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elisa kits for mcp1  (R&D Systems)


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    R&D Systems elisa kits for mcp1
    AhR inhibition has no effect on the anti-inflammatory actions of Kyn-CKA in BMDMs. (A) Mouse AhR reporter cells expressing luciferase under the control of the xenobiotic response element (XRE) were incubated with Kyn-CKA or kynurenine for 24 h prior to luminescence measurement (n = 3). Data were fitted to a sigmoidal four-parameter logistic curve (L-Kyn: r 2 = 0.824, IC 50 = 28 μM, span = 3218 RFU. Kyn-CKA: r 2 = 0.970, IC 50 = 13 μM, span = 47,901 RFU). (B) Inhibition of AhR-dependent luciferase expression by CH223191 (AhRinh). (C–F) Kyn-CKA inhibits the expression of the NF-κB-regulated genes IL6, <t>MCP1,</t> Nos2 and IL1β in BMDM following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA both in the presence or absence of CH223191 (10 μM). Data are n = 3–4, ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test. (G – H) Extracellular cytokine levels from BMDM treated as in C–F for 5 h. Data are n = 3–4 (all replicates shown), ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test.
    Elisa Kits For Mcp1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 217 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2"

    Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

    Journal: Redox Biology

    doi: 10.1016/j.redox.2026.104009

    AhR inhibition has no effect on the anti-inflammatory actions of Kyn-CKA in BMDMs. (A) Mouse AhR reporter cells expressing luciferase under the control of the xenobiotic response element (XRE) were incubated with Kyn-CKA or kynurenine for 24 h prior to luminescence measurement (n = 3). Data were fitted to a sigmoidal four-parameter logistic curve (L-Kyn: r 2 = 0.824, IC 50 = 28 μM, span = 3218 RFU. Kyn-CKA: r 2 = 0.970, IC 50 = 13 μM, span = 47,901 RFU). (B) Inhibition of AhR-dependent luciferase expression by CH223191 (AhRinh). (C–F) Kyn-CKA inhibits the expression of the NF-κB-regulated genes IL6, MCP1, Nos2 and IL1β in BMDM following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA both in the presence or absence of CH223191 (10 μM). Data are n = 3–4, ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test. (G – H) Extracellular cytokine levels from BMDM treated as in C–F for 5 h. Data are n = 3–4 (all replicates shown), ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test.
    Figure Legend Snippet: AhR inhibition has no effect on the anti-inflammatory actions of Kyn-CKA in BMDMs. (A) Mouse AhR reporter cells expressing luciferase under the control of the xenobiotic response element (XRE) were incubated with Kyn-CKA or kynurenine for 24 h prior to luminescence measurement (n = 3). Data were fitted to a sigmoidal four-parameter logistic curve (L-Kyn: r 2 = 0.824, IC 50 = 28 μM, span = 3218 RFU. Kyn-CKA: r 2 = 0.970, IC 50 = 13 μM, span = 47,901 RFU). (B) Inhibition of AhR-dependent luciferase expression by CH223191 (AhRinh). (C–F) Kyn-CKA inhibits the expression of the NF-κB-regulated genes IL6, MCP1, Nos2 and IL1β in BMDM following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA both in the presence or absence of CH223191 (10 μM). Data are n = 3–4, ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test. (G – H) Extracellular cytokine levels from BMDM treated as in C–F for 5 h. Data are n = 3–4 (all replicates shown), ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test.

    Techniques Used: Inhibition, Expressing, Luciferase, Control, Incubation

    The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).
    Figure Legend Snippet: The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).

    Techniques Used: Expressing, Knock-Out, Incubation



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    Image Search Results


    AhR inhibition has no effect on the anti-inflammatory actions of Kyn-CKA in BMDMs. (A) Mouse AhR reporter cells expressing luciferase under the control of the xenobiotic response element (XRE) were incubated with Kyn-CKA or kynurenine for 24 h prior to luminescence measurement (n = 3). Data were fitted to a sigmoidal four-parameter logistic curve (L-Kyn: r 2 = 0.824, IC 50 = 28 μM, span = 3218 RFU. Kyn-CKA: r 2 = 0.970, IC 50 = 13 μM, span = 47,901 RFU). (B) Inhibition of AhR-dependent luciferase expression by CH223191 (AhRinh). (C–F) Kyn-CKA inhibits the expression of the NF-κB-regulated genes IL6, MCP1, Nos2 and IL1β in BMDM following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA both in the presence or absence of CH223191 (10 μM). Data are n = 3–4, ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test. (G – H) Extracellular cytokine levels from BMDM treated as in C–F for 5 h. Data are n = 3–4 (all replicates shown), ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test.

    Journal: Redox Biology

    Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

    doi: 10.1016/j.redox.2026.104009

    Figure Lengend Snippet: AhR inhibition has no effect on the anti-inflammatory actions of Kyn-CKA in BMDMs. (A) Mouse AhR reporter cells expressing luciferase under the control of the xenobiotic response element (XRE) were incubated with Kyn-CKA or kynurenine for 24 h prior to luminescence measurement (n = 3). Data were fitted to a sigmoidal four-parameter logistic curve (L-Kyn: r 2 = 0.824, IC 50 = 28 μM, span = 3218 RFU. Kyn-CKA: r 2 = 0.970, IC 50 = 13 μM, span = 47,901 RFU). (B) Inhibition of AhR-dependent luciferase expression by CH223191 (AhRinh). (C–F) Kyn-CKA inhibits the expression of the NF-κB-regulated genes IL6, MCP1, Nos2 and IL1β in BMDM following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA both in the presence or absence of CH223191 (10 μM). Data are n = 3–4, ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test. (G – H) Extracellular cytokine levels from BMDM treated as in C–F for 5 h. Data are n = 3–4 (all replicates shown), ∗∗∗∗p < 0.0001 by one-way ANOVA and Tukey's post-test.

    Article Snippet: ELISA kits for MCP1 (DY479 and MJE00B) and IL6 (DY406) were obtained from R&D Systems (Minneapolis, MN).

    Techniques: Inhibition, Expressing, Luciferase, Control, Incubation

    The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).

    Journal: Redox Biology

    Article Title: The electrophilic metabolite of kynurenine, kynurenine-CKA, requires C151 in Keap1 to derepress Nrf2

    doi: 10.1016/j.redox.2026.104009

    Figure Lengend Snippet: The low-dose anti-inflammatory effects of Kyn-CKA in BMDMs are dependent on Nrf2. (A – B) Treatment with Kyn-CKA (5 h) fails to induce the expression of Nqo1 and Gclm in BMDMs obtained from Nrf2-knockout (Nrf2 −/− ) mice. Data are n = 3, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. (C – G) Effects of Kyn-CKA on the expression of NF-κB−regulated genes in WT and Nrf2-KO BMDMs following 5 h incubation with LPS (0.5 μg/mL) and the indicated concentrations of Kyn-CKA. Data are n = 6, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001 by two-way ANOVA and Tukey's post-test. Nrf2 was identified as a significant source of variation for MCP1, IL6, TNFα, Nos2, (p < 0.0001) and IL1β (p < 0.005).

    Article Snippet: ELISA kits for MCP1 (DY479 and MJE00B) and IL6 (DY406) were obtained from R&D Systems (Minneapolis, MN).

    Techniques: Expressing, Knock-Out, Incubation