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R&D Systems human en rage duoset elisas
Human En Rage Duoset Elisas, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 13 article reviews

human en rage duoset elisas - by Bioz Stars, 2026-05

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Fig. 2. SC79 induces the shedding of the RAGE ectodomain. HAECs were incubated with 10 µM SC79 for various times (5, 10, 30, and 60 min) (n = 4) (A) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (n = 3) (B). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and an anti-actin antibody. To compare the size of RAGE in cell lysate and culture supernatant, untreated cell lysate (a) and conditioned media from cells treated with 10 µM SC79 for 30 min (b) were run on the same gel and immunoblotted with the RAGE antibody (C). The cell lysates of HAECs treated with different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min were immunoblotted with an antibody to the C-terminal domain of human RAGE and an anti-actin antibody (n = 4) (D). (*p < 0.05 vs. control)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 2. SC79 induces the shedding of the RAGE ectodomain. HAECs were incubated with 10 µM SC79 for various times (5, 10, 30, and 60 min) (n = 4) (A) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (n = 3) (B). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and an anti-actin antibody. To compare the size of RAGE in cell lysate and culture supernatant, untreated cell lysate (a) and conditioned media from cells treated with 10 µM SC79 for 30 min (b) were run on the same gel and immunoblotted with the RAGE antibody (C). The cell lysates of HAECs treated with different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min were immunoblotted with an antibody to the C-terminal domain of human RAGE and an anti-actin antibody (n = 4) (D). (*p < 0.05 vs. control)

Article Snippet: Anti-RAGE (JF0975) rabbit monoclonal antibody against amino acids 350–390 corresponding to the C-terminal region of human RAGE was from R&D Systems, Inc. (Minneapolis, MN, USA).

Techniques: Incubation, Control

Fig. 3. Inhibitors of AKT and ADAM10 diminish SC79-induced RAGE ectodomain shedding. HAECs were preincubated with or without MK-2206 (1 µM), GI 254023X (2 µM), or DMSO (vehicle) for 60 min. Following this, they were further incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and an anti-actin antibody. (n = 3, *p < 0.05 vs. control, #p < 0.05 vs. SC79 treatment alone)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 3. Inhibitors of AKT and ADAM10 diminish SC79-induced RAGE ectodomain shedding. HAECs were preincubated with or without MK-2206 (1 µM), GI 254023X (2 µM), or DMSO (vehicle) for 60 min. Following this, they were further incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and an anti-actin antibody. (n = 3, *p < 0.05 vs. control, #p < 0.05 vs. SC79 treatment alone)

Techniques: Incubation, Control

Fig. 4. AKT1 activation is required for SC79-induced RAGE ectodomain shedding. (A) HAECs express all three AKT isoforms, and AKT1-, AKT2-, and AKT3-siRNAs selectively deplete each AKT isoform. HAECs were transfected with AKT1-, AKT2-, AKT3-siRNAs, or control siRNAs, and the cell lysates were immunoblotted with antibodies to AKT1, AKT2, AKT3, or actin. (n = 3, *p < 0.05 vs. control). (B) SC79 activates AKT1. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT1 (Ser473) and AKT1. (n = 3, *p < 0.05 vs. control). (C) AKT1 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT1-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT1 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (D) AKT1 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT1-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT1, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT1-siRNA)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 4. AKT1 activation is required for SC79-induced RAGE ectodomain shedding. (A) HAECs express all three AKT isoforms, and AKT1-, AKT2-, and AKT3-siRNAs selectively deplete each AKT isoform. HAECs were transfected with AKT1-, AKT2-, AKT3-siRNAs, or control siRNAs, and the cell lysates were immunoblotted with antibodies to AKT1, AKT2, AKT3, or actin. (n = 3, *p < 0.05 vs. control). (B) SC79 activates AKT1. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT1 (Ser473) and AKT1. (n = 3, *p < 0.05 vs. control). (C) AKT1 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT1-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT1 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (D) AKT1 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT1-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT1, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT1-siRNA)

Techniques: Activation Assay, Transfection, Control, Incubation, Knockdown

Fig. 5. AKT2 activation is required for SC79-induced RAGE ectodomain shedding. (A) SC79 activates AKT2. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT2 (Ser474) and AKT2. (n = 4, *p < 0.05 vs. control). (B) AKT2 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT2-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT2 and actin. (n = 4, *p < 0.05 vs. control cells transfected with control siRNA). (C) AKT2 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT2-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE-BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT2, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT2-siRNA)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 5. AKT2 activation is required for SC79-induced RAGE ectodomain shedding. (A) SC79 activates AKT2. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT2 (Ser474) and AKT2. (n = 4, *p < 0.05 vs. control). (B) AKT2 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT2-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT2 and actin. (n = 4, *p < 0.05 vs. control cells transfected with control siRNA). (C) AKT2 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT2-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE-BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT2, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT2-siRNA)

Techniques: Activation Assay, Incubation, Control, Knockdown, Transfection

Fig. 6. AKT3 activation is required for SC79-induced RAGE ectodomain shedding. (A) SC79 activates AKT3. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT3 (Ser472) and AKT3. (n = 3, *p < 0.05 vs. control). (B) AKT3 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT3-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT3 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) AKT3 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT3-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE-BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT3, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT3-siRNA)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 6. AKT3 activation is required for SC79-induced RAGE ectodomain shedding. (A) SC79 activates AKT3. HAECs were incubated with 10 µM SC79 for various times (1, 5, 10, and 30 min) (upper panel) or different concentrations of SC79 (0.1, 1, 5, and 10 µM) for 30 min (lower panel). The cell lysates were immunoblotted with antibodies to p-AKT3 (Ser472) and AKT3. (n = 3, *p < 0.05 vs. control). (B) AKT3 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with AKT3-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to AKT3 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) AKT3 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with AKT3-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE-BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, AKT3, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with AKT3-siRNA)

Techniques: Activation Assay, Incubation, Control, Knockdown, Transfection

Fig. 7. SC79 induces RAGE ectodomain shedding by promoting ADAM10 cell surface translocation. (A) Immunofluorescence staining to evaluate the effect of SC79 on ADAM10 localization. HAECs grown in culture dishes with a coverslip were treated with SC79 (10 µM) for 10–120 min. (a) The cells on the coverslip were fixed for 10 min with 4% paraformaldehyde without permeabilization, then immunostained with an antibody to an extracellular portion of ADAM10 and examined using confocal microscopy. DAPI was used to label the nuclei of the cells. Representative photos and the relative fluorescence intensities are shown (scale bar: 100 μm). (b) Cell lysates from cells that were not on the coverslip in the same culture plate were immunoblotted with antibodies to ADAM10 and actin. (n = 3, *p < 0.05 vs. control). (B) ADAM10 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with ADAM10-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to ADAM10 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) ADAM10 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with ADAM10-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, ADAM10, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with ADAM10- siRNA)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 7. SC79 induces RAGE ectodomain shedding by promoting ADAM10 cell surface translocation. (A) Immunofluorescence staining to evaluate the effect of SC79 on ADAM10 localization. HAECs grown in culture dishes with a coverslip were treated with SC79 (10 µM) for 10–120 min. (a) The cells on the coverslip were fixed for 10 min with 4% paraformaldehyde without permeabilization, then immunostained with an antibody to an extracellular portion of ADAM10 and examined using confocal microscopy. DAPI was used to label the nuclei of the cells. Representative photos and the relative fluorescence intensities are shown (scale bar: 100 μm). (b) Cell lysates from cells that were not on the coverslip in the same culture plate were immunoblotted with antibodies to ADAM10 and actin. (n = 3, *p < 0.05 vs. control). (B) ADAM10 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with ADAM10-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to ADAM10 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) ADAM10 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with ADAM10-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, ADAM10, and actin. (n = 3, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with ADAM10- siRNA)

Techniques: Translocation Assay, Immunofluorescence, Staining, Confocal Microscopy, Fluorescence, Control, Knockdown, Transfection, Incubation

Fig. 10. Rab14 is required for SC79-induced ADAM10 cell surface translocation. (A) Rab14 knockdown prevents SC79-induced ADAM10 cell surface translocation. HAECs grown in culture dishes with a coverslip were transfected with Rab14-siRNA or control siRNA and then incubated for 20 min with DMSO or SC79 (10 µM). (a) Cells grown on the coverslip were immunostained with an antibody to an extracellular portion of ADAM10. Representative photos and the relative fluorescence intensities are shown (scale bar: 100 μm). (b) Cell lysates from cells that were not on the coverslip in the same culture plate were immunoblotted with antibodies to Rab14 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (B) Rab14 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with Rab14-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to Rab14 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) Rab14 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with Rab14-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, Rab14, and actin. (n = 4, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with Rab14-siRNA)

Journal: Scientific reports

Article Title: AKT activation triggers Rab14-mediated ADAM10 translocation to the cell surface in human aortic endothelial cells.

doi: 10.1038/s41598-025-90624-w

Figure Lengend Snippet: Fig. 10. Rab14 is required for SC79-induced ADAM10 cell surface translocation. (A) Rab14 knockdown prevents SC79-induced ADAM10 cell surface translocation. HAECs grown in culture dishes with a coverslip were transfected with Rab14-siRNA or control siRNA and then incubated for 20 min with DMSO or SC79 (10 µM). (a) Cells grown on the coverslip were immunostained with an antibody to an extracellular portion of ADAM10. Representative photos and the relative fluorescence intensities are shown (scale bar: 100 μm). (b) Cell lysates from cells that were not on the coverslip in the same culture plate were immunoblotted with antibodies to Rab14 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (B) Rab14 knockdown inhibits SC79-induced RAGE ectodomain shedding. HAECs were transfected with Rab14-siRNA or control siRNA and then incubated for 30 min with or without SC79 (10 µM). The cell lysate and culture supernatant were immunoblotted with a monoclonal antibody to the extracellular domain of human RAGE and antibodies to Rab14 and actin. (n = 3, *p < 0.05 vs. control cells transfected with control siRNA). (C) Rab14 knockdown abolishes SC79’s inhibitory effect against AGE-BSA. HAECs transfected with Rab14-siRNA or control siRNA were treated for 30 min with or without SC79 (10 µM). The cells were then treated with AGE- BSA (100 µg/ml) for 24 h. The cell lysates were immunoblotted with antibodies to ICAM-1, Rab14, and actin. (n = 4, *p < 0.05 vs. control; #p < 0.05 vs. AGE-BSA; †p < 0.05 vs. control cells transfected with Rab14-siRNA)

Techniques: Translocation Assay, Knockdown, Transfection, Control, Incubation, Fluorescence

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