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h 151  (InvivoGen)


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    InvivoGen h 151
    H 151, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 155 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/h 151/product/InvivoGen
    Average 96 stars, based on 155 article reviews
    h 151 - by Bioz Stars, 2026-05
    96/100 stars

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    (A) Cells were pretreated (t = −1 hr) with BAY 11-7082 (10 μM) to inhibit NFκB activation. IL-6 secretion was measured 24 hrs after dopamine treatment using AlphaLISA, demonstrating that dopamine-induced IL-6 secretion is mediated through the NFκB pathway, (Biological replicates: N=19). Data are presented as box and whisker plot (min to max). See and . (B-F) Cells were treated with dopamine in a time-course experiment (5, 15, 30, 60, and 360 minutes) and assessed for cGAS protein expression (normalized to total protein expression, Biological replicate: N=5-14) as well as phosphorylation of STING (Biological replicate: N=7-9), TBK1 (Biological replicate: N=5-7), and IRF3 (Biological replicate: N=5), (normalized to the total expression level of each protein) by western blotting. Individual values are shown with line demonstrating mean. See and . (G-I) Cells were pretreated (t = −1 hr) with G-140 (1 μM) <t>or</t> <t>H-151</t> (1 μM) to inhibit the cGAS-STING pathway, and the inhibitory effects were validated by western blotting. Cells were then treated with dopamine (t = 0). IL-6 secretion was measured 24 hrs post-treatment using AlphaLISA (Biological replicate: G-140:N=14 and H-151: N=10), demonstrating that activation of the cGAS-STING pathway contributes to dopamine-induced IL-6 secretion. Data are presented as box and whisker plot (min to max). Paired comparisons were analyzed using a paired t -test (non-parametric: Wilcoxon test) in panel C-F or paired one-way ANOVA (non-parametric: Friedman test) in panel A, H and I. Significance levels are indicated as follows: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).
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    (A) Cells were pretreated (t = −1 hr) with BAY 11-7082 (10 μM) to inhibit NFκB activation. IL-6 secretion was measured 24 hrs after dopamine treatment using AlphaLISA, demonstrating that dopamine-induced IL-6 secretion is mediated through the NFκB pathway, (Biological replicates: N=19). Data are presented as box and whisker plot (min to max). See and . (B-F) Cells were treated with dopamine in a time-course experiment (5, 15, 30, 60, and 360 minutes) and assessed for cGAS protein expression (normalized to total protein expression, Biological replicate: N=5-14) as well as phosphorylation of STING (Biological replicate: N=7-9), TBK1 (Biological replicate: N=5-7), and IRF3 (Biological replicate: N=5), (normalized to the total expression level of each protein) by western blotting. Individual values are shown with line demonstrating mean. See and . (G-I) Cells were pretreated (t = −1 hr) with G-140 (1 μM) <t>or</t> <t>H-151</t> (1 μM) to inhibit the cGAS-STING pathway, and the inhibitory effects were validated by western blotting. Cells were then treated with dopamine (t = 0). IL-6 secretion was measured 24 hrs post-treatment using AlphaLISA (Biological replicate: G-140:N=14 and H-151: N=10), demonstrating that activation of the cGAS-STING pathway contributes to dopamine-induced IL-6 secretion. Data are presented as box and whisker plot (min to max). Paired comparisons were analyzed using a paired t -test (non-parametric: Wilcoxon test) in panel C-F or paired one-way ANOVA (non-parametric: Friedman test) in panel A, H and I. Significance levels are indicated as follows: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).
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    sting inhibitor h 151  (InvivoGen)
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    (A) Cells were pretreated (t = −1 hr) with BAY 11-7082 (10 μM) to inhibit NFκB activation. IL-6 secretion was measured 24 hrs after dopamine treatment using AlphaLISA, demonstrating that dopamine-induced IL-6 secretion is mediated through the NFκB pathway, (Biological replicates: N=19). Data are presented as box and whisker plot (min to max). See and . (B-F) Cells were treated with dopamine in a time-course experiment (5, 15, 30, 60, and 360 minutes) and assessed for cGAS protein expression (normalized to total protein expression, Biological replicate: N=5-14) as well as phosphorylation of STING (Biological replicate: N=7-9), TBK1 (Biological replicate: N=5-7), and IRF3 (Biological replicate: N=5), (normalized to the total expression level of each protein) by western blotting. Individual values are shown with line demonstrating mean. See and . (G-I) Cells were pretreated (t = −1 hr) with G-140 (1 μM) <t>or</t> <t>H-151</t> (1 μM) to inhibit the cGAS-STING pathway, and the inhibitory effects were validated by western blotting. Cells were then treated with dopamine (t = 0). IL-6 secretion was measured 24 hrs post-treatment using AlphaLISA (Biological replicate: G-140:N=14 and H-151: N=10), demonstrating that activation of the cGAS-STING pathway contributes to dopamine-induced IL-6 secretion. Data are presented as box and whisker plot (min to max). Paired comparisons were analyzed using a paired t -test (non-parametric: Wilcoxon test) in panel C-F or paired one-way ANOVA (non-parametric: Friedman test) in panel A, H and I. Significance levels are indicated as follows: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).
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    (A) Cells were pretreated (t = −1 hr) with BAY 11-7082 (10 μM) to inhibit NFκB activation. IL-6 secretion was measured 24 hrs after dopamine treatment using AlphaLISA, demonstrating that dopamine-induced IL-6 secretion is mediated through the NFκB pathway, (Biological replicates: N=19). Data are presented as box and whisker plot (min to max). See and . (B-F) Cells were treated with dopamine in a time-course experiment (5, 15, 30, 60, and 360 minutes) and assessed for cGAS protein expression (normalized to total protein expression, Biological replicate: N=5-14) as well as phosphorylation of STING (Biological replicate: N=7-9), TBK1 (Biological replicate: N=5-7), and IRF3 (Biological replicate: N=5), (normalized to the total expression level of each protein) by western blotting. Individual values are shown with line demonstrating mean. See and . (G-I) Cells were pretreated (t = −1 hr) with G-140 (1 μM) or H-151 (1 μM) to inhibit the cGAS-STING pathway, and the inhibitory effects were validated by western blotting. Cells were then treated with dopamine (t = 0). IL-6 secretion was measured 24 hrs post-treatment using AlphaLISA (Biological replicate: G-140:N=14 and H-151: N=10), demonstrating that activation of the cGAS-STING pathway contributes to dopamine-induced IL-6 secretion. Data are presented as box and whisker plot (min to max). Paired comparisons were analyzed using a paired t -test (non-parametric: Wilcoxon test) in panel C-F or paired one-way ANOVA (non-parametric: Friedman test) in panel A, H and I. Significance levels are indicated as follows: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

    Journal: bioRxiv

    Article Title: It’s Not Rewarding for Mitochondria: Dopamine-Induced Mitochondrial Dysfunction Activates cGAS-STING to Drive IL-6 Secretion in Macrophages

    doi: 10.64898/2026.04.23.719926

    Figure Lengend Snippet: (A) Cells were pretreated (t = −1 hr) with BAY 11-7082 (10 μM) to inhibit NFκB activation. IL-6 secretion was measured 24 hrs after dopamine treatment using AlphaLISA, demonstrating that dopamine-induced IL-6 secretion is mediated through the NFκB pathway, (Biological replicates: N=19). Data are presented as box and whisker plot (min to max). See and . (B-F) Cells were treated with dopamine in a time-course experiment (5, 15, 30, 60, and 360 minutes) and assessed for cGAS protein expression (normalized to total protein expression, Biological replicate: N=5-14) as well as phosphorylation of STING (Biological replicate: N=7-9), TBK1 (Biological replicate: N=5-7), and IRF3 (Biological replicate: N=5), (normalized to the total expression level of each protein) by western blotting. Individual values are shown with line demonstrating mean. See and . (G-I) Cells were pretreated (t = −1 hr) with G-140 (1 μM) or H-151 (1 μM) to inhibit the cGAS-STING pathway, and the inhibitory effects were validated by western blotting. Cells were then treated with dopamine (t = 0). IL-6 secretion was measured 24 hrs post-treatment using AlphaLISA (Biological replicate: G-140:N=14 and H-151: N=10), demonstrating that activation of the cGAS-STING pathway contributes to dopamine-induced IL-6 secretion. Data are presented as box and whisker plot (min to max). Paired comparisons were analyzed using a paired t -test (non-parametric: Wilcoxon test) in panel C-F or paired one-way ANOVA (non-parametric: Friedman test) in panel A, H and I. Significance levels are indicated as follows: p < 0.05 (*), p < 0.01 (**), p < 0.001 (***).

    Article Snippet: Dopamine hydrochloride (DA; #H8502, Sigma-Aldrich), lipopolysaccharide from Escherichia coli O55:B5 (LPS; #L2880, MilliporeSigma), carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP; #0453, Tocris), 2′3′-cGAMP (#HY-12512, MedChemExpress), Mdivi-1 (#HY-15886, MedChemExpress), G140 (#HY-133916, MedChemExpress), H-151 (#HY-112693, MedChemExpress), ethidium bromide (EtBr; #HY-D0021, MedChemExpress), BAY 11-7082 (#S2913, Selleck Chemicals) were purchased from the indicated vendors.

    Techniques: Activation Assay, Whisker Assay, Expressing, Phospho-proteomics, Western Blot