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plc inhibitor d609  (Tocris)


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    Tocris plc inhibitor d609
    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the <t>PLC</t> inhibitor <t>D609</t> for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
    Plc Inhibitor D609, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/plc+inhibitor+d609/pmc08125753-171-53-56?v=Tocris
    Average 93 stars, based on 31 article reviews
    plc inhibitor d609 - by Bioz Stars, 2026-07
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    1) Product Images from "Oxaliplatin Causes Transient Changes in TRPM8 Channel Activity"

    Article Title: Oxaliplatin Causes Transient Changes in TRPM8 Channel Activity

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms22094962

    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the PLC inhibitor D609 for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
    Figure Legend Snippet: Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the PLC inhibitor D609 for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.

    Techniques Used: Plasmid Preparation, Transfection, Saline, Comparison, Activation Assay



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    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the <t>PLC</t> inhibitor <t>D609</t> for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
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    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the <t>PLC</t> inhibitor <t>D609</t> for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
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    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the <t>PLC</t> inhibitor <t>D609</t> for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
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    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the <t>PLC</t> inhibitor <t>D609</t> for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.
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    Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the PLC inhibitor D609 for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.

    Journal: International Journal of Molecular Sciences

    Article Title: Oxaliplatin Causes Transient Changes in TRPM8 Channel Activity

    doi: 10.3390/ijms22094962

    Figure Lengend Snippet: Phosphatidyl 4,5-bisphosphate concentrations are altered after oxaliplatin treatment. ( A ) Relative PIP 2 (phosphatidylinositol 4,5-bisphosphate) concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells treated with vehicle (saline) or 10 µM oxaliplatin for 24 h. Data represent the means ± SEM from n = 10–12 dishes per condition. * p < 0.05; *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( B ) Relative PIP 2 concentrations of untransfected HEK cells, empty-vector-transfected and TRPM8-transfected HEK cells that were treated with vehicle (saline), 10 µM oxaliplatin ±10 µM of the PLC inhibitor D609 for 5 h. Data represent the means ± SEM from n = 4–6 dishes per condition. *** p < 0.001; one-way ANOVA and Dunnett´s multiple comparison test. ( C ) Schematic overview of the proposed mechanisms leading to TRPM8 channel desensitization after acute oxaliplatin treatment. TRPM8 channel activation causes PLC pathway activation. In turn, PLC hydrolyzes PIP 2 to IP 3 (inositol 1,4,5-triphosphate) and DAG (1,2-diacylglycerol). PIP 2 -depletion is responsible for TRPM8 channel desensitization after oxaliplatin treatment.

    Article Snippet: For PI (4,5) P2 ELISA measurement analysis, (r)TRPM8-transfected or empty-vector-transfected and untransfected HEK cells were treated with 10 μM oxaliplatin for 24 h. For investigating the contribution of the PLC pathway to the PIP 2 amount, (r)TRPM8-transfected or empty-vector-transfected and untransfected HEK cells were treated with 10 μM oxaliplatin ±10 μM of the PLC inhibitor D609 (Tocris) for 5 h.

    Techniques: Plasmid Preparation, Transfection, Saline, Comparison, Activation Assay