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Huabio Inc anti cd206 primary antibody
Anti Cd206 Primary Antibody, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The effects of patches on angiogenesis and inflammation in infarcted tissues 4 weeks post-MI. a) Immunofluorescence staining of α-smooth muscle actin (α-SMA, a vascular protein marker, green) and von Willebrand factor (vWF, an endothelial marker, red) of the infarct region in the MI, BMN-P, BMN-CP and CBMN-CP groups. b, c) Quantitative analysis of α-SMA (b) and vWF (c) in different groups based on fluorescent staining images (n = 4). d) Representative immunofluorescence staining of the infarct region in different groups for CD86 (green) and <t>CD206</t> (red). e, f) Fluorescence intensity statistics of CD86 (e) and CD206 (f) in different groups based on fluorescent staining images (n = 4). Nuclei are stained blue with DAPI. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.
Rabbit Cd206 Primary Antibody, supplied by Wuhan Sanying Biotechnology, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti cd206 primary antibody
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
Anti Cd206 Primary Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd206+primary+antibody/CD206+Antibody/pmc12918416-113-0-3
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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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd206+primary+antibody/CD206+Antibody/pmc12918416-120-0-4
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primary antibody against cd206 - by Bioz Stars, 2026-09
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Proteintech cd206 primary antibody
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
Cd206 Primary Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd206+primary+antibody/CD206+Antibody/pm41512500-378-6-9
Average 96 stars, based on 1 article reviews
cd206 primary antibody - by Bioz Stars, 2026-09
96/100 stars
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96
Proteintech primary antibodies 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 Antibodies Against Cd206, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cd206+primary+antibody/CD206+Antibody/pm41480959-252-5-10
Average 96 stars, based on 1 article reviews
primary antibodies against cd206 - by Bioz Stars, 2026-09
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Image Search Results


The effects of patches on angiogenesis and inflammation in infarcted tissues 4 weeks post-MI. a) Immunofluorescence staining of α-smooth muscle actin (α-SMA, a vascular protein marker, green) and von Willebrand factor (vWF, an endothelial marker, red) of the infarct region in the MI, BMN-P, BMN-CP and CBMN-CP groups. b, c) Quantitative analysis of α-SMA (b) and vWF (c) in different groups based on fluorescent staining images (n = 4). d) Representative immunofluorescence staining of the infarct region in different groups for CD86 (green) and CD206 (red). e, f) Fluorescence intensity statistics of CD86 (e) and CD206 (f) in different groups based on fluorescent staining images (n = 4). Nuclei are stained blue with DAPI. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Journal: Bioactive Materials

Article Title: A self-locking conductive cardiac patch for immediate electrical integration with infarcted rat myocardium

doi: 10.1016/j.bioactmat.2025.10.045

Figure Lengend Snippet: The effects of patches on angiogenesis and inflammation in infarcted tissues 4 weeks post-MI. a) Immunofluorescence staining of α-smooth muscle actin (α-SMA, a vascular protein marker, green) and von Willebrand factor (vWF, an endothelial marker, red) of the infarct region in the MI, BMN-P, BMN-CP and CBMN-CP groups. b, c) Quantitative analysis of α-SMA (b) and vWF (c) in different groups based on fluorescent staining images (n = 4). d) Representative immunofluorescence staining of the infarct region in different groups for CD86 (green) and CD206 (red). e, f) Fluorescence intensity statistics of CD86 (e) and CD206 (f) in different groups based on fluorescent staining images (n = 4). Nuclei are stained blue with DAPI. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001.

Article Snippet: The tissue sections were then incubated with the following primary antibodies: rabbit Connexin 43 primary antibody (BOSTER, BA1727, 1:200, China), mouse α-actinin primary antibody (Abcam, AB9465, 1:200, UK), mouse α-SMA primary antibody (Wuhan Sanying, 67735-1-IG, 1:400, China), rabbit vWF primary antibody (Wuhan Sanying, 27186-1-AP, 1:300, China), mouse CD86 primary antibody (BOSTER, BA4121, 1:100, China) and rabbit CD206 primary antibody (Wuhan Sanying, 18704-1-AP, 1:400, China).

Techniques: Immunofluorescence, Staining, Marker, Fluorescence

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: Anti-CD206 primary antibody (Proteintech, 18704-1-AP) was added at a dilution of 1:200, followed by incubation in the dark for 30 min.

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

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