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rig i inhibitor bx795  (MedChemExpress)


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    MedChemExpress rig i inhibitor bx795
    Rig I Inhibitor Bx795, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 53 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/bx795/BX795/pm42316185-92-22-29
    Average 95 stars, based on 53 article reviews
    rig i inhibitor bx795 - by Bioz Stars, 2026-10
    95/100 stars

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    Related Articles

    Infection:

    Article Title: PARP10 condensation inhibits viral infection via targeting NAD + homeostasis
    Article Snippet: The Vesicular Stomatitis Virus (VSV) DNA plasmid, driven by a T7 promoter, was purchased from Miaoling Biology. .. Cells were treated with 500 μM sodium arsenite (Merck, 1.06277.1003) for 1 h, 20 ng/mL human IFNβ (Peprotech, 300-02BC), IFNγ (Peprotech, 300-02), TNFα (Peprotech, 300-01A) for 24 h, 10 μM Olaparib (MCE, HY-10162) or OUL-35 (R&D, 6344) for 5 h, VSV at MOI=1.5 for indicated times, SFV at MOI=0.5 for indicated times, 50 μg/mL poly(I:C) LMW (Invivogen, tlrl-picw) for 5 h, 100 μg/mL RNAse A (Takara, 740505) in PBS, 0.5 μM LysoTracker (Thermo Fisher Scientific, L12492) for 30 min at 37 °C, 1 μM CellTracker CM-Dil Dye (Invitrogen, C7000) for 30 min at 37 °C, 10 μM BX795 (MCE, HY-10514) 3 h before and during viral infection, 1-2 mM Nicotinamide riboside chloride (NR) (MCE, HY-123033A) or 1 μM FK866 (MCE, HY-50876) 24 h before and during viral infection. .. DNA fragments encoding human PARP10 were amplified from U2OS cDNA library by PCR and ligated into the HindIII and BamHI sites of mEGFP-C1 construct (Addgene #54759) using ClonExpress II One Step Cloning kit (Vazyme, C112).

    other:

    Article Title: A TAK1-Driven NLRP1 Inflammasome Pathway Revealed by Phosphatase-Targeting Environmental Toxins
    Article Snippet: Next day, when indicated, cells were pre-incubated for 1 hour in OPTI-MEM (Gibco, 51985034) with inhibitors before the addition of toxins or control stimuli.



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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    <t>TLR2/TBK1</t> signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor <t>BX795</t> (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .
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    Image Search Results


    TLR2/TBK1 signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor BX795 (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .

    Journal: Frontiers in Immunology

    Article Title: Nuclear IL-33 amplifies NF-κB signaling to drive neutrophil recruitment and activation in the endocervical epithelium during Mycoplasma genitalium infection

    doi: 10.3389/fimmu.2026.1820874

    Figure Lengend Snippet: TLR2/TBK1 signaling drives IL-33 mRNA expression. (A) IL-33 mRNA expression in cells stimulated with M. genitalium (100 MOI), heat-killed M. genitalium (HK-Mg, equivalent to MOI 100), or purified membrane lipoproteins (LP, 10μg/ml). (B) Cells were pretreated with anti-TLR2 Ab (10μg/ml), C29 (50μmol/L), or TAK-242 (1μmol/L) for 1h prior to infection; IL-33 levels were measured by qPCR. DMSO (0.1%) employed as the vehicle control. (C) Immunoblot of p-TBK1 (Ser172) and total TBK1 kinetics following infection. (D) Cells were treated with the TBK1 inhibitor BX795 (10 μmol/L) and IL-33 mRNA was quantified by qPCR. (E) End1/E6E7 cells were transfected with TBK1 siRNA, and the knockdown efficiency was assessed by qPCR. (F) IL-33 mRNA levels were measured in TBK1−depleted cells by qPCR. (G) Co-IP of TLR2 and TBK1 from cell lysates infected with M. genitalium . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05, **p < 0.01 as compared with the uninfected control (A) or indicated groups (B, D–G) . ns, no significant difference between groups (B, E) .

    Article Snippet: Specific pharmacological inhibitors included: the TLR2 inhibitor C29 (MedChemExpress); the TLR4 signaling inhibitor TAK-242 (CLI-095, InvivoGen); and the specific TBK1/IKKε inhibitor BX795 (InvivoGen).

    Techniques: Expressing, Purification, Membrane, Infection, Control, Western Blot, Transfection, Knockdown, Co-Immunoprecipitation Assay

    IRF1 and IRF7 are transcriptional regulators of IL-33 . (A) Immunoblot of IRF1 and IRF7 in nuclear fractions of cells infected with M. genitalium for 24 h. (B) Impact of TBK1 inhibitor BX795 on the nuclear accumulation of IRF1 and IRF7, DMSO (0.1%) employed as the vehicle control. (C, D) ChIP-qPCR analysis of IRF1 and IRF7 binding to the IL-33 promoter. Data are expressed as the percentage of input DNA (% Input). (E–G) End1/E6E7 cells were transfected with shRNA targeting IRF1 or IRF7, followed by M. genitalium infection. IL-33 mRNA and protein levels were assessed by qPCR (E, F) and immunoblot (G) . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05 vs. indicated groups (C–F) .

    Journal: Frontiers in Immunology

    Article Title: Nuclear IL-33 amplifies NF-κB signaling to drive neutrophil recruitment and activation in the endocervical epithelium during Mycoplasma genitalium infection

    doi: 10.3389/fimmu.2026.1820874

    Figure Lengend Snippet: IRF1 and IRF7 are transcriptional regulators of IL-33 . (A) Immunoblot of IRF1 and IRF7 in nuclear fractions of cells infected with M. genitalium for 24 h. (B) Impact of TBK1 inhibitor BX795 on the nuclear accumulation of IRF1 and IRF7, DMSO (0.1%) employed as the vehicle control. (C, D) ChIP-qPCR analysis of IRF1 and IRF7 binding to the IL-33 promoter. Data are expressed as the percentage of input DNA (% Input). (E–G) End1/E6E7 cells were transfected with shRNA targeting IRF1 or IRF7, followed by M. genitalium infection. IL-33 mRNA and protein levels were assessed by qPCR (E, F) and immunoblot (G) . Data are mean ± SEM of three independent biological experiments (n=3). *p < 0.05 vs. indicated groups (C–F) .

    Article Snippet: Specific pharmacological inhibitors included: the TLR2 inhibitor C29 (MedChemExpress); the TLR4 signaling inhibitor TAK-242 (CLI-095, InvivoGen); and the specific TBK1/IKKε inhibitor BX795 (InvivoGen).

    Techniques: Western Blot, Infection, Control, ChIP-qPCR, Analysis, Binding Assay, Transfection, shRNA, Real-time Polymerase Chain Reaction