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phycoerythrin (pe)-conjugated antibodies against human cell differentiation antigen 86 (cd86)  (Thermo Fisher)


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    Thermo Fisher phycoerythrin (pe)-conjugated antibodies against human cell differentiation antigen 86 (cd86)
    Phycoerythrin (Pe) Conjugated Antibodies Against Human Cell Differentiation Antigen 86 (Cd86), supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/phycoerythrin (pe)-conjugated antibodies against human cell differentiation antigen 86 (cd86)/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    phycoerythrin (pe)-conjugated antibodies against human cell differentiation antigen 86 (cd86) - by Bioz Stars, 2026-03
    90/100 stars

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    Figure 4. The aortas of patients with AD exhibit abundant M1 macrophages, with significant activation of the TLR2/NLRP3 signaling pathway, and increased release of MMP2 and MMP9. Representative immunofluorescence (A) of aortas from patients with AD (n=4) and normal controls (n=4), with quantification of INOS (B), TLR2 (C), NLRP3 (D), MMP2 (E), and MMP9 (F) expression in patients with AD and normal controls. Representative western blot (G) of aortas from patients with AD (n=8) and normal controls (n=8), with quantification of TLR2 (H), NLRP3 (I), CD86 (J), INOS (K), MMP2 (L), and MMP9 (M) expression in patients with AD and normal controls. Data are presented as mean±SEM. Bars represent the means, and caps represent the SEM. Statistical significance was determined by Mann–Whitney U test in (B) and (C) and by unpaired t test in D through F and H through M. A value of P<0.05 was considered significant. AD indicates aortic dissection; CD, cluster of differentiation; INOS, inducible nitric oxide synthase; MMP, matrix metalloproteinase; NLRP3, NOD-like receptor pyrin domain containing 3; and TLR2, Toll-like receptor 2.

    Journal: Journal of the American Heart Association

    Article Title: Hepatic Abnormal Secretion of Apolipoprotein C3 Promotes Inflammation in Aortic Dissection

    doi: 10.1161/jaha.124.037172

    Figure Lengend Snippet: Figure 4. The aortas of patients with AD exhibit abundant M1 macrophages, with significant activation of the TLR2/NLRP3 signaling pathway, and increased release of MMP2 and MMP9. Representative immunofluorescence (A) of aortas from patients with AD (n=4) and normal controls (n=4), with quantification of INOS (B), TLR2 (C), NLRP3 (D), MMP2 (E), and MMP9 (F) expression in patients with AD and normal controls. Representative western blot (G) of aortas from patients with AD (n=8) and normal controls (n=8), with quantification of TLR2 (H), NLRP3 (I), CD86 (J), INOS (K), MMP2 (L), and MMP9 (M) expression in patients with AD and normal controls. Data are presented as mean±SEM. Bars represent the means, and caps represent the SEM. Statistical significance was determined by Mann–Whitney U test in (B) and (C) and by unpaired t test in D through F and H through M. A value of P<0.05 was considered significant. AD indicates aortic dissection; CD, cluster of differentiation; INOS, inducible nitric oxide synthase; MMP, matrix metalloproteinase; NLRP3, NOD-like receptor pyrin domain containing 3; and TLR2, Toll-like receptor 2.

    Article Snippet: The membranes were blocked with 5% nonfat milk at room temperature for 2 hours and then incubated overnight at 4 °C with primary antibodies against apo C3 (1:1000; Affinity; DF8054), TLR2 (1:1000; Proteintech; 17 236- 1- AP), NLRP3 (1:1000; Invitrogen; MA5- 23919), cluster of differentiation 86 (CD86) (1:1000; Proteintech; 13 395- 1- AP), inducible nitric oxide synthase (INOS) (1:1000; Invitrogen; PA1- 036), matrix metalloproteinase (MMP) 2 (1:1000; Proteintech; 10 373- 2- AP), and MMP9 (1:1000; Proteintech; 10 375- 2- AP).

    Techniques: Activation Assay, Immunofluorescence, Expressing, Western Blot, MANN-WHITNEY, Dissection