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constructs for pparα  (Addgene inc)


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    Addgene inc constructs for pparα
    (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated <t>PPAR</t> antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 <t>nM</t> <t>(PPARγ</t> agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.
    Constructs For Pparα, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/constructs+for+ppar%CE%B1/pSG5+PPAR+alpha+(Plasmid+%2322751)/pmc04752002-134-2-0
    Average 93 stars, based on 28 article reviews
    constructs for pparα - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "PPARδ repression in Huntington’s disease and its essential role in CNS translate into a potent agonist therapy"

    Article Title: PPARδ repression in Huntington’s disease and its essential role in CNS translate into a potent agonist therapy

    Journal: Nature medicine

    doi: 10.1038/nm.4003

    (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated PPAR antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 nM (PPARγ agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.
    Figure Legend Snippet: (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated PPAR antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 nM (PPARγ agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.

    Techniques Used: Luciferase, Activity Assay, Transgenic Assay, Control, Transfection, Plasmid Preparation, Expressing, Construct, Membrane, Fluorescence, Positive Control, Immunofluorescence, Staining, shRNA

    Related Articles

    Construct:

    Article Title: PPARδ repression in Huntington’s disease and its essential role in CNS translate into a potent agonist therapy
    Article Snippet: Co-transfection with the indicated constructs (previously described ) was done with Lipofectamine 2000, as per manufacturer’s protocol (Invitrogen). .. Addgene provided constructs for PPARα (22751) and PPARγ (8895). .. PPARδ-Flag (Origene, MR207001) truncation constructs [ΔA–C (Δ1-141), ΔA–D (Δ1-214), ΔD–F (Δ143-440), and ΔE–F (Δ215-440)] were made by standard techniques and verified by sequencing.



    Similar Products

    constructs for pparα  (Addgene inc)
    93
    Addgene inc constructs for pparα
    (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated <t>PPAR</t> antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 <t>nM</t> <t>(PPARγ</t> agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.
    Constructs For Pparα, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/constructs+for+ppar%CE%B1/pSG5+PPAR+alpha+(Plasmid+%2322751)/pmc04752002-134-2-0
    Average 93 stars, based on 1 article reviews
    constructs for pparα - by Bioz Stars, 2026-09
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated PPAR antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 nM (PPARγ agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.

    Journal: Nature medicine

    Article Title: PPARδ repression in Huntington’s disease and its essential role in CNS translate into a potent agonist therapy

    doi: 10.1038/nm.4003

    Figure Lengend Snippet: (a) 3X-PPRE luciferase reporter activity in primary cortical neurons from BAC-HD or non-transgenic (Non-Tg) control mice, co-transfected with Renilla luciferase vector, and PPARδ and/or PGC-1α expression constructs, as indicated, and treated with GW501516 (100 nM) or vehicle. Results were normalized to Non-Tg neurons at baseline. * P < .05; t-test. (b) Mitochondrial membrane potential of primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated, was determined from the ratio of mitochondrial to cytosolic JC-1 fluorescence. Results were normalized to Non-Tg neurons at baseline, and CCCP treatment served as a positive control for depolarization. * P < .05, ** P < .01; t-test. (c) Immunofluorescence of active caspase-3 (red) and microtubule-associated protein 2 (green) in primary cortical neurons from BAC-HD and Non-Tg mice, treated as indicated. Scale bar = 20 μm. (d) Quantification of active caspase-3 staining shown in (e) . Results were normalized to Non-Tg neurons at baseline. * P < .05, ** P < .01; t-test. (e) Cortex from Non-Tg mice immunostained with the indicated PPAR antibody (green) and NeuN antibody (red). Merged images reveal expression of indicated PPAR. Scale bar = 50 μm. (f) Immunofluorescence of active caspase-3 in primary cortical neurons from BAC-HD mice, transfected with the indicated shRNA construct for 3 days, or treated with fenofibrate 100 nM (PPARα agonist), GW501516 100 nM (PPARδ agonist), or pioglitazone 20 nM (PPARγ agonist) for 24 h, prior to exposure to 25 μM H 2 O 2 . * P < .05, ** P < .01; ANOVA with post-hoc Tukey. Error bars = s.e.m. All experiments were performed with 3 biological replicates and 9 technical replicates per condition.

    Article Snippet: Addgene provided constructs for PPARα (22751) and PPARγ (8895).

    Techniques: Luciferase, Activity Assay, Transgenic Assay, Control, Transfection, Plasmid Preparation, Expressing, Construct, Membrane, Fluorescence, Positive Control, Immunofluorescence, Staining, shRNA