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recombinant ppar γ  (Sino Biological)


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    Sino Biological recombinant ppar γ
    Recombinant Ppar γ, supplied by Sino Biological, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ppar+%CE%B3+protein/Human+PPARG+%2F+Nr1c3+%2F+PPARgamma+Protein/pm41969066-407-10-14
    Average 94 stars, based on 8 article reviews
    recombinant ppar γ - by Bioz Stars, 2026-10
    94/100 stars

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    other:

    Article Title: 1,8-Cineole ameliorates vascular endothelial senescence in diabetes mellitus by directly targeting and deubiquitinating PPAR-γ in vivo and in vitro
    Article Snippet: 10 PPAR-γ protein (12019-H20B) was supplied by Sino biological (Beijing, China).



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    AS attenuates steatosis via the multi-target and <t>PPARγ</t> pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant <t>PPARγ</t> <t>protein</t> upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    AS attenuates steatosis via the multi-target and <t>PPARγ</t> pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant <t>PPARγ</t> <t>protein</t> upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    AS attenuates steatosis via the multi-target and <t>PPARγ</t> pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant <t>PPARγ</t> <t>protein</t> upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    AS attenuates steatosis via the multi-target and <t>PPARγ</t> pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant <t>PPARγ</t> <t>protein</t> upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    AS attenuates steatosis via the multi-target and <t>PPARγ</t> pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant <t>PPARγ</t> <t>protein</t> upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.
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    Image Search Results


    AS attenuates steatosis via the multi-target and PPARγ pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant PPARγ protein upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.

    Journal: Frontiers in Pharmacology

    Article Title: Acetylshikonin mitigates diet-induced MASLD by targeting PPARγ-mediated metabolic dysfunction

    doi: 10.3389/fphar.2026.1735481

    Figure Lengend Snippet: AS attenuates steatosis via the multi-target and PPARγ pathways. (A) Molecular docking models showing AS binding to key targets including PPARγ, PPARα, mTOR, FASN, HIF1A, and ESR1, generated using AutoDock Vina. (B) Thermal shift assay showing increased thermal stability of recombinant PPARγ protein upon AS binding at various temperatures. (C) qPCR analysis showing reduced hepatic Pparγ mRNA levels in AS-treated HFHC-fed mice (n = 6). (D) Western blot analysis demonstrating dose-dependent downregulation of the PPARγ protein in PA/OA-stimulated Hepa1-6 cells treated with AS (n = 3); representative blots and quantification are shown. (E,F) Lipid droplet accumulation assessed using BODIPY staining in Hepa1-6 cells co-treated with AS and the PPARγ antagonist GW9662; fluorescence quantification confirms the synergistic effect; scale bar: 10 μm. All quantitative data are shown as the mean ± SD; * p < 0.05, ** p < 0.01, and *** p < 0.001.

    Article Snippet: To block non-specific binding, the membranes were incubated in 5% skimmed milk powder for 2 h. The membranes were incubated overnight at 4 °C with primary antibodies against PPARγ protein (16643-1-AP, 1:1000, Proteintech) and GAPDH (60004-1-Ig, 1:10,000, Proteintech).

    Techniques: Binding Assay, Generated, Thermal Shift Assay, Recombinant, Western Blot, Staining, Fluorescence