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rabbit polyclonal anti stat6  (Proteintech)


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    Structured Review

    Proteintech rabbit polyclonal anti stat6
    Rabbit Polyclonal Anti Stat6, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 71 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+stat6/STAT6+Antibody/pmc13049607-9-0-4
    Average 95 stars, based on 71 article reviews
    rabbit polyclonal anti stat6 - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Transfection:

    Article Title: ADGRG6 Promotes Pancreatic Adenocarcinoma Progression Through the NF-κB/STAT6 Axis and Modulation of the Tumor Immune Microenvironment
    Article Snippet: .. Total protein lysates were prepared from AsPC-1 cells transfected with si-ADGRG6 or si-NC for 48 h. Blots were probed using anti-ADGRG6 (1:1000, Proteintech, Rosemont, IL, USA), anti-phospho-NF-κB p65 (Ser468) (1:1000, Proteintech), anti-NF-κB p65 (1:1000, Proteintech), anti-STAT6 (1:1000, Proteintech), anti-phospho-STAT6 (Tyr641) (1:1000, Proteintech), anti-GATA3 (1:1000, Proteintech), and anti-GAPDH (1:3000, Proteintech) antibodies. .. Bands were visualized using Enhanced Chemiluminescence (ECL, Meilunbio, Dalian, China) and imaged with a ChemiDoc TM ; Imaging System (Bio-Rad, Hercules, CA, USA).

    Saline:

    Article Title: Tumor-derived CCL16 Normalizes Tumor Vasculature through Macrophage ICAM-1 Receptor and Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma
    Article Snippet: Hepatocellular carcinoma (HCC) is characterized by aberrant tumor vasculature and an immunosuppressive tumor microenvironment (TME), both of which compromise immunotherapy efficacy while promoting circulating tumor cell (CTC) dissemination and immune escape.. In this study, we aimed to identify potential therapeutic targets for remodeling aberrant tumor vasculature by analyzing CTCs from patients with early-stage HCC.. HCC tissue samples derived from patients with elevated CTC counts demonstrated significant CCL16 downregulation accompanied by vascular structural abnormalities and an immunosuppressive TME.

    Article Title: Tumor-Derived CCL16 Normalizes Tumor Vasculature through Macrophage ICAM-1 Receptor and Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma
    Article Snippet: Equal amounts of protein (30 μg per lane) were separated by 10% SDS-PAGE and transferred to polyvinylidene difluoride membranes (Millipore). .. The membranes were blocked with 5% non-fat milk in Tris-Buffered Saline with Tween 20 (TBST) for 1 hour at room temperature, followed by overnight incubation at 4°C with the following primary antibodies: anti–β-tubulin (TA-10, ZsBio), anti–β-actin (TA-09, ZsBio), anti-CCL16 (YN1319, Immunoway), anti–ICAM-1 (10831-1-AP, Proteintech), anti-JAK2 (ET1607-35, HUABIO), anti–pJAK2 (ET1607-34, HUABIO), anti-STAT6 (51073-1-AP, Proteintech), anti–pSTAT6 (ab188080, Abcam), anti-DPP4 (DF12387, Affinity), anti-IL24 (26772-1-AP, Proteintech), anti-F4/80 (28463-1-AP, Proteintech), anti-CCR1 (DF2710, Affinity), anti-CD31 (ab124432, Abcam), anti-SMA (ZM-0003, ZsBio), anti-GST (#2625, Cell Signaling Technology), and anti-FLAG (F1804, Sigma-Aldrich). ..

    Incubation:

    Article Title: Tumor-derived CCL16 Normalizes Tumor Vasculature through Macrophage ICAM-1 Receptor and Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma
    Article Snippet: Hepatocellular carcinoma (HCC) is characterized by aberrant tumor vasculature and an immunosuppressive tumor microenvironment (TME), both of which compromise immunotherapy efficacy while promoting circulating tumor cell (CTC) dissemination and immune escape.. In this study, we aimed to identify potential therapeutic targets for remodeling aberrant tumor vasculature by analyzing CTCs from patients with early-stage HCC.. HCC tissue samples derived from patients with elevated CTC counts demonstrated significant CCL16 downregulation accompanied by vascular structural abnormalities and an immunosuppressive TME.

    Article Title: Tumor-Derived CCL16 Normalizes Tumor Vasculature through Macrophage ICAM-1 Receptor and Enhances Immunotherapy Efficacy in Hepatocellular Carcinoma
    Article Snippet: Equal amounts of protein (30 μg per lane) were separated by 10% SDS-PAGE and transferred to polyvinylidene difluoride membranes (Millipore). .. The membranes were blocked with 5% non-fat milk in Tris-Buffered Saline with Tween 20 (TBST) for 1 hour at room temperature, followed by overnight incubation at 4°C with the following primary antibodies: anti–β-tubulin (TA-10, ZsBio), anti–β-actin (TA-09, ZsBio), anti-CCL16 (YN1319, Immunoway), anti–ICAM-1 (10831-1-AP, Proteintech), anti-JAK2 (ET1607-35, HUABIO), anti–pJAK2 (ET1607-34, HUABIO), anti-STAT6 (51073-1-AP, Proteintech), anti–pSTAT6 (ab188080, Abcam), anti-DPP4 (DF12387, Affinity), anti-IL24 (26772-1-AP, Proteintech), anti-F4/80 (28463-1-AP, Proteintech), anti-CCR1 (DF2710, Affinity), anti-CD31 (ab124432, Abcam), anti-SMA (ZM-0003, ZsBio), anti-GST (#2625, Cell Signaling Technology), and anti-FLAG (F1804, Sigma-Aldrich). ..

    Western Blot:

    Article Title: Bone Marrow Mesenchymal Stem Cell‐Derived Exosomes Promote <scp>M2</scp> Polarization and Protect Against Acute Lung Injury
    Article Snippet: The lysates were then subjected to immunoprecipitation using 4 μg of anti- HA antibody or normal rabbit IgG (ab9100/ab125938, Abcam), together with protein A- Sepharose (Santa Cruz Biotechnology, Texas, USA). .. The immune complexes were washed and analyzed by immunoblotting with anti- STAT6 (1:800) and anti- pan Acetylation (66289, Proteintech, USA) (1:500) antibodies. ..

    Article Title: Bone Marrow Mesenchymal Stem Cell‐Derived Exosomes Promote M2 Polarization and Protect Against Acute Lung Injury
    Article Snippet: The lysates were then subjected to immunoprecipitation using 4 μg of anti‐HA antibody or normal rabbit IgG (ab9100/ab125938, Abcam), together with protein A‐Sepharose (Santa Cruz Biotechnology, Texas, USA). .. The immune complexes were washed and analyzed by immunoblotting with anti‐STAT6 (1:800) and anti‐pan Acetylation (66289, Proteintech, USA) (1:500) antibodies. ..



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    HA from myofibroblasts induces macrophage M2 polarization via the <t>CD44/STAT6</t> axis. (A) RAW264.7 macrophages were stimulated with HA for 24 h, and flow cytometry was performed to assess the expression of CD206 (FITC) and CD86 (PE) (n=3 for each group). (B) The content of TGF-β1 in macrophages following HA treatment over 48 h was quantified using ELISA (n=3 for each group). (C) Western blotting analysis of p-STAT6 and total STAT6 expression at various time points following 100 μ g/ml HA stimulation (n=4 for each group). (D) Flow cytometric analysis of CD86 and CD206 expression in macrophages after 24-h treatment with 100 μ g/ml HA and CD44 inhibitor at indicated concentrations (n=3 for each group). (E) TGF-β1 quantification by ELISA in culture supernatants (n=3 for each group). (F) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and CD44 inhibitor at varying concentrations (n=3 for each group). (G) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and STAT6 inhibitor (AS1517499) at varying concentrations (n=4 for each group). (H) Schematic workflow: Conditioned medium from TGF-β1-stimulated NIH/3T3 fibroblasts was used to culture RAW264.7 macrophages for 24 h. Where indicated, RAW264.7 cells were co-treated with a CD44 inhibitor or a STAT6 inhibitor. Macrophage polarization was subsequently analyzed by flow cytometry. (I) Flow cytometry was used to measure the expression levels of CD206 (FITC) and CD86 (PE) (n=3 for each group). * P<0.05, ** P<0.01, *** P<0.001. HA, hyaluronic acid; FITC, fluorescein isothiocyanate; PE, phycoerythrin; p-, phosphorylated.
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    Image Search Results


    HA from myofibroblasts induces macrophage M2 polarization via the CD44/STAT6 axis. (A) RAW264.7 macrophages were stimulated with HA for 24 h, and flow cytometry was performed to assess the expression of CD206 (FITC) and CD86 (PE) (n=3 for each group). (B) The content of TGF-β1 in macrophages following HA treatment over 48 h was quantified using ELISA (n=3 for each group). (C) Western blotting analysis of p-STAT6 and total STAT6 expression at various time points following 100 μ g/ml HA stimulation (n=4 for each group). (D) Flow cytometric analysis of CD86 and CD206 expression in macrophages after 24-h treatment with 100 μ g/ml HA and CD44 inhibitor at indicated concentrations (n=3 for each group). (E) TGF-β1 quantification by ELISA in culture supernatants (n=3 for each group). (F) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and CD44 inhibitor at varying concentrations (n=3 for each group). (G) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and STAT6 inhibitor (AS1517499) at varying concentrations (n=4 for each group). (H) Schematic workflow: Conditioned medium from TGF-β1-stimulated NIH/3T3 fibroblasts was used to culture RAW264.7 macrophages for 24 h. Where indicated, RAW264.7 cells were co-treated with a CD44 inhibitor or a STAT6 inhibitor. Macrophage polarization was subsequently analyzed by flow cytometry. (I) Flow cytometry was used to measure the expression levels of CD206 (FITC) and CD86 (PE) (n=3 for each group). * P<0.05, ** P<0.01, *** P<0.001. HA, hyaluronic acid; FITC, fluorescein isothiocyanate; PE, phycoerythrin; p-, phosphorylated.

    Journal: International Journal of Molecular Medicine

    Article Title: Orcinol glucoside ameliorates pulmonary fibrosis by suppressing hyaluronic acid synthesis and macrophage M2 polarization via targeting hyaluronic acid synthase 2

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    Figure Lengend Snippet: HA from myofibroblasts induces macrophage M2 polarization via the CD44/STAT6 axis. (A) RAW264.7 macrophages were stimulated with HA for 24 h, and flow cytometry was performed to assess the expression of CD206 (FITC) and CD86 (PE) (n=3 for each group). (B) The content of TGF-β1 in macrophages following HA treatment over 48 h was quantified using ELISA (n=3 for each group). (C) Western blotting analysis of p-STAT6 and total STAT6 expression at various time points following 100 μ g/ml HA stimulation (n=4 for each group). (D) Flow cytometric analysis of CD86 and CD206 expression in macrophages after 24-h treatment with 100 μ g/ml HA and CD44 inhibitor at indicated concentrations (n=3 for each group). (E) TGF-β1 quantification by ELISA in culture supernatants (n=3 for each group). (F) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and CD44 inhibitor at varying concentrations (n=3 for each group). (G) Western blotting analysis of p-STAT6 and total STAT6 in macrophages following 2-h treatment with HA and STAT6 inhibitor (AS1517499) at varying concentrations (n=4 for each group). (H) Schematic workflow: Conditioned medium from TGF-β1-stimulated NIH/3T3 fibroblasts was used to culture RAW264.7 macrophages for 24 h. Where indicated, RAW264.7 cells were co-treated with a CD44 inhibitor or a STAT6 inhibitor. Macrophage polarization was subsequently analyzed by flow cytometry. (I) Flow cytometry was used to measure the expression levels of CD206 (FITC) and CD86 (PE) (n=3 for each group). * P<0.05, ** P<0.01, *** P<0.001. HA, hyaluronic acid; FITC, fluorescein isothiocyanate; PE, phycoerythrin; p-, phosphorylated.

    Article Snippet: Antibodies for Collagen type I α 1 chain (COL1A1; cat. no. 72026; 1:1,000), Phospho-STAT6 (Tyr641; cat. no. 56554S; 1:1,000) and α-smooth muscle actin (α-SMA; cat. no. 19245; 1:1,000) were obtained from Cell Signaling Technology, Inc.

    Techniques: Flow Cytometry, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot