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13 hode  (Proteintech)


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    Structured Review

    Proteintech 13 hode
    PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing <t>increased</t> <t>13-HODE</t> levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5
    13 Hode, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/13+hode/pmc12829093-326-19-24?v=Proteintech
    Average 93 stars, based on 2 article reviews
    13 hode - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "Targeting OxLDL-mediated CD36 + CAF reprogramming potentiates PD-1 immunotherapy in osteosarcoma"

    Article Title: Targeting OxLDL-mediated CD36 + CAF reprogramming potentiates PD-1 immunotherapy in osteosarcoma

    Journal: Molecular Cancer

    doi: 10.1186/s12943-025-02516-2

    PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing increased 13-HODE levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5
    Figure Legend Snippet: PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing increased 13-HODE levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5

    Techniques Used: Activity Assay, Expressing, Quantitative RT-PCR, Biomarker Discovery, Western Blot, Knockdown, ChIP-qPCR, Binding Assay, Enzyme-linked Immunosorbent Assay, Ligand Binding Assay, Co-Immunoprecipitation Assay



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    Larodan 9 10 13 s s s trihydroxyoctadec 11e enoic acid
    PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing <t>increased</t> <t>13-HODE</t> levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5
    9 10 13 S S S Trihydroxyoctadec 11e Enoic Acid, supplied by Larodan, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing increased 13-HODE levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5

    Journal: Molecular Cancer

    Article Title: Targeting OxLDL-mediated CD36 + CAF reprogramming potentiates PD-1 immunotherapy in osteosarcoma

    doi: 10.1186/s12943-025-02516-2

    Figure Lengend Snippet: PPARG-mediated lipid metabolism reprograms CD36⁺ CAFs through the CD36–FABP4 axis. a – d PPARG activity and expression in CAFs, showing positive correlations with CD36 and FABP4. e – f qRT-PCR validation of PPARG, CD36, and FABP4 expression in ( e ) CD36⁺ CAFs ( n = 5 per group, ** p < 0.01) and ( f ) in response to OxLDL treatment (50 µg/mL; n = 3 per group, ** p < 0.01, * p < 0.05). g Western blot analysis of CD36, PPARG, ANGPTL4, and FABP4 expression in CAFs treated with OxLDL, siCD36, or CD36 inhibitor (SSO) ( n = 3 per group). h – i qRT-PCR and Western blot showing that PPARG knockdown reduces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001, ** p < 0.01, * p < 0.05). j ChIP-qPCR confirming PPARG binding to CD36 and FABP4 promoters ( n = 3 per group, ** p < 0.01, * p < 0.05). k ELISA showing increased 13-HODE levels in CAFs after OxLDL stimulation ( n = 3 per group, *** p < 0.001). (l–m) qRT-PCR and Western blot showing that 13-HODE induces CD36, FABP4, and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). n – o qRT-PCR and Western blot showing that FABP4 knockdown impairs 13-HODE–induced CD36 and ANGPTL4 expression ( n = 5 per group, **** p < 0.0001, *** p < 0.001). p Molecular docking analysis predicting binding interactions among 13-HODE, FABP4, and the PPARG ligand-binding domain (LBD). q – r AlphaFold modeling, and co-IP validating FABP4–PPARG interaction. See also Supplementary Figure S5

    Article Snippet: Blood samples were collected from cardiac puncture separated by centrifugation at 3000 g, 4°C, 10 min. OxLDL (Elabscience, E-EL-M0066), 13-HODE (MEIMIAN, MM-60095H2) and ANGPTL4 (Proteintech, KE00186) levels were measured using ELISA kits following the manufacturer’s instructions.

    Techniques: Activity Assay, Expressing, Quantitative RT-PCR, Biomarker Discovery, Western Blot, Knockdown, ChIP-qPCR, Binding Assay, Enzyme-linked Immunosorbent Assay, Ligand Binding Assay, Co-Immunoprecipitation Assay