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ppar γ agonist  (MedChemExpress)


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    MedChemExpress ppar γ agonist
    The enhanced APC function of B cells by OA in vitro is achieved through H3K27ac-mediated upregulation of <t>PPAR</t> γ expression. A Protein expression of β -actin and H3K27ac in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS and treated with OA was assessed by WB. β -Actin was used as the internal control to calculate the relative expression level of H3K27ac. B The enrichment percentage of H3K27ac at the PPAR γ , CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. C Correlation analysis of PPAR γ and APC function-related genes (CD80, CD86, CD83, MHC II) in B cells in OvCa patients in the TCGA database (n = 426). D Analysis of protein interaction among FABP4, PPAR γ , CD80, CD86, and CD83. E The enrichment percentage of PPAR γ at the CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. F Mean fluorescence intensity of CD80, CD86, and CD83 in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS, GW9662/Trog, and treated with OA was detected by flow cytometry. AS, Ascites; Ag, Antigen; OA, oleic acid; BMS, BMS309403. Data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, not significant
    Ppar γ Agonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Promoting APC function of B cells via reprogramming the fatty acid metabolism enhances anticancer immunity in metastatic ovarian cancer"

    Article Title: Promoting APC function of B cells via reprogramming the fatty acid metabolism enhances anticancer immunity in metastatic ovarian cancer

    Journal: Cancer Immunology, Immunotherapy : CII

    doi: 10.1007/s00262-026-04387-y

    The enhanced APC function of B cells by OA in vitro is achieved through H3K27ac-mediated upregulation of PPAR γ expression. A Protein expression of β -actin and H3K27ac in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS and treated with OA was assessed by WB. β -Actin was used as the internal control to calculate the relative expression level of H3K27ac. B The enrichment percentage of H3K27ac at the PPAR γ , CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. C Correlation analysis of PPAR γ and APC function-related genes (CD80, CD86, CD83, MHC II) in B cells in OvCa patients in the TCGA database (n = 426). D Analysis of protein interaction among FABP4, PPAR γ , CD80, CD86, and CD83. E The enrichment percentage of PPAR γ at the CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. F Mean fluorescence intensity of CD80, CD86, and CD83 in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS, GW9662/Trog, and treated with OA was detected by flow cytometry. AS, Ascites; Ag, Antigen; OA, oleic acid; BMS, BMS309403. Data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, not significant
    Figure Legend Snippet: The enhanced APC function of B cells by OA in vitro is achieved through H3K27ac-mediated upregulation of PPAR γ expression. A Protein expression of β -actin and H3K27ac in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS and treated with OA was assessed by WB. β -Actin was used as the internal control to calculate the relative expression level of H3K27ac. B The enrichment percentage of H3K27ac at the PPAR γ , CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. C Correlation analysis of PPAR γ and APC function-related genes (CD80, CD86, CD83, MHC II) in B cells in OvCa patients in the TCGA database (n = 426). D Analysis of protein interaction among FABP4, PPAR γ , CD80, CD86, and CD83. E The enrichment percentage of PPAR γ at the CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. F Mean fluorescence intensity of CD80, CD86, and CD83 in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS, GW9662/Trog, and treated with OA was detected by flow cytometry. AS, Ascites; Ag, Antigen; OA, oleic acid; BMS, BMS309403. Data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, not significant

    Techniques Used: In Vitro, Expressing, Control, ChIP-sequencing, Fluorescence, Flow Cytometry

    The mechanism diagram of combining adoptive immunotherapy with APC-function-enhanced B cells and LDC improves anticancer immunity in metastatic OvCa mice. In vitro, OA enhances the expression of CD80/CD86/CD83 of B cells through the H3K27ac-mediated upregulation of PPAR γ expression. Then, the B cells are adoptively transferred into the abdominal cavity of metastatic OvCa mice. In the abdominal cavity, LDC facilitates the APC function of the transferred B cells by causing apoptosis of cancer cells. The transferred B cells promote the activation, proliferation, and differentiation of T cells, which release higher levels of effector molecules (IL-2, GZMB, and IFN- γ , etc.), and facilitate the formation of lymphoid aggregates, finally improving anticancer immunity. LDC, low-dose chemotherapy
    Figure Legend Snippet: The mechanism diagram of combining adoptive immunotherapy with APC-function-enhanced B cells and LDC improves anticancer immunity in metastatic OvCa mice. In vitro, OA enhances the expression of CD80/CD86/CD83 of B cells through the H3K27ac-mediated upregulation of PPAR γ expression. Then, the B cells are adoptively transferred into the abdominal cavity of metastatic OvCa mice. In the abdominal cavity, LDC facilitates the APC function of the transferred B cells by causing apoptosis of cancer cells. The transferred B cells promote the activation, proliferation, and differentiation of T cells, which release higher levels of effector molecules (IL-2, GZMB, and IFN- γ , etc.), and facilitate the formation of lymphoid aggregates, finally improving anticancer immunity. LDC, low-dose chemotherapy

    Techniques Used: In Vitro, Expressing, Activation Assay

    Related Articles

    Recombinant:

    Article Title: Schistosome egg-derived extracellular vesicles deliver Sja-miR-71a inhibits host macrophage and neutrophil extracellular traps via targeting Sema4D
    Article Snippet: .. They were then treated with Schistosome egg-derived EVs (E-EVs, 10 μg/ml) for 24 h, a Sja-miR-71a mimic (50 nM, Ribobio China) for 24 h, recombinant Sema4D protein (10 μg/ml; Abclonal, USA) for 24 h, IL-10 antibodies (15 μg/ml; Proteintech, China) for 24 h, and a PPAR-γ agonist (30μΜ; MedchemExpress, USA) and antagonist (20 μM; MedchemExpress, USA) for 24 h. phorbol-12-myristate-13-acetate (PMA) (500 nM; ETs-inducer; Sigma-Aldrich, USA) Reagent was used to stimulate neutrophils and macrophages 4 h before harvesting. .. As described in our previous study [ ], the rAAV HBAAV2/9-Sja-miR-71a was purchased from Hanbio Biotechnology Co., Ltd. Mice were randomized into groups and inoculated with rAAV (1.5 × 10 [ ] v.g./mouse) via tail vein injection 10 days after infection with S. japonicum .

    Article Title: Schistosome egg-derived extracellular vesicles deliver Sja-miR-71a inhibits host macrophage and neutrophil extracellular traps via targeting Sema4D.
    Article Snippet: .. They were then treated with Schistosome egg-derived EVs (E-EVs, 10 μg/ml) for 24 h, a Sja-miR-71a mimic (50 nM, Ribobio China) for 24 h, recombinant Sema4D protein (10 μg/ml; Abclonal, USA) for 24 h, IL-10 antibodies (15 μg/ml; Proteintech, China) for 24 h, and a PPAR-γ agonist (30μΜ; MedchemExpress, USA) and antagonist (20 μM; MedchemExpress, USA) for 24 h. phorbol-12-myristate-13-acetate (PMA) (500 nM; ETs-inducer; Sigma-Aldrich, USA) Reagent was used to stimulate neutrophils and macrophages 4 h before harvesting. .. Recombinant adeno‐associated virus (rAAV) vectors and transduction As described in our previous study [13], the rAAV HBAAV2/9-Sja-miR-71a was purchased from Hanbio Biotechnology Co., Ltd. Mice were randomized into groups and inoculated with rAAV (1.5 × 10 [11] v.g./ mouse) via tail vein injection 10 days after infection with S. japonicum.

    Binding Assay:

    Article Title: Promoting APC function of B cells via reprogramming the fatty acid metabolism enhances anticancer immunity in metastatic ovarian cancer
    Article Snippet: .. In the mechanistic study, mouse ascitic CD19 + B cells (1 × 10 6 /ml) were pretreated with fatty acid binding protein 4 gene (FABP4) inhibitor (BMS309403, MedChemExpress; Cat# HY-101903; 50 μM), PPARγ antagonist (GW9662, MedChemExpress; Cat# HY-16578; 25 μM), and PPAR γ agonist (Troglitazone, Trog, MedChemExpress; Cat# HY-50935; 10 μM) for 2h, respectively. ..



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    The enhanced APC function of B cells by OA in vitro is achieved through H3K27ac-mediated upregulation of PPAR γ expression. A Protein expression of β -actin and H3K27ac in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS and treated with OA was assessed by WB. β -Actin was used as the internal control to calculate the relative expression level of H3K27ac. B The enrichment percentage of H3K27ac at the PPAR γ , CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. C Correlation analysis of PPAR γ and APC function-related genes (CD80, CD86, CD83, MHC II) in B cells in OvCa patients in the TCGA database (n = 426). D Analysis of protein interaction among FABP4, PPAR γ , CD80, CD86, and CD83. E The enrichment percentage of PPAR γ at the CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. F Mean fluorescence intensity of CD80, CD86, and CD83 in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS, GW9662/Trog, and treated with OA was detected by flow cytometry. AS, Ascites; Ag, Antigen; OA, oleic acid; BMS, BMS309403. Data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, not significant

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Promoting APC function of B cells via reprogramming the fatty acid metabolism enhances anticancer immunity in metastatic ovarian cancer

    doi: 10.1007/s00262-026-04387-y

    Figure Lengend Snippet: The enhanced APC function of B cells by OA in vitro is achieved through H3K27ac-mediated upregulation of PPAR γ expression. A Protein expression of β -actin and H3K27ac in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS and treated with OA was assessed by WB. β -Actin was used as the internal control to calculate the relative expression level of H3K27ac. B The enrichment percentage of H3K27ac at the PPAR γ , CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. C Correlation analysis of PPAR γ and APC function-related genes (CD80, CD86, CD83, MHC II) in B cells in OvCa patients in the TCGA database (n = 426). D Analysis of protein interaction among FABP4, PPAR γ , CD80, CD86, and CD83. E The enrichment percentage of PPAR γ at the CD80, CD86, and CD83 promoter regions was quantified using ChIP-seq analysis. F Mean fluorescence intensity of CD80, CD86, and CD83 in 3 w OvCa-bearing mouse ascitic CD19 + B cells pretreated with BMS, GW9662/Trog, and treated with OA was detected by flow cytometry. AS, Ascites; Ag, Antigen; OA, oleic acid; BMS, BMS309403. Data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, ns, not significant

    Article Snippet: In the mechanistic study, mouse ascitic CD19 + B cells (1 × 10 6 /ml) were pretreated with fatty acid binding protein 4 gene (FABP4) inhibitor (BMS309403, MedChemExpress; Cat# HY-101903; 50 μM), PPARγ antagonist (GW9662, MedChemExpress; Cat# HY-16578; 25 μM), and PPAR γ agonist (Troglitazone, Trog, MedChemExpress; Cat# HY-50935; 10 μM) for 2h, respectively.

    Techniques: In Vitro, Expressing, Control, ChIP-sequencing, Fluorescence, Flow Cytometry

    The mechanism diagram of combining adoptive immunotherapy with APC-function-enhanced B cells and LDC improves anticancer immunity in metastatic OvCa mice. In vitro, OA enhances the expression of CD80/CD86/CD83 of B cells through the H3K27ac-mediated upregulation of PPAR γ expression. Then, the B cells are adoptively transferred into the abdominal cavity of metastatic OvCa mice. In the abdominal cavity, LDC facilitates the APC function of the transferred B cells by causing apoptosis of cancer cells. The transferred B cells promote the activation, proliferation, and differentiation of T cells, which release higher levels of effector molecules (IL-2, GZMB, and IFN- γ , etc.), and facilitate the formation of lymphoid aggregates, finally improving anticancer immunity. LDC, low-dose chemotherapy

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Promoting APC function of B cells via reprogramming the fatty acid metabolism enhances anticancer immunity in metastatic ovarian cancer

    doi: 10.1007/s00262-026-04387-y

    Figure Lengend Snippet: The mechanism diagram of combining adoptive immunotherapy with APC-function-enhanced B cells and LDC improves anticancer immunity in metastatic OvCa mice. In vitro, OA enhances the expression of CD80/CD86/CD83 of B cells through the H3K27ac-mediated upregulation of PPAR γ expression. Then, the B cells are adoptively transferred into the abdominal cavity of metastatic OvCa mice. In the abdominal cavity, LDC facilitates the APC function of the transferred B cells by causing apoptosis of cancer cells. The transferred B cells promote the activation, proliferation, and differentiation of T cells, which release higher levels of effector molecules (IL-2, GZMB, and IFN- γ , etc.), and facilitate the formation of lymphoid aggregates, finally improving anticancer immunity. LDC, low-dose chemotherapy

    Article Snippet: In the mechanistic study, mouse ascitic CD19 + B cells (1 × 10 6 /ml) were pretreated with fatty acid binding protein 4 gene (FABP4) inhibitor (BMS309403, MedChemExpress; Cat# HY-101903; 50 μM), PPARγ antagonist (GW9662, MedChemExpress; Cat# HY-16578; 25 μM), and PPAR γ agonist (Troglitazone, Trog, MedChemExpress; Cat# HY-50935; 10 μM) for 2h, respectively.

    Techniques: In Vitro, Expressing, Activation Assay

    Effect of trans- 10, cis- 12 CLA and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist troglitazone (TG) and antagonist T0070907 (T07) on lipogenesis in a bovine mammary epithelial cell line (MAC-T). Lipogenesis was measured by incorporation of 14 C acetate into lipids during the last 4 h of treatment and expressed relative to the control. Cells were treated for 24 h in basal medium with 75 μ M trans- 10, cis- 12 CLA, 5 μ M TG, 5 μ M T07, or combinations of these treatments in the presence or absence of 10 μ M of 9- cis retinoic acid (9c RA). Values represent LSM ± SEM (includes intra- and interexperimental run error). Means are scaled relative to control (control set to 100; n = 6 wells per treatment across 2 independent experiments). Means that do not share a letter (a–d) differ ( P < 0.05).

    Journal: Journal of dairy science

    Article Title: Potential involvement of peroxisome proliferator-activated receptors in the inhibition of mammary lipid synthesis during diet-induced milk fat depression

    doi: 10.3168/jds.2024-25575

    Figure Lengend Snippet: Effect of trans- 10, cis- 12 CLA and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist troglitazone (TG) and antagonist T0070907 (T07) on lipogenesis in a bovine mammary epithelial cell line (MAC-T). Lipogenesis was measured by incorporation of 14 C acetate into lipids during the last 4 h of treatment and expressed relative to the control. Cells were treated for 24 h in basal medium with 75 μ M trans- 10, cis- 12 CLA, 5 μ M TG, 5 μ M T07, or combinations of these treatments in the presence or absence of 10 μ M of 9- cis retinoic acid (9c RA). Values represent LSM ± SEM (includes intra- and interexperimental run error). Means are scaled relative to control (control set to 100; n = 6 wells per treatment across 2 independent experiments). Means that do not share a letter (a–d) differ ( P < 0.05).

    Article Snippet: Treatments included 5 μM PPAR-γ agonist troglitazone (TG; Calbiochem, San Diego, CA), 5 μM PPAR-γ antagonist T0070907 (T07; Calbiochem, San Diego, CA), 10 μM cis-9 retinoic acid (9cRA; Sigma, St. Louis, MO), and 75 μM trans-10,cis-12 CLA, either individually or in combination.

    Techniques: Control

    Effect of trans- 10, cis- 12 CLA and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist troglitazone (TG) and antagonist T0070907 (T07) on gene expression in a bovine mammary epithelial cell line (MAC-T). Cells were treated for 24 h in basal media with 75 μ M CLA, 5 μ M of the agonist or antagoinist, or combinations of these treatments. (A) Expression of PPAR- γ; (B) expression of fatty acid synthase ( FASN ); (C) expression of sterol response element binding factor 1c ( SREBF1c ); (D) expression of thyroid hormone responsive ( THRSP ). Values are LSM ± SEM scaled relative to control (n = 5 to 8 per treatment). Means that do not share a letter differ (a–d) differ ( P < 0.05).

    Journal: Journal of dairy science

    Article Title: Potential involvement of peroxisome proliferator-activated receptors in the inhibition of mammary lipid synthesis during diet-induced milk fat depression

    doi: 10.3168/jds.2024-25575

    Figure Lengend Snippet: Effect of trans- 10, cis- 12 CLA and peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist troglitazone (TG) and antagonist T0070907 (T07) on gene expression in a bovine mammary epithelial cell line (MAC-T). Cells were treated for 24 h in basal media with 75 μ M CLA, 5 μ M of the agonist or antagoinist, or combinations of these treatments. (A) Expression of PPAR- γ; (B) expression of fatty acid synthase ( FASN ); (C) expression of sterol response element binding factor 1c ( SREBF1c ); (D) expression of thyroid hormone responsive ( THRSP ). Values are LSM ± SEM scaled relative to control (n = 5 to 8 per treatment). Means that do not share a letter differ (a–d) differ ( P < 0.05).

    Article Snippet: Treatments included 5 μM PPAR-γ agonist troglitazone (TG; Calbiochem, San Diego, CA), 5 μM PPAR-γ antagonist T0070907 (T07; Calbiochem, San Diego, CA), 10 μM cis-9 retinoic acid (9cRA; Sigma, St. Louis, MO), and 75 μM trans-10,cis-12 CLA, either individually or in combination.

    Techniques: Gene Expression, Expressing, Binding Assay, Control