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ppar γ agonist  (MedChemExpress)


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    Structured Review

    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

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    Article Title: PPARG-centric transcriptional re-wiring during differentiation of human trophoblast stem cells into extravillous trophoblasts
    Article Snippet: The following were used: T0070907 (Selleck Chemicals, S2871; 1 μM), Rosiglitazone (MedChemExpress, HY-17386; 1 μM), LGD1069 (Selleck Chemicals, S2098; 1 μM), CD3254 (Fisher Scientific, 33-025-0; 1 μM), Troglitazone (MedChemExpress, HY-50935; 1 μM), DMOG (Selleck Chemicals, S7483; 500 μM), and SCH772984 (MedChemExpress, HY-50846; 0.5 μM).

    Article Title: Structural Elucidation and Covalent Modulation of the Autorepressed Orphan Nuclear Receptor NR2F6
    Article Snippet: 9-cis-retinoic acid was ordered from Sigma Aldrich.

    Article Title: Fluoropolymer-Mediated Delivery of a Dual TSHR/IGF1R-Targeting CRISPR-Cas9 System for Localized Therapy in Thyroid-Associated Ophthalmopathy.
    Article Snippet: Thyroid-associated ophthalmopathy (TAO), a vision-threatening and disfiguring autoimmune orbital disorder, remains a therapeutic challenge due to the lack of therapies with orbital specificity, sustained efficacy, and minimal side effects.. Herein, we present G4F7-CRISPR, a fluoropolymer-based CRISPR-Cas9 delivery platform engineered for localized and efficient disruption of thyroid-stimulating hormone receptor (TSHR) and insulin-like growth factor 1 receptor (IGF1R), two key mediators of TAO pathogenesis.. G4F7-CRISPR achieved high insertion/deletion frequencies in primary orbital fibroblasts (Tshr: 37.2%; Igf1r: 42.8%) and mature adipocytes (Tshr: 22.4%; Igf1r: 24.3%), and maintained robust editing efficiency in orbital adipose tissue of TAOmouse models (Tshr: 30.7%; Igf1r: 32.4%).

    Article Title: Generation and applications of an expandable and mature hiPSC-derived liver organoid
    Article Snippet: Troglitazone (HY-50935), benzbromarone (HY-B1135), acetaminophen (APAP, HY-66005), trovafloxacin (HY-A0170), cyclosporin A (HY-B0579), rifampicin (HY-B0272), rosiglitazone (HY-17386), levofloxacin (HY-B0330), elafibranor (HY-16737), liraglutide (HY-P0014), metformin (HY-B0627), obeticholic acid (HY-12222), saroglitazar (HY-19937), Nile red (HY-D0718), and sodium oleate (HY-N1446B) were purchased from MCE.

    Article Title: A novel synthetic bile acid derivative inhibits hepatitis B virus infection at entry step by interfering with the oligomerization of sodium taurocholate co-transporting polypeptide.
    Article Snippet: Hepatitis B virus (HBV) infection is a major global health burden worldwide despite the availability of an effective vaccine and effective anti-HBV drugs.. The currently approved anti-HBV drugs—i.e., nucleos(t)ide analogues and pegylated interferon α—can effectively suppress HBV replication, but rarely achieve a functional cure.. Accordingly, new anti-HBV agents targeting different aspects of the HBV life cycle are needed.

    Article Title: Generation and applications of an expandable and mature hiPSC-derived liver organoid
    Article Snippet: Troglitazone (HY-50935), benzbromarone (HY-B1135), acetaminophen (APAP, HY-66005), trovafloxacin (HY-A0170), cyclosporin A (HY-B0579), rifampicin (HY-B0272), rosiglitazone (HY-17386), levofloxacin (HY-B0330), elafibranor (HY-16737), liraglutide (HY-P0014), metformin (HY-B0627), obeticholic acid (HY-12222), saroglitazar (HY-19937), Nile red (HY-D0718), and sodium oleate (HY-N1446B) were purchased from MCE.



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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