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mouse phospho stat6  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mouse phospho stat6
    Mouse Phospho Stat6, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 233 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+stat6/Phospho-Stat6+(Tyr641)+Rabbit+mAb/pmc13049607-338-66-69
    Average 96 stars, based on 233 article reviews
    mouse phospho stat6 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    other:

    Article Title: Baihua Dangen Tang inhibits the peritoneal metastasis of colon cancer by modulating the bacterial metabolite gentisic acid to suppress MDSCs
    Article Snippet: Background: The treatment principle of Lingnan traditional compound Baihua Dangen Tang includes ̳clearing heat and removing toxins, resolving stasis and dispersing stagnation, and dispelling wind and removing dampness‘, which is compatible with the pathogenesis of peritoneal cancer, which is characterized by ̳dampness, heat, stasis and toxin‘.. Therefore, Baihua Dangen Tang may be an effective treatment for peritoneal metastasis of colon cancer.. Objective: To systematically elucidate the effects and mechanisms of Baihua Dangen Tang in inhibiting the peritoneal metastasis of colon cancer.

    Article Title: Cooperative Interaction Between IL-4 Signaling and FLT3 in Multipotent Progenitors Restore Lymphopoiesis in Inflammation and Aging
    Article Snippet: Primary antibodies used included anti-HA (1:2,000, Cell Signaling Technology), anti-Myc (1:2,000, Bio-Rad), anti-Flag (1:2,000, Sigma-Aldrich), anti-STAT6 (1:2,000, Cell Signaling Technology), anti-Phospho-STAT6 (Tyr641) (1:2,000, Cell Signaling Technology) and anti-β-actin (1:3,000, Cell Signaling Technology).

    Article Title: Atf3 Integrates Lipid and Cytoskeletal Remodeling to Drive Macrophage Fusion
    Article Snippet: The following primary antibodies were used: anti-ATP5a [15H4C4] (mouse, 1:1000; Abcam #ab14748, RRID:AB_301447), anti-ATF3 (rabbit, 1:500, Novus #NBP1-85816, RRID:AB_11014863), anti-actin (rabbit, 1:1000, Sigma-Aldrich #A2066, RRID:AB_476693), anti-STAT6 (rabbit, 1:1000, Cell Signaling Technology #5397, RRID:AB_11220421), anti-phospho-STAT6 (Tyr641) (D8S9Y) (rabbit, 1:1000, Cell Signaling Technology #56554, RRID:AB_2799514), anti-STAT1 (rabbit, 1:1000; Cell Signaling Technology #9172, RRID:AB_2198300), anti-phospho-STAT1 (Tyr701) (58D6) (rabbit, 1:1000, Cell Signaling Technology #9167, RRID:AB_561284), anti-WASP (mouse; 1:500; Santa Cruz #sc-13139, RRID:AB_628445), anti-lamin A/C (mouse, 1:1000, Cell Signaling Technology #4777, RRID:AB_10545756), anti-Phospho-Cofilin (Ser3) (77G2) (rabbit, 1:1000; Cell Signaling Technology #3313, RRID:AB_2080597), anti-Cofilin (D3F9) (rabbit, 1:1000; Cell Signaling Technology #5175, RRID:AB_10622000), anti-HMGCR (mouse, 1:500, Atlas Antibodies #AMAb90619, RRID:AB_2665607), anti-HMGCS1 (mouse, 1:500; Novus #NBP2-36554, RRID:AB_3295882).

    Article Title: TREM1 deficiency attenuates LPS-induced sepsis-associated acute kidney injury by modulating macrophage polarization
    Article Snippet: Protein samples of the same content were separated through SDS‒PAGE, and subsequently transferred to PVDF membranes, and finally immunoblotted with primary antibodies (Abs): anti-phospho PI3K, anti-PI3K, anti-phospho AKT, anti-AKT, anti-phospho mTOR, anti-mTOR, anti-phospho STAT6, anti-STAT6 (CST, Danvers, USA), anti-IRF4 (Proteintech, Wuhan, China), and anti-β-actin (Affinity Biosciences, OH, USA).

    Article Title: Uncovering the individual immunotherapeutic roles of PTPN1 and PTPN2 in T cells during dual inhibition
    Article Snippet: anti-STAT6 , Cell Signalling Technologies , Cat# 5397; RRID: AB_11220421.

    Article Title: Baitong Decoction Ameliorates DSS-Induced Colitis via Modulation of STING and JAK/STAT Pathways
    Article Snippet: The membranes were probed with primary antibodies overnight at 4 °C, including anti-STING (CST, 72971S), antiphospho-STING (CST, 72971S), anti-TBK1 (CST, 3504S), antiphospho-TBK1 (CST, 5483S), anti-IκB (CST, 4814S), antiphospho-IκB (CST, 2859S), anti-STAT3 (CST, 12640S), anti-STAT6 (CST, 5397S), anti-NF-κB (CST, 6956S), anti-JAK1 (CST, 3344S), antiphospho-JAK1 (CST, 3331S), anti-JAK2 (CST, 3230S), antiphospho-JAK2 (CST, 3771S), anti-Histone H3 (CST, 4499S) and anti-GAPDH (CST, 2118S).

    Incubation:

    Article Title: Ruxolitinib, a novel JAK/STAT-targeted therapy through restoring mucosal homeostasis for chronic rhinosinusitis with nasal polyps.
    Article Snippet: Ruxolitinib, a novel JAK/STAT-targeted therapy through restoring mucosal homeostasis for chronic rhinosinusitis with nasal polyps

    Article Title: Extracellular vesicles derived from live or apoptotic mesenchymal stem cells: comparison of the effects of two extracellular vesicles on liver fibrosis.
    Article Snippet: Subsequently, equal amounts of protein samples (30 μg) were loaded onto SDS-PAGE gels and transferred to nitrocellulose membranes (Bio-Rad Biotechnology, USA). .. The membranes were blocked in TBST buffer containing 2.5% skim milk for 30 min. Then, the membranes were incubated overnight at 4 °C with the following primary antibodies: anti-Caspase-3 (9662, Cell Signaling Technology, USA; diluted at 1:1000), anti-GM130 (ab52649, Abcam, UK; diluted at 1:1000), anti-Calnexin (10427-2-AP, Proteintech, USA; diluted at 1:1000), anti-CD81 (ab79559, Abcam, UK; diluted at 1:1000), anti-CD9 (ab236630, Abcam, UK; diluted at 1:1000), anti-Collagen I (ab270993, Abcam, UK; diluted at 1:1000), anti-αSMA (19245, Cell Signaling Technology, USA; diluted at 1:1000), anti-NOS2 (ab15323, Abcam, UK; diluted at 1:1000), antiARG-1 (ab124917, Abcam, UK; diluted at 1:1000), anti-STAT3 (10253-2-AP, Proteintech, USA; diluted at 1:1000), anti-STAT6 (9362, Cell Signaling Technology, USA; diluted at 1:1000), anti- NF-κB (8242, Cell Signaling Technology, USA; diluted at 1:1000), anti-AKT (4691, Cell Signaling Technology, USA; diluted at 1:1000), and anti-β-Actin (66009-1-Ig, Proteintech, USA; diluted at 1:5000). ..



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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

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    doi: 10.3892/ijmm.2026.5764

    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