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primary antibody against cd206  (Proteintech)


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    Proteintech primary antibody against cd206
    ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and <t>CD206</t> (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001
    Primary Antibody Against Cd206, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1182 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+against+cd206/pmc12918416-120-0-4?v=Proteintech
    Average 96 stars, based on 1182 article reviews
    primary antibody against cd206 - by Bioz Stars, 2026-07
    96/100 stars

    Images

    1) Product Images from "Ferroptosis-dependent small extracellular vesicles ULK1 enhances mitophagy and suppresses breast cancer migration"

    Article Title: Ferroptosis-dependent small extracellular vesicles ULK1 enhances mitophagy and suppresses breast cancer migration

    Journal: Hereditas

    doi: 10.1186/s41065-025-00621-2

    ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and CD206 (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001
    Figure Legend Snippet: ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and CD206 (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001

    Techniques Used: Migration, Fluorescence, Knockdown, Western Blot, Marker, Immunofluorescence, Staining, Expressing, Activation Assay, Transwell Migration Assay, Cell Culture



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    ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and <t>CD206</t> (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001
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    ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and <t>CD206</t> (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001
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    Image Search Results


    ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and CD206 (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Hereditas

    Article Title: Ferroptosis-dependent small extracellular vesicles ULK1 enhances mitophagy and suppresses breast cancer migration

    doi: 10.1186/s41065-025-00621-2

    Figure Lengend Snippet: ULK1 in Fer-sEVs inhibits M2 polarization of macrophages and suppresses breast cancer cell migration through mitophagy. A Mitophagy analysis using mCherry-GFP-LC3B tandem fluorescence reporters in macrophages with ULK1 knockdown following Fer-sEVs treatment. B Western blot analysis of macrophage polarization markers of CD86 (M1 marker) and CD206 (M2 marker) after ULK1 knockdown and autophagy induction. C Immunofluorescence staining of CD206 in macrophages after treatment with siNC- Fer-sEVs or siULK1-Fer-sEVs, with or without the autophagy inducer rapamycin. CD206 expression was increased in the siULK1-Fer-sEVs group and suppressed by rapamycin treatment. Scale bar: 50 μm. D Flow cytometric analysis of CD206⁺ macrophages. ULK1 knockdown in Fer-sEVs significantly increased the proportion of CD206⁺ cells, which was reversed by autophagy activation. E Transwell migration assay of MDA-MB-231 cells co-cultured with macrophages pretreated with different sEVs groups. Fer-sEVs-treated macrophages inhibited tumor cell migration, whereas ULK1-deficient Fer-sEVs-treated macrophages restored pro-migratory effects. Scale bar: 50 μm. Data are presented as mean ± SD; ns p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: Primary antibody against CD206 (Proteintech, 18704-1-AP) was diluted 1:500 in PBS and incubated with cells overnight at 4 °C.

    Techniques: Migration, Fluorescence, Knockdown, Western Blot, Marker, Immunofluorescence, Staining, Expressing, Activation Assay, Transwell Migration Assay, Cell Culture

    Effects of mAF treatment on hepatic macrophages in CGI-58 LivKO mice. (A) Representative IHC images and quantification of the (B) M1 macrophage marker CD68, (C) M2 macrophage marker CD206, and (D) ratio of CD68 to CD206 in the liver of mice. Data are presented as mean ± SD. n = 8 for treatment group, and n = 3 for ALB- group. *P < 0.05, **P < 0.01 by Student’s t-test. Scale bars: 50 μm.

    Journal: Frontiers in Bioengineering and Biotechnology

    Article Title: An engineered adipose formulation decreases hepatic inflammation and fibrosis in a rodent model of metabolic dysfunction-associated steatotic liver disease

    doi: 10.3389/fbioe.2025.1579062

    Figure Lengend Snippet: Effects of mAF treatment on hepatic macrophages in CGI-58 LivKO mice. (A) Representative IHC images and quantification of the (B) M1 macrophage marker CD68, (C) M2 macrophage marker CD206, and (D) ratio of CD68 to CD206 in the liver of mice. Data are presented as mean ± SD. n = 8 for treatment group, and n = 3 for ALB- group. *P < 0.05, **P < 0.01 by Student’s t-test. Scale bars: 50 μm.

    Article Snippet: The expression of CD68 and CD206 in the liver was evaluated by immunohistochemical staining using primary antibodies against mouse CD68 (1:4,000 dilution, Abcam, Waltham, MA) or mouse CD206 (1:1,600 dilution, Cell Signaling Technology ® , Danvers, MA).

    Techniques: Marker