monoclonal c9 neoepitope specific capture antibody Search Results


murine monoclonal neoepitope anti human c9  (BioPorto Inc)
86
BioPorto Inc murine monoclonal neoepitope anti human c9
CC induce PTF1.2 dependent on the TF pathway. (A) PTF1.2 induction over time (60, 120, and 240 min) upon exposure to CC 2000 μg/ml, PBS/HSA, E. coli (1 × 107 particles/ml), or glass (n = 7 donors) in human whole blood. (B) Effect of TF inhibition following exposure of CC (500, 1000, and 2000 μg/ml) or E.coli after addition of the functional-grade inhibitory Ab against TF (anti-TF) or the corresponding Ultra-LEAF purified IgG1κ control Ab (Ctr <t>IgG)</t> for 240 min in human whole blood (n = 6 donors). (C) Effect of factor XII inhibition by CTI (40 μg/ml) in PFP following incubation with CC (2000 μg/ml) or glass for 60 min (n = 5). Effect of CC on platelet aggregation in human whole blood measured by electrical impedance aggregometry in (D) by CC (2000 μg/ml) or its controls, HSA/PBS, or TRAP (n = 6), (E) by additional stimulation with ADP (n = 3), and in (F) with TRAP following 6 min of incubation (n = 3), given as arbitrary units × min. In all experiments, thrombin was inhibited with lepirudin. All data are given as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Murine Monoclonal Neoepitope Anti Human C9, supplied by BioPorto Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/murine monoclonal neoepitope anti human c9/product/BioPorto Inc
Average 86 stars, based on 1 article reviews
murine monoclonal neoepitope anti human c9 - by Bioz Stars, 2025-07
86/100 stars
  Buy from Supplier
alkaline phosphatase conjugated mouse anti human c9 neoepitope monoclonal antibody  (Diatec Inc)
86
Diatec Inc alkaline phosphatase conjugated mouse anti human c9 neoepitope monoclonal antibody
CC induce PTF1.2 dependent on the TF pathway. (A) PTF1.2 induction over time (60, 120, and 240 min) upon exposure to CC 2000 μg/ml, PBS/HSA, E. coli (1 × 107 particles/ml), or glass (n = 7 donors) in human whole blood. (B) Effect of TF inhibition following exposure of CC (500, 1000, and 2000 μg/ml) or E.coli after addition of the functional-grade inhibitory Ab against TF (anti-TF) or the corresponding Ultra-LEAF purified IgG1κ control Ab (Ctr <t>IgG)</t> for 240 min in human whole blood (n = 6 donors). (C) Effect of factor XII inhibition by CTI (40 μg/ml) in PFP following incubation with CC (2000 μg/ml) or glass for 60 min (n = 5). Effect of CC on platelet aggregation in human whole blood measured by electrical impedance aggregometry in (D) by CC (2000 μg/ml) or its controls, HSA/PBS, or TRAP (n = 6), (E) by additional stimulation with ADP (n = 3), and in (F) with TRAP following 6 min of incubation (n = 3), given as arbitrary units × min. In all experiments, thrombin was inhibited with lepirudin. All data are given as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Alkaline Phosphatase Conjugated Mouse Anti Human C9 Neoepitope Monoclonal Antibody, supplied by Diatec Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/alkaline phosphatase conjugated mouse anti human c9 neoepitope monoclonal antibody/product/Diatec Inc
Average 86 stars, based on 1 article reviews
alkaline phosphatase conjugated mouse anti human c9 neoepitope monoclonal antibody - by Bioz Stars, 2025-07
86/100 stars
  Buy from Supplier
mouse monoclonal nti human c9 neoepitope antibody  (Quidel)
86
Quidel mouse monoclonal nti human c9 neoepitope antibody
CC induce PTF1.2 dependent on the TF pathway. (A) PTF1.2 induction over time (60, 120, and 240 min) upon exposure to CC 2000 μg/ml, PBS/HSA, E. coli (1 × 107 particles/ml), or glass (n = 7 donors) in human whole blood. (B) Effect of TF inhibition following exposure of CC (500, 1000, and 2000 μg/ml) or E.coli after addition of the functional-grade inhibitory Ab against TF (anti-TF) or the corresponding Ultra-LEAF purified IgG1κ control Ab (Ctr <t>IgG)</t> for 240 min in human whole blood (n = 6 donors). (C) Effect of factor XII inhibition by CTI (40 μg/ml) in PFP following incubation with CC (2000 μg/ml) or glass for 60 min (n = 5). Effect of CC on platelet aggregation in human whole blood measured by electrical impedance aggregometry in (D) by CC (2000 μg/ml) or its controls, HSA/PBS, or TRAP (n = 6), (E) by additional stimulation with ADP (n = 3), and in (F) with TRAP following 6 min of incubation (n = 3), given as arbitrary units × min. In all experiments, thrombin was inhibited with lepirudin. All data are given as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
Mouse Monoclonal Nti Human C9 Neoepitope Antibody, supplied by Quidel, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse monoclonal nti human c9 neoepitope antibody/product/Quidel
Average 86 stars, based on 1 article reviews
mouse monoclonal nti human c9 neoepitope antibody - by Bioz Stars, 2025-07
86/100 stars
  Buy from Supplier

Image Search Results


CC induce PTF1.2 dependent on the TF pathway. (A) PTF1.2 induction over time (60, 120, and 240 min) upon exposure to CC 2000 μg/ml, PBS/HSA, E. coli (1 × 107 particles/ml), or glass (n = 7 donors) in human whole blood. (B) Effect of TF inhibition following exposure of CC (500, 1000, and 2000 μg/ml) or E.coli after addition of the functional-grade inhibitory Ab against TF (anti-TF) or the corresponding Ultra-LEAF purified IgG1κ control Ab (Ctr IgG) for 240 min in human whole blood (n = 6 donors). (C) Effect of factor XII inhibition by CTI (40 μg/ml) in PFP following incubation with CC (2000 μg/ml) or glass for 60 min (n = 5). Effect of CC on platelet aggregation in human whole blood measured by electrical impedance aggregometry in (D) by CC (2000 μg/ml) or its controls, HSA/PBS, or TRAP (n = 6), (E) by additional stimulation with ADP (n = 3), and in (F) with TRAP following 6 min of incubation (n = 3), given as arbitrary units × min. In all experiments, thrombin was inhibited with lepirudin. All data are given as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: The Journal of Immunology Author Choice

Article Title: Cholesterol Crystals Induce Coagulation Activation through Complement-Dependent Expression of Monocytic Tissue Factor

doi: 10.4049/jimmunol.1900503

Figure Lengend Snippet: CC induce PTF1.2 dependent on the TF pathway. (A) PTF1.2 induction over time (60, 120, and 240 min) upon exposure to CC 2000 μg/ml, PBS/HSA, E. coli (1 × 107 particles/ml), or glass (n = 7 donors) in human whole blood. (B) Effect of TF inhibition following exposure of CC (500, 1000, and 2000 μg/ml) or E.coli after addition of the functional-grade inhibitory Ab against TF (anti-TF) or the corresponding Ultra-LEAF purified IgG1κ control Ab (Ctr IgG) for 240 min in human whole blood (n = 6 donors). (C) Effect of factor XII inhibition by CTI (40 μg/ml) in PFP following incubation with CC (2000 μg/ml) or glass for 60 min (n = 5). Effect of CC on platelet aggregation in human whole blood measured by electrical impedance aggregometry in (D) by CC (2000 μg/ml) or its controls, HSA/PBS, or TRAP (n = 6), (E) by additional stimulation with ADP (n = 3), and in (F) with TRAP following 6 min of incubation (n = 3), given as arbitrary units × min. In all experiments, thrombin was inhibited with lepirudin. All data are given as means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Abs for histology included murine monoclonal neoepitope anti-human C9 (DIA011-01, clone E11, isotype IgG2a) from BioPorto Diagnostics (DK-2820; Gentofte, Denmark), neoepitope anti-human iC3b (A209, isotype IgG1) from Quidel (San Diego, CA), mAb against human TF (CD142, ADG4509, clone IIID8, isotype IgG1) from Sekisui (American Diagnostica, Pfungstdt, Germany), a monoclonal anti-human CD14 (18D11, isotype IgG1) synthesized in-house, monoclonal mouse anti-human CD68 (clone KP1, M0814, isotype IgG1), and anti-human CD61 (clone Y2/51, M0753, isotype IgG1) from Dako (Glostrup, Denmark).

Techniques: Inhibition, Functional Assay, Purification, Incubation

Immunohistochemistry of frozen sections of human intracranial thrombus retracted from a patient with advanced carotid atherosclerosis and explored with polarization filter reflected light microscopy. (A and B) Staining against the monocyte marker CD14. (C) Staining against TF. (D) Staining against the complement neoepitopes C5b–9. (E) Staining against the complement neoepitope iC3b. The thicknesses of the sections are 4 μm. Pictures in the left column are taken by original magnification ×4 objective, and the CC-rich area (blue frame) is further augmented with an original magnification ×40 objective (middle and right columns). Examples of birefringent structures are shown by yellow arrows, whereas blue arrows point to the outer thrombi sections stained heavily for neoepitope iC3b. Scale bars, 200 μm for pictures in left column and 30 μm for pictures in middle and right columns.

Journal: The Journal of Immunology Author Choice

Article Title: Cholesterol Crystals Induce Coagulation Activation through Complement-Dependent Expression of Monocytic Tissue Factor

doi: 10.4049/jimmunol.1900503

Figure Lengend Snippet: Immunohistochemistry of frozen sections of human intracranial thrombus retracted from a patient with advanced carotid atherosclerosis and explored with polarization filter reflected light microscopy. (A and B) Staining against the monocyte marker CD14. (C) Staining against TF. (D) Staining against the complement neoepitopes C5b–9. (E) Staining against the complement neoepitope iC3b. The thicknesses of the sections are 4 μm. Pictures in the left column are taken by original magnification ×4 objective, and the CC-rich area (blue frame) is further augmented with an original magnification ×40 objective (middle and right columns). Examples of birefringent structures are shown by yellow arrows, whereas blue arrows point to the outer thrombi sections stained heavily for neoepitope iC3b. Scale bars, 200 μm for pictures in left column and 30 μm for pictures in middle and right columns.

Article Snippet: Abs for histology included murine monoclonal neoepitope anti-human C9 (DIA011-01, clone E11, isotype IgG2a) from BioPorto Diagnostics (DK-2820; Gentofte, Denmark), neoepitope anti-human iC3b (A209, isotype IgG1) from Quidel (San Diego, CA), mAb against human TF (CD142, ADG4509, clone IIID8, isotype IgG1) from Sekisui (American Diagnostica, Pfungstdt, Germany), a monoclonal anti-human CD14 (18D11, isotype IgG1) synthesized in-house, monoclonal mouse anti-human CD68 (clone KP1, M0814, isotype IgG1), and anti-human CD61 (clone Y2/51, M0753, isotype IgG1) from Dako (Glostrup, Denmark).

Techniques: Immunohistochemistry, Light Microscopy, Staining, Marker

Human vulnerable plaque and whole blood show corresponding patterns in monocyte TF/CD14 expression and complement activation to CC. (A) Immunohistochemistry of the vulnerable plaque with the monocyte marker CD14, TF, and activated complement neoepitope iC3b and neoepitopes C5b–9. Staining areas for CD14bright monocytes are marked with yellow arrows, and CD14low/TF+-expressing monocytes are marked by blue arrows; specified also are the CC-rich areas, lumen, and adventitia. Sections are 4 μm and are taken by original magnification ×4 objective and given for two adjacent areas in each staining. Scale bar, 200 μm. Whole blood following CC exposure showing effects on (B) monocyte CD14 expression, (C) correlation between CD14 and TF in monocytes, (D) the increase in monocyte granularity, (E) monocyte CD14 following inhibition of complement C3 (120 min), (F) monocyte CD14 following inhibition of complement C5 (120 min), (G) monocyte granularity following inhibition of C3 (120 min), and (H) monocyte granularity following inhibition of C5 (120 min). Data are given as mean fluorescence intensity (MFI; mean ± SEM, n = 6 donors). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: The Journal of Immunology Author Choice

Article Title: Cholesterol Crystals Induce Coagulation Activation through Complement-Dependent Expression of Monocytic Tissue Factor

doi: 10.4049/jimmunol.1900503

Figure Lengend Snippet: Human vulnerable plaque and whole blood show corresponding patterns in monocyte TF/CD14 expression and complement activation to CC. (A) Immunohistochemistry of the vulnerable plaque with the monocyte marker CD14, TF, and activated complement neoepitope iC3b and neoepitopes C5b–9. Staining areas for CD14bright monocytes are marked with yellow arrows, and CD14low/TF+-expressing monocytes are marked by blue arrows; specified also are the CC-rich areas, lumen, and adventitia. Sections are 4 μm and are taken by original magnification ×4 objective and given for two adjacent areas in each staining. Scale bar, 200 μm. Whole blood following CC exposure showing effects on (B) monocyte CD14 expression, (C) correlation between CD14 and TF in monocytes, (D) the increase in monocyte granularity, (E) monocyte CD14 following inhibition of complement C3 (120 min), (F) monocyte CD14 following inhibition of complement C5 (120 min), (G) monocyte granularity following inhibition of C3 (120 min), and (H) monocyte granularity following inhibition of C5 (120 min). Data are given as mean fluorescence intensity (MFI; mean ± SEM, n = 6 donors). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Abs for histology included murine monoclonal neoepitope anti-human C9 (DIA011-01, clone E11, isotype IgG2a) from BioPorto Diagnostics (DK-2820; Gentofte, Denmark), neoepitope anti-human iC3b (A209, isotype IgG1) from Quidel (San Diego, CA), mAb against human TF (CD142, ADG4509, clone IIID8, isotype IgG1) from Sekisui (American Diagnostica, Pfungstdt, Germany), a monoclonal anti-human CD14 (18D11, isotype IgG1) synthesized in-house, monoclonal mouse anti-human CD68 (clone KP1, M0814, isotype IgG1), and anti-human CD61 (clone Y2/51, M0753, isotype IgG1) from Dako (Glostrup, Denmark).

Techniques: Expressing, Activation Assay, Immunohistochemistry, Marker, Staining, Inhibition, Fluorescence