t> pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).
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    Image Search Results


    a Schematic representation of TLR4 signaling, ligands used and contact point of the MyD88 inhibitor ST2825. HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) ( b ) or S. minnesota (100 ng/ml) or preincubated with 10 µM of the MyD88 inhibitor ST2825. c Immunofluorescence microscopy for localization experiments of MyD88 (green) in transfected HEK293 KO-MyD88 cells before and after stimulation with LPS E. coli and LPS S. minnesota (100 ng/ml) for 5 min, 15 min or 45 min. Cells are transfected with 500 ng MyD88-Venus construct and counterstained with the nuclear probe Hoechst (blue). Scale bars, 5 µm. Images are representative of three biologically independent experiments. d HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) or S. minnesota (100 ng/ml). Baseline-corrected DMR recordings are mean + SEM and representative of three biologically independent experiments. Source data are provided as a Source Data file. ( a ) was created in BioRender. Weindl, G. (2024) BioRender.com/x63i940.

    Journal: Nature Communications

    Article Title: Label-free biosensor assay decodes the dynamics of Toll-like receptor signaling

    doi: 10.1038/s41467-024-53770-9

    Figure Lengend Snippet: a Schematic representation of TLR4 signaling, ligands used and contact point of the MyD88 inhibitor ST2825. HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) ( b ) or S. minnesota (100 ng/ml) or preincubated with 10 µM of the MyD88 inhibitor ST2825. c Immunofluorescence microscopy for localization experiments of MyD88 (green) in transfected HEK293 KO-MyD88 cells before and after stimulation with LPS E. coli and LPS S. minnesota (100 ng/ml) for 5 min, 15 min or 45 min. Cells are transfected with 500 ng MyD88-Venus construct and counterstained with the nuclear probe Hoechst (blue). Scale bars, 5 µm. Images are representative of three biologically independent experiments. d HEK293 TLR4/MD-2/CD14 reporter cells were stimulated with LPS from E. coli (100 ng/ml) or S. minnesota (100 ng/ml). Baseline-corrected DMR recordings are mean + SEM and representative of three biologically independent experiments. Source data are provided as a Source Data file. ( a ) was created in BioRender. Weindl, G. (2024) BioRender.com/x63i940.

    Article Snippet: The inhibitor ST2825 (MyD88) was obtained from MedChemExpress (New Jersey, USA).

    Techniques: Immunofluorescence, Microscopy, Transfection, Construct

    RABV inducing the activation of the Myd88 pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Journal: International Journal of Molecular Sciences

    Article Title: Rabies Virus Regulates Inflammatory Response in BV-2 Cells through Activation of Myd88 and NF-κB Signaling Pathways via TLR7

    doi: 10.3390/ijms25179144

    Figure Lengend Snippet: RABV inducing the activation of the Myd88 pathway through TLR7. ( A ) The expression levels of TLR7, MyD88, IRAK4 and TRAF6 assessed via Western blotting. ( B ) BV-2 cells pre-treated for 2 h with the inhibitor (HY-124603) and agonist (HY-117602) of TLR7 before stimulation with CVS-11 for 6 h. TRL7, Myd88, IRAK4 and TRAF6 were analyzed via Western blotting. ( C ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6, normalized against β-actin. ( D ) Quantitative assessment of the relative expression levels of TLR7, Myd88, IRAK4 and TRAF6 following normalization against β-actin, in response to treatment with TLR7 inhibitors (HY-124603) and agonists (HY-117602). ( E ) The expression levels of viral P gene mRNA, quantified using qRT-PCR following treatment with the TLR7 inhibitor (HY-124603) and agonist (HY-117602). ( F ) BV-2 cells pre-treated for 2 h with the TLR7 inhibitor (HY-124603) and for 30 min with the Myd88 inhibitor (HY-50937). The supernatants were collected, and the concentration of CCL2 was quantified at 24 h. ( G ) The expression of CXCL10 was measured at 24 h. ( H ) The expression of IL-6 was measured at 24 h. Statistical evaluations were conducted utilizing ANOVA (* p < 0.05, ** p < 0.01).

    Article Snippet: The TLR7 inhibitor (HY-124603, MCE, Princeton, NJ, USA), agonist (HY-117602, MCE, USA) and Myd88 inhibitor (HY-50937) were purchased from Med-Chem-Express.

    Techniques: Activation Assay, Expressing, Western Blot, Quantitative RT-PCR, Concentration Assay