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myd88 inhibitor t6167923  (MedChemExpress)


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    Structured Review

    MedChemExpress myd88 inhibitor t6167923
    Recombinant Ts‐HSP70 promotes the expression of TLR2 and <t>MyD88.</t> Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.
    Myd88 Inhibitor T6167923, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway"

    Article Title: Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway

    Journal: Transboundary and Emerging Diseases

    doi: 10.1155/tbed/5533482

    Recombinant Ts‐HSP70 promotes the expression of TLR2 and MyD88. Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.
    Figure Legend Snippet: Recombinant Ts‐HSP70 promotes the expression of TLR2 and MyD88. Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.

    Techniques Used: Recombinant, Expressing, Western Blot

    Recombinant Ts‐HSP70 affects mouse macrophage immune function via the TLR2/MyD88/ERK signaling pathway. Mouse macrophages were pretreated with a TLR2‐specific antibody (or control IgG) for 1 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min) and harvested for Western blot. In the MyD88 inhibition assay, RAW264.7 cells were pretreated with the MyD88 inhibitor T6167923 (5, 10 μg/mL; DMSO control) for 18 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min), and harvested for Western blot analysis. A. TLR2 blocking assay. B. MyD88 inhibition assay. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above bars indicate significant differences ( p < 0.05); the same letter indicates no significant difference.
    Figure Legend Snippet: Recombinant Ts‐HSP70 affects mouse macrophage immune function via the TLR2/MyD88/ERK signaling pathway. Mouse macrophages were pretreated with a TLR2‐specific antibody (or control IgG) for 1 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min) and harvested for Western blot. In the MyD88 inhibition assay, RAW264.7 cells were pretreated with the MyD88 inhibitor T6167923 (5, 10 μg/mL; DMSO control) for 18 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min), and harvested for Western blot analysis. A. TLR2 blocking assay. B. MyD88 inhibition assay. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above bars indicate significant differences ( p < 0.05); the same letter indicates no significant difference.

    Techniques Used: Recombinant, Control, Western Blot, Inhibition, Blocking Assay

    Related Articles

    Cell Culture:

    Article Title: Free heme induces neuroinflammation and cognitive impairment by microglial activation via the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: On the first day, BV2 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) supplemented with 10% fetal bovine serum (FBS) (Sigma–Aldrich, MO, USA) and 1% penicillin/ streptomycin (Gibco) in humidified 5% CO2 air environment at 37 °C. .. On the second day, the BV2 cell culture medium was replaced, and the cells were divided into 4 groups: 1) the Control group (BV2), in which BV2 cells were incubated with medium only for 24 h; 2) the Heme group (BV2 + Heme) in which BV2 cells were treated with 40 μM hemin (H9039, Sigma, USA) for 24 h; 3) the MyD88 inhibition group (BV2 + Heme + T6167923) in which BV2 cells were treated with 40 μM hemin and 2 μM MyD88 inhibitor (T6167923, #HY-19744, MedChemExpress, USA) for 24 h; and 4) the NF-κB inhibition group (BV2 + Heme + JSH-23), in which BV2 cells were treated with 40 μM hemin and 20 μM NF-κB inhibitor (JSH-23, #S7351, Selleck, USA) for 24 h. Then, the BV2 cells were harvested for subsequent experiments. .. The BV2 and HT22 cell coculture system was conducted using Corning Transwell polycarbonate membrane cell inserts (Corning Costar Corp, USA).

    Control:

    Article Title: Free heme induces neuroinflammation and cognitive impairment by microglial activation via the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: On the first day, BV2 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) supplemented with 10% fetal bovine serum (FBS) (Sigma–Aldrich, MO, USA) and 1% penicillin/ streptomycin (Gibco) in humidified 5% CO2 air environment at 37 °C. .. On the second day, the BV2 cell culture medium was replaced, and the cells were divided into 4 groups: 1) the Control group (BV2), in which BV2 cells were incubated with medium only for 24 h; 2) the Heme group (BV2 + Heme) in which BV2 cells were treated with 40 μM hemin (H9039, Sigma, USA) for 24 h; 3) the MyD88 inhibition group (BV2 + Heme + T6167923) in which BV2 cells were treated with 40 μM hemin and 2 μM MyD88 inhibitor (T6167923, #HY-19744, MedChemExpress, USA) for 24 h; and 4) the NF-κB inhibition group (BV2 + Heme + JSH-23), in which BV2 cells were treated with 40 μM hemin and 20 μM NF-κB inhibitor (JSH-23, #S7351, Selleck, USA) for 24 h. Then, the BV2 cells were harvested for subsequent experiments. .. The BV2 and HT22 cell coculture system was conducted using Corning Transwell polycarbonate membrane cell inserts (Corning Costar Corp, USA).

    Article Title: TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/TXNIP/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways
    Article Snippet: .. The cells were divided into the control, LPS, LPS + CB13 and LPS + MyD88 inhibitor + CB13 groups, and the MyD88 inhibitor (MCE, HY-139397) was 40 μM. ..

    Article Title: TXM-CB13 Improves the Intestinal Mucosal Barrier and Alleviates Colitis by Inhibiting the ROS/TXNIP/TRX/NLRP3 and TLR4/MyD88/NF-κB/NLRP3 Pathways.
    Article Snippet: .. The cells were divided into the control, LPS, LPS + CB13 and LPS + MyD88 inhibitor + CB13 groups, and the MyD88 inhibitor (MCE, HY-139397) was 40 μM. ..

    Incubation:

    Article Title: Free heme induces neuroinflammation and cognitive impairment by microglial activation via the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: On the first day, BV2 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) supplemented with 10% fetal bovine serum (FBS) (Sigma–Aldrich, MO, USA) and 1% penicillin/ streptomycin (Gibco) in humidified 5% CO2 air environment at 37 °C. .. On the second day, the BV2 cell culture medium was replaced, and the cells were divided into 4 groups: 1) the Control group (BV2), in which BV2 cells were incubated with medium only for 24 h; 2) the Heme group (BV2 + Heme) in which BV2 cells were treated with 40 μM hemin (H9039, Sigma, USA) for 24 h; 3) the MyD88 inhibition group (BV2 + Heme + T6167923) in which BV2 cells were treated with 40 μM hemin and 2 μM MyD88 inhibitor (T6167923, #HY-19744, MedChemExpress, USA) for 24 h; and 4) the NF-κB inhibition group (BV2 + Heme + JSH-23), in which BV2 cells were treated with 40 μM hemin and 20 μM NF-κB inhibitor (JSH-23, #S7351, Selleck, USA) for 24 h. Then, the BV2 cells were harvested for subsequent experiments. .. The BV2 and HT22 cell coculture system was conducted using Corning Transwell polycarbonate membrane cell inserts (Corning Costar Corp, USA).

    Article Title: Teleost-specific TLR23 in Takifugu rubripes recruits MyD88 to trigger ERK pathway and promotes antibacterial defense.
    Article Snippet: Takifugu rubripes is a highly valued cultured fish in Asia, while pathogen infections can result in severe diseases and lead to substantial economic losses.. Toll-like receptors (TLRs), as pattern recognition receptors, play a crucial role on recognition pathogens and initiation innate immune response.. However, the immunological properties of teleost-specific TLR23 remain largely unknown.

    Inhibition:

    Article Title: Free heme induces neuroinflammation and cognitive impairment by microglial activation via the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: On the first day, BV2 cells were maintained in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) supplemented with 10% fetal bovine serum (FBS) (Sigma–Aldrich, MO, USA) and 1% penicillin/ streptomycin (Gibco) in humidified 5% CO2 air environment at 37 °C. .. On the second day, the BV2 cell culture medium was replaced, and the cells were divided into 4 groups: 1) the Control group (BV2), in which BV2 cells were incubated with medium only for 24 h; 2) the Heme group (BV2 + Heme) in which BV2 cells were treated with 40 μM hemin (H9039, Sigma, USA) for 24 h; 3) the MyD88 inhibition group (BV2 + Heme + T6167923) in which BV2 cells were treated with 40 μM hemin and 2 μM MyD88 inhibitor (T6167923, #HY-19744, MedChemExpress, USA) for 24 h; and 4) the NF-κB inhibition group (BV2 + Heme + JSH-23), in which BV2 cells were treated with 40 μM hemin and 20 μM NF-κB inhibitor (JSH-23, #S7351, Selleck, USA) for 24 h. Then, the BV2 cells were harvested for subsequent experiments. .. The BV2 and HT22 cell coculture system was conducted using Corning Transwell polycarbonate membrane cell inserts (Corning Costar Corp, USA).

    Activation Assay:

    Article Title: Teleost-specific TLR23 in Takifugu rubripes recruits MyD88 to trigger ERK pathway and promotes antibacterial defense.
    Article Snippet: Takifugu rubripes is a highly valued cultured fish in Asia, while pathogen infections can result in severe diseases and lead to substantial economic losses.. Toll-like receptors (TLRs), as pattern recognition receptors, play a crucial role on recognition pathogens and initiation innate immune response.. However, the immunological properties of teleost-specific TLR23 remain largely unknown.

    Western Blot:

    Article Title: Teleost-specific TLR23 in Takifugu rubripes recruits MyD88 to trigger ERK pathway and promotes antibacterial defense.
    Article Snippet: Takifugu rubripes is a highly valued cultured fish in Asia, while pathogen infections can result in severe diseases and lead to substantial economic losses.. Toll-like receptors (TLRs), as pattern recognition receptors, play a crucial role on recognition pathogens and initiation innate immune response.. However, the immunological properties of teleost-specific TLR23 remain largely unknown.



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    Image Search Results


    Recombinant Ts‐HSP70 promotes the expression of TLR2 and MyD88. Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.

    Journal: Transboundary and Emerging Diseases

    Article Title: Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway

    doi: 10.1155/tbed/5533482

    Figure Lengend Snippet: Recombinant Ts‐HSP70 promotes the expression of TLR2 and MyD88. Mouse macrophages were stimulated with 5, 10, 20, or 40 μg/mL rTs‐HSP70 for 12 h. Following stimulation, total cellular RNA and protein were extracted and analyzed. A. The effect of rTs‐HSP70 on the transcription level of TLR2 and MyD88 in mouse macrophage cells. B. Western blot analysis of the TLR2 and MyD88 expression in mouse macrophage cells after rTs‐HSP70 stimulation. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above the bars denote statistically significant differences ( p < 0.05), while the same letters indicate no significant difference.

    Article Snippet: To verify whether rTs‐HSP70 activates the NF‐κB and MAPK pathways via the TLR2/MyD88 signaling pathway, we pretreated cells with a TLR2‐specific antibody (Novus Biologicals, Centennial, CO, USA) and the MyD88 inhibitor T6167923 (MedChemExpress, Monmouth Junction, NJ, USA).

    Techniques: Recombinant, Expressing, Western Blot

    Recombinant Ts‐HSP70 affects mouse macrophage immune function via the TLR2/MyD88/ERK signaling pathway. Mouse macrophages were pretreated with a TLR2‐specific antibody (or control IgG) for 1 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min) and harvested for Western blot. In the MyD88 inhibition assay, RAW264.7 cells were pretreated with the MyD88 inhibitor T6167923 (5, 10 μg/mL; DMSO control) for 18 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min), and harvested for Western blot analysis. A. TLR2 blocking assay. B. MyD88 inhibition assay. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above bars indicate significant differences ( p < 0.05); the same letter indicates no significant difference.

    Journal: Transboundary and Emerging Diseases

    Article Title: Trichinella spiralis HSP70 Mediates Mice Immune Responses via TLR2/MyD88/ERK Signaling Pathway

    doi: 10.1155/tbed/5533482

    Figure Lengend Snippet: Recombinant Ts‐HSP70 affects mouse macrophage immune function via the TLR2/MyD88/ERK signaling pathway. Mouse macrophages were pretreated with a TLR2‐specific antibody (or control IgG) for 1 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min) and harvested for Western blot. In the MyD88 inhibition assay, RAW264.7 cells were pretreated with the MyD88 inhibitor T6167923 (5, 10 μg/mL; DMSO control) for 18 h, then stimulated with rTs‐HSP70 (1 μg/mL, 15 min), and harvested for Western blot analysis. A. TLR2 blocking assay. B. MyD88 inhibition assay. Statistical differences among groups were determined by one‐way ANOVA followed by Duncan’s multiple range test. Different letters above bars indicate significant differences ( p < 0.05); the same letter indicates no significant difference.

    Article Snippet: To verify whether rTs‐HSP70 activates the NF‐κB and MAPK pathways via the TLR2/MyD88 signaling pathway, we pretreated cells with a TLR2‐specific antibody (Novus Biologicals, Centennial, CO, USA) and the MyD88 inhibitor T6167923 (MedChemExpress, Monmouth Junction, NJ, USA).

    Techniques: Recombinant, Control, Western Blot, Inhibition, Blocking Assay

    (a) Effects of water intake on changes in lymph volume collected over set intervals of 60 min in rat jejunum‐derived lymph vessels in the absence (white column) and presence of a MyD88 inhibitor (oblique line column). (b) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐1β in the lymph. (c) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐6 in the lymph. (d) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐10 in the lymph. The error bars represent the SDs.

    Journal: Physiological Reports

    Article Title: Water intake regulates mucosal immunity in rat jejunal villi via IL ‐1β, IL ‐6, and IL ‐10

    doi: 10.14814/phy2.70891

    Figure Lengend Snippet: (a) Effects of water intake on changes in lymph volume collected over set intervals of 60 min in rat jejunum‐derived lymph vessels in the absence (white column) and presence of a MyD88 inhibitor (oblique line column). (b) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐1β in the lymph. (c) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐6 in the lymph. (d) Effects of water intake without (white column) and with a MyD88 inhibitor (oblique line column) on changes in the concentration of IL‐10 in the lymph. The error bars represent the SDs.

    Article Snippet: Clodronate‐containing liposomes (catalog no 16001004, Sigma‐Aldrich, USA) and an inhibitor of MyD88 (catalog no 2‐29328 Novus Bio, USA) are purchased.

    Techniques: Derivative Assay, Concentration Assay

    eHSP90α exerts its function through the TLR4‐MyD88 signaling axis. (A) The immunoprecipitation with anti‐HSP90α and anti‐TLR4 antibody was performed in neutrophils. (B) Immunofluorescence analysis of colocalization of FITC‐HSP90α and TLR4 in neutrophils. Control: unlabeled HSP90α. (C) Immunoblot and quantification analysis for LC3B and p62 in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 3) in absence or presence of TLR4 inhibitor (30 µ m ) ( n = 3), MyD88 inhibitor (1 µ m ) ( n = 3), 3‐MA (5 m m ) ( n = 3) and bafilomycin A1 (1 µ m ) ( n = 3). (D) The immunoprecipitation with anti‐MyD88 and anti‐Beclin 1 antibody was performed in neutrophils incubated with or without recombinant HSP90α (10 µg/mL). (E) Immunoblot and quantification analysis of p‐Beclin 1 and Beclin 1 in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 5) in absence or presence of anti‐HSP90α antibody (10 µg/mL) ( n = 5), TLR4 inhibitor (30 µ m ) ( n = 5), MyD88 inhibitor (1 µM) ( n = 5). (F,G) Immunofluorescence and quantification analysis of NETs in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 5) in absence or presence of TLR4 inhibitor (30 µM) ( n = 5) and MyD88 inhibitor (1 µM) ( n = 5). Cells were stained with DAPI for DNA (blue) and anti‐MPO for PMNs or NETs (green). Scale bars: 50 µm. (H) Quantification of MPO‐DNA in the supernatant of neutrophils from each group ( n = 5). All data are presented as the mean ± SD. Statistical analysis was conducted using one‐way ANOVA and Holm‐Šídák's multiple comparisons test (C, E–H). * P < 0.05, ** P < 0.01, *** P < 0.001. Each data point represents one experiment well (C, E, G, H). For A–H, three independent experiments were performed. LC3B, microtubule associated protein 1 light chain 3 beta.

    Journal: Advanced Science

    Article Title: Activated Platelet–Released Heat Shock Protein 90α Triggers Autophagy‐Dependent Neutrophil Extracellular Trap Formation and Amplifies Sepsis

    doi: 10.1002/advs.202515933

    Figure Lengend Snippet: eHSP90α exerts its function through the TLR4‐MyD88 signaling axis. (A) The immunoprecipitation with anti‐HSP90α and anti‐TLR4 antibody was performed in neutrophils. (B) Immunofluorescence analysis of colocalization of FITC‐HSP90α and TLR4 in neutrophils. Control: unlabeled HSP90α. (C) Immunoblot and quantification analysis for LC3B and p62 in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 3) in absence or presence of TLR4 inhibitor (30 µ m ) ( n = 3), MyD88 inhibitor (1 µ m ) ( n = 3), 3‐MA (5 m m ) ( n = 3) and bafilomycin A1 (1 µ m ) ( n = 3). (D) The immunoprecipitation with anti‐MyD88 and anti‐Beclin 1 antibody was performed in neutrophils incubated with or without recombinant HSP90α (10 µg/mL). (E) Immunoblot and quantification analysis of p‐Beclin 1 and Beclin 1 in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 5) in absence or presence of anti‐HSP90α antibody (10 µg/mL) ( n = 5), TLR4 inhibitor (30 µ m ) ( n = 5), MyD88 inhibitor (1 µM) ( n = 5). (F,G) Immunofluorescence and quantification analysis of NETs in neutrophils incubated with recombinant HSP90α (10 µg/mL) ( n = 5) in absence or presence of TLR4 inhibitor (30 µM) ( n = 5) and MyD88 inhibitor (1 µM) ( n = 5). Cells were stained with DAPI for DNA (blue) and anti‐MPO for PMNs or NETs (green). Scale bars: 50 µm. (H) Quantification of MPO‐DNA in the supernatant of neutrophils from each group ( n = 5). All data are presented as the mean ± SD. Statistical analysis was conducted using one‐way ANOVA and Holm‐Šídák's multiple comparisons test (C, E–H). * P < 0.05, ** P < 0.01, *** P < 0.001. Each data point represents one experiment well (C, E, G, H). For A–H, three independent experiments were performed. LC3B, microtubule associated protein 1 light chain 3 beta.

    Article Snippet: For TLR4‐mediated NET formation, isolated HD neutrophils were cultured with 10 μg/mL recombinant HSP90α, or supplemented with 30 μ m TLR4 inhibitor VIPER (Novus Biologicals, NBP2‐26244) or 1 μ m MYD88 inhibitor MyD88‐IN‐1 (MCE, HY‐149992).

    Techniques: Immunoprecipitation, Immunofluorescence, Control, Western Blot, Incubation, Recombinant, Staining