complement system inhibitors Search Results


92
Athens Research fxi
(A) Non-reducing Western blot analysis of <t>FXI,</t> C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with <t>FXI</t> <t>purified</t> protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.
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90
Shanghai Korain Biotech Co Ltd elisa kit
(A) Non-reducing Western blot analysis of <t>FXI,</t> C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with <t>FXI</t> <t>purified</t> protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.
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93
Proteintech clu
(A) Non-reducing Western blot analysis of <t>FXI,</t> C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with <t>FXI</t> <t>purified</t> protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.
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90
Boster Bio anti apolipoprotein j clusterin antibody
(A) Non-reducing Western blot analysis of <t>FXI,</t> C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with <t>FXI</t> <t>purified</t> protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.
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93
Boster Bio human clusterin elisa kit
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Boster Bio monoclonal antibody
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Achillion inc therapeutic complement inhibitors
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Omeros Inc therapeutic inhibitors for the lectin activation pathway of complement
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Federation of European Neuroscience Societies complement pathway inhibitor
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Genentech inc complement cascade amd, geographic atrophy inhibitor (factor d
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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90
Diamedix Corporation complement inhibitors
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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IVERIC Bio Inc complement inhibitors avacincaptad
CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using <t>ELISA</t> after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.
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Image Search Results


(A) Non-reducing Western blot analysis of FXI, C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with FXI purified protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.

Journal: Journal of thrombosis and haemostasis : JTH

Article Title: The Alzheimer’s disease peptide Aβ promotes thrombin generation through activation of coagulation factor XII

doi: 10.1111/jth.13209

Figure Lengend Snippet: (A) Non-reducing Western blot analysis of FXI, C1inh, and transferrin loading control in plasma of 10 AD patients and 10 ND controls from Group 1. Lanes loaded with FXI purified protein (FXI) and FXI-deficient human plasma (FXI-def) show that the band just above the FXI band is non-specific. (B) FXI levels normalized to transferrin were lower in AD than ND plasma (p = 0.008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (C) C1inh levels were lower in AD than ND plasma (p = 0.0008). Levels of FXIIa normalized to transferrin in these samples were determined previously [25], and mean values for each group are designated by asterisk. (D) Levels of FXI, C1inh, and transferrin were analyzed in 10 AD and 10 ND plasmas from Group 2. (E) FXI levels were lower in AD than ND plasma (p = 0.0003). (F) C1inh levels were lower in AD than ND plasma (p = 0.01). (G) Levels of fibrin monomer were analyzed under reducing conditions in 10 AD and 10 ND plasma samples from Group 2 using antibody 59D8 specific for fibrin beta chain [46]. (H) D-dimer levels were analyzed under non-reducing conditions in 10 AD and 10 ND plasma samples from Group 2. (I) Fibrin (p = 0.009) and D-dimer (p = 0.018) levels were increased in Group 2 AD plasma compared to control. (J) Fibrin (r = −0.49; p = 0.03) and D-dimer (r = −0.57, p = 0.008) levels were negatively correlated with FXI levels in samples from Group 2.

Article Snippet: Purified FXI, C1 esterase inhibitor (Athens Research and Technology), and FXI-deficient plasma (George King Biomedical) served as controls.

Techniques: Western Blot, Control, Clinical Proteomics, Purification

CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using ELISA after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.

Journal: Scientific Reports

Article Title: Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells

doi: 10.1038/s41598-024-82140-0

Figure Lengend Snippet: CLU protein concentration in HL-60 cells exposed to different concentrations of HQ. CLU protein levels were quantified using ELISA after treatment with HQ at concentrations of 0, 10, 25, and 50 µmol/L ( n = 3 per group). The error bars represent SD, and the mean is shown as horizontal bars. The control group (0 µmol/L HQ) exhibited the highest CLU concentration (19.05 ± 2.32 ng/mL), while HQ-treated groups showed a progressive decrease: 14.45 ± 1.23 ng/mL at 10 µmol/L, 9.43 ± 0.40 ng/mL at 25 µmol/L, and 9.46 ± 0.67 ng/mL at 50 µmol/L. Significant differences were determined by ANOVA followed by Tukey post hoc test (* p < 0.05, ** p < 0.01, *** p < 0.001, ns p > 0.05), ns : not significant.

Article Snippet: The concentration of sCLU proteins was measured using the Human Clusterin ELISA Kit (Boster Biological Technology, China) according to the instructions.

Techniques: Protein Concentration, Enzyme-linked Immunosorbent Assay, Control, Concentration Assay

Concentration of sCLU protein in the cell culture supernatant after exposure to varying HQ concentrations. The concentration of sCLU protein in the supernatant of HL -60 cell cultures was determined using ELISA following treatment with HQ at 0, 10, 25, and 50 µmol/L ( n = 3 per group). The control group (0 µmol/L HQ) exhibited the highest concentration (25.88 ± 4.24 ng/mL), while the 10 µmol/L HQ group showed a slight, non-significant decrease (23.73 ± 2.03 ng/mL, p = 0.696). Significant reductions were observed in the 25 µmol/L (17.45 ± 0.36 ng/mL) and 50 µmol/L (12.96 ± 0.67 ng/mL) groups compared to the control (* p < 0.05, *** p < 0.001, ns p > 0.05), ns : not significant.

Journal: Scientific Reports

Article Title: Clusterin mediates hydroquinone-induced cytotoxic responses in HL-60 differentiated cells

doi: 10.1038/s41598-024-82140-0

Figure Lengend Snippet: Concentration of sCLU protein in the cell culture supernatant after exposure to varying HQ concentrations. The concentration of sCLU protein in the supernatant of HL -60 cell cultures was determined using ELISA following treatment with HQ at 0, 10, 25, and 50 µmol/L ( n = 3 per group). The control group (0 µmol/L HQ) exhibited the highest concentration (25.88 ± 4.24 ng/mL), while the 10 µmol/L HQ group showed a slight, non-significant decrease (23.73 ± 2.03 ng/mL, p = 0.696). Significant reductions were observed in the 25 µmol/L (17.45 ± 0.36 ng/mL) and 50 µmol/L (12.96 ± 0.67 ng/mL) groups compared to the control (* p < 0.05, *** p < 0.001, ns p > 0.05), ns : not significant.

Article Snippet: The concentration of sCLU proteins was measured using the Human Clusterin ELISA Kit (Boster Biological Technology, China) according to the instructions.

Techniques: Concentration Assay, Cell Culture, Enzyme-linked Immunosorbent Assay, Control