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differentiation 63 cd63  (Proteintech)


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    Proteintech differentiation 63 cd63
    Differentiation 63 Cd63, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 963 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/differentiation+63+cd63/CD63+Antibody/pm41015146-117-7-17
    Average 96 stars, based on 963 article reviews
    differentiation 63 cd63 - by Bioz Stars, 2026-11
    96/100 stars

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    Related Articles

    Expressing:

    Article Title: Protective effects of adipose-derived biogenic nanoparticles on the pulmonary microvascular endothelial barrier in mice with ventilator-induced lung injury via the TRPV4/ROCK1 signalling pathway.
    Article Snippet: Purpose: The "obesity paradox" phenomenon occurs in critically ill patients who receive mechanical ventilation.. Our previous studies found that the adipose-derived exosomes secreted by obese mice have a protective effect on the pulmonary microvascular endothelial barrier.. However, the extraction of exosomes is cumbersome, their yield is low, and their storage is difficult.

    Marker:

    Article Title: Protective effects of adipose-derived biogenic nanoparticles on the pulmonary microvascular endothelial barrier in mice with ventilator-induced lung injury via the TRPV4/ROCK1 signalling pathway.
    Article Snippet: Purpose: The "obesity paradox" phenomenon occurs in critically ill patients who receive mechanical ventilation.. Our previous studies found that the adipose-derived exosomes secreted by obese mice have a protective effect on the pulmonary microvascular endothelial barrier.. However, the extraction of exosomes is cumbersome, their yield is low, and their storage is difficult.

    Western Blot:

    Article Title: Protective effects of adipose-derived biogenic nanoparticles on the pulmonary microvascular endothelial barrier in mice with ventilator-induced lung injury via the TRPV4/ROCK1 signalling pathway.
    Article Snippet: Purpose: The "obesity paradox" phenomenon occurs in critically ill patients who receive mechanical ventilation.. Our previous studies found that the adipose-derived exosomes secreted by obese mice have a protective effect on the pulmonary microvascular endothelial barrier.. However, the extraction of exosomes is cumbersome, their yield is low, and their storage is difficult.

    Article Title: Exosomal FGG promotes colorectal cancer liver metastases through inducing angiogenic pre-metastatic niche formation.
    Article Snippet: Angiogenesis is a defining feature of a pre-metastatic niche and is essential for primary colorectal cancer (CRC) tumor metastasis.. Epithelial-mesenchymal transition (EMT) also serves as a critical driver of CRC tumor metastatic progression.. Here, we hypothesized that exosomes from CRC cells promoted liver metastasis by remodeling tumor microenvironment.

    Biomarker Discovery:

    Article Title: Exosomal FGG promotes colorectal cancer liver metastases through inducing angiogenic pre-metastatic niche formation.
    Article Snippet: Angiogenesis is a defining feature of a pre-metastatic niche and is essential for primary colorectal cancer (CRC) tumor metastasis.. Epithelial-mesenchymal transition (EMT) also serves as a critical driver of CRC tumor metastatic progression.. Here, we hypothesized that exosomes from CRC cells promoted liver metastasis by remodeling tumor microenvironment.

    Lysis:

    Article Title: Exosomal FGG promotes colorectal cancer liver metastases through inducing angiogenic pre-metastatic niche formation.
    Article Snippet: Angiogenesis is a defining feature of a pre-metastatic niche and is essential for primary colorectal cancer (CRC) tumor metastasis.. Epithelial-mesenchymal transition (EMT) also serves as a critical driver of CRC tumor metastatic progression.. Here, we hypothesized that exosomes from CRC cells promoted liver metastasis by remodeling tumor microenvironment.



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    Eight weeks of aerobic exercise improved the proliferation and migration capabilities of circulating EPC in both humans and rats with obesity through circulating exosomes. (A) Representative transmission electron microscopy image of exosomes derived from human peripheral blood. Scale bar = 200 nm. (B) Exosome characterization and identification. Exosomes derived from human peripheral blood express TSG101 and <t>CD63.</t> (C) Nanoparticle tracking analysis confirms the presence of exosomes with a peak diameter of 100 nm, characteristic of exosomal size. Quantitative analysis of exosomes derived from human peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood between the control group and the exercise group ( n = 30 for each group). (D) Cell proliferation assay results showed that exosomes derived from the exercise group significantly enhanced the proliferative capacity of human EPC compared to those from the control group, as measured by the CCK-8 method ( n = 20 for each group). *** p < 0.001, Exercise vs . Control. (E) Scratch assay results showed that exosomes derived from the exercise group significantly promoted the migratory ability of human EPC compared to those from the control group ( n = 5 for each group). * p < 0.05, Exercise vs . Control. (F) Representative images of wound healing in the scratch assay, showcasing the migratory response of human EPC. (G) Characterization of circulating exosomes from rat peripheral blood. (H) Quantitative analysis of exosomes derived from rat peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood among all groups ( n = 3 for each group). (I) Cell proliferation assays revealed that exosomes derived from the HC group exhibited a diminished capacity to promote EPC proliferation compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC proliferation ( n : 5–6 for each group). * p < 0.05, HC vs . NC; ## p < 0.01, HE vs . HC. (J) Scratch assays indicated that exosomes derived from the HC group exhibited a diminished capacity to enhance EPC migration rates compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC migration rates ( n = 4 for each group). ** p < 0.01, HC vs . NC; ## p < 0.01, HE vs . HC. (K) Representative images of wound healing in the scratch assay, showcasing the migratory response of rat EPC. CCK-8 = cell counting kit-8; CD63 = cluster of differentiation 63; EPC = endothelial progenitor cells; HC = the high-fat diet with sedentary group; HE = the high-fat diet with exercise group; NC = the normal diet with sedentary group; TSG101 = tumor susceptibility gene 101.
    Differentiation 63 Cd63, supplied by Affinity Biosciences, 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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    Fisetin reduced the co-localization between ASGR1 and lysosomes and regulated mTORC1/AMPK-BRCA1/BARD1 pathway. ( A ) Representative immunofluorescence images and statistical results of ASGR1 and <t>CD63</t> protein expression in AML12 cells. Scale bar (20 μm), magnification (400 ×). ( B-G ) Western blot analysis of p-mTOR, p-S6K, p-AMPK, BRCA1 and BARD1 in AML12 cells. Data are mean ± SD, n = 3. * p < 0.05, ** p < 0.01
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    Eight weeks of aerobic exercise improved the proliferation and migration capabilities of circulating EPC in both humans and rats with obesity through circulating exosomes. (A) Representative transmission electron microscopy image of exosomes derived from human peripheral blood. Scale bar = 200 nm. (B) Exosome characterization and identification. Exosomes derived from human peripheral blood express TSG101 and CD63. (C) Nanoparticle tracking analysis confirms the presence of exosomes with a peak diameter of 100 nm, characteristic of exosomal size. Quantitative analysis of exosomes derived from human peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood between the control group and the exercise group ( n = 30 for each group). (D) Cell proliferation assay results showed that exosomes derived from the exercise group significantly enhanced the proliferative capacity of human EPC compared to those from the control group, as measured by the CCK-8 method ( n = 20 for each group). *** p < 0.001, Exercise vs . Control. (E) Scratch assay results showed that exosomes derived from the exercise group significantly promoted the migratory ability of human EPC compared to those from the control group ( n = 5 for each group). * p < 0.05, Exercise vs . Control. (F) Representative images of wound healing in the scratch assay, showcasing the migratory response of human EPC. (G) Characterization of circulating exosomes from rat peripheral blood. (H) Quantitative analysis of exosomes derived from rat peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood among all groups ( n = 3 for each group). (I) Cell proliferation assays revealed that exosomes derived from the HC group exhibited a diminished capacity to promote EPC proliferation compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC proliferation ( n : 5–6 for each group). * p < 0.05, HC vs . NC; ## p < 0.01, HE vs . HC. (J) Scratch assays indicated that exosomes derived from the HC group exhibited a diminished capacity to enhance EPC migration rates compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC migration rates ( n = 4 for each group). ** p < 0.01, HC vs . NC; ## p < 0.01, HE vs . HC. (K) Representative images of wound healing in the scratch assay, showcasing the migratory response of rat EPC. CCK-8 = cell counting kit-8; CD63 = cluster of differentiation 63; EPC = endothelial progenitor cells; HC = the high-fat diet with sedentary group; HE = the high-fat diet with exercise group; NC = the normal diet with sedentary group; TSG101 = tumor susceptibility gene 101.

    Journal: Journal of Sport and Health Science

    Article Title: Long-term aerobic exercise enhances circulating exosomal miR-214-3p to promote endothelial progenitor cell-mediated repair of endothelial damage induced by obesity

    doi: 10.1016/j.jshs.2025.101094

    Figure Lengend Snippet: Eight weeks of aerobic exercise improved the proliferation and migration capabilities of circulating EPC in both humans and rats with obesity through circulating exosomes. (A) Representative transmission electron microscopy image of exosomes derived from human peripheral blood. Scale bar = 200 nm. (B) Exosome characterization and identification. Exosomes derived from human peripheral blood express TSG101 and CD63. (C) Nanoparticle tracking analysis confirms the presence of exosomes with a peak diameter of 100 nm, characteristic of exosomal size. Quantitative analysis of exosomes derived from human peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood between the control group and the exercise group ( n = 30 for each group). (D) Cell proliferation assay results showed that exosomes derived from the exercise group significantly enhanced the proliferative capacity of human EPC compared to those from the control group, as measured by the CCK-8 method ( n = 20 for each group). *** p < 0.001, Exercise vs . Control. (E) Scratch assay results showed that exosomes derived from the exercise group significantly promoted the migratory ability of human EPC compared to those from the control group ( n = 5 for each group). * p < 0.05, Exercise vs . Control. (F) Representative images of wound healing in the scratch assay, showcasing the migratory response of human EPC. (G) Characterization of circulating exosomes from rat peripheral blood. (H) Quantitative analysis of exosomes derived from rat peripheral blood revealed no statistically significant difference in the number of exosomes isolated from equal volumes of circulating blood among all groups ( n = 3 for each group). (I) Cell proliferation assays revealed that exosomes derived from the HC group exhibited a diminished capacity to promote EPC proliferation compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC proliferation ( n : 5–6 for each group). * p < 0.05, HC vs . NC; ## p < 0.01, HE vs . HC. (J) Scratch assays indicated that exosomes derived from the HC group exhibited a diminished capacity to enhance EPC migration rates compared to those from the NC group in rats. In contrast, exosomes induced by 8 weeks of aerobic exercise significantly enhanced EPC migration rates ( n = 4 for each group). ** p < 0.01, HC vs . NC; ## p < 0.01, HE vs . HC. (K) Representative images of wound healing in the scratch assay, showcasing the migratory response of rat EPC. CCK-8 = cell counting kit-8; CD63 = cluster of differentiation 63; EPC = endothelial progenitor cells; HC = the high-fat diet with sedentary group; HE = the high-fat diet with exercise group; NC = the normal diet with sedentary group; TSG101 = tumor susceptibility gene 101.

    Article Snippet: The primary antibodies used included PI3K (SC-365290, 1:1000; Santa Cruz Biotechnology, Dallas, TX, USA), Akt1 (SC-5298, 1:1000; Santa Cruz), p-Akt (Ser473) (66444-1-lg, 1:1000; Proteintech Group, Rosemont, IL, USA), phosphatase and tensin homolog (PTEN) (60300-1-Ig, 1:1000; Proteintech), tumor susceptibility gene 101 (TSG101) (DF8427, 1:1000; Affinity Biosciences, Cincinnati, OH, USA), cluster of differentiation 63 (CD63) (AF5117, 1:1000; Affinity), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) (GB15002-100, 1:4000; Servicebio).

    Techniques: Migration, Transmission Assay, Electron Microscopy, Derivative Assay, Isolation, Control, Proliferation Assay, CCK-8 Assay, Wound Healing Assay, Cell Counting

    Fisetin reduced the co-localization between ASGR1 and lysosomes and regulated mTORC1/AMPK-BRCA1/BARD1 pathway. ( A ) Representative immunofluorescence images and statistical results of ASGR1 and CD63 protein expression in AML12 cells. Scale bar (20 μm), magnification (400 ×). ( B-G ) Western blot analysis of p-mTOR, p-S6K, p-AMPK, BRCA1 and BARD1 in AML12 cells. Data are mean ± SD, n = 3. * p < 0.05, ** p < 0.01

    Journal: Journal of Nanobiotechnology

    Article Title: Fisetin-loaded nanoparticles as a novel approach for cholesterol regulation in hypercholesterolemia: targeting the ASGR1-mediated mTORC1/AMPK pathway

    doi: 10.1186/s12951-026-04181-z

    Figure Lengend Snippet: Fisetin reduced the co-localization between ASGR1 and lysosomes and regulated mTORC1/AMPK-BRCA1/BARD1 pathway. ( A ) Representative immunofluorescence images and statistical results of ASGR1 and CD63 protein expression in AML12 cells. Scale bar (20 μm), magnification (400 ×). ( B-G ) Western blot analysis of p-mTOR, p-S6K, p-AMPK, BRCA1 and BARD1 in AML12 cells. Data are mean ± SD, n = 3. * p < 0.05, ** p < 0.01

    Article Snippet: Following permeabilization with 0.1% Triton X-100 for 10 min, the cells were blocked with 5% BSA for 1 h. Next, the cells were incubated with primary antibodies against ASGR1 (Proteintech, Wuhan, China, 11739-1-AP, 1:200) and Cluster of Differentiation 63 (CD63) (Abmart, Shanghai, China, M051014, 1:200) for 2 h. Subsequently, the cells were incubated with FITC-conjugated Goat Anti-Mouse IgG (Abbkine, Wuhan, China, A22110, 1:500) and TRITC-conjugated Goat Anti-Rabbit IgG (Zenbio, Chengdu, China, 511202, 1:500) for 1.5 h. The nuclei were then stained with 1 μg/mL DAPI for 10 min.

    Techniques: Immunofluorescence, Expressing, Western Blot

    Distribution of particle counts and EV biomarker levels in plasma ADEVs. ( A ) Distribution of ADEV particle counts measured by nano-flow cytometry (NFCM) and nanoparticle tracking analysis (NTA). ( B ) Distribution of five EV biomarkers (CD9, CD63, CD81, TSG101, and Alix) in ADEVs

    Journal: BMC Psychiatry

    Article Title: Normalization strategies for protein quantification in plasma astrocyte-derived extracellular vesicles: a clinical applicability study

    doi: 10.1186/s12888-026-07796-6

    Figure Lengend Snippet: Distribution of particle counts and EV biomarker levels in plasma ADEVs. ( A ) Distribution of ADEV particle counts measured by nano-flow cytometry (NFCM) and nanoparticle tracking analysis (NTA). ( B ) Distribution of five EV biomarkers (CD9, CD63, CD81, TSG101, and Alix) in ADEVs

    Article Snippet: The levels of CD9 (Cat# CSB-EL004969HU, CUSABIO, China), CD63 (Cat# CSB-E14107h-IS, CUSABIO, China), CD81 (Cat# CSB-EL004960HU-IS, CUSABIO, China), Alix (Cat# CSB-EL017673HU, CUSABIO, China), TSG101 (Cat# CSB-EL025125HU, CUSABIO, China), and BDNF (Cat# E-EL-H0010, Elabscience, China) in ADEVs were measured using enzyme-linked immunosorbent assay (ELISA) kits.

    Techniques: Biomarker Discovery, Clinical Proteomics, Flow Cytometry