Human RAGE ELISA Kit

Kit Components

 1. Recombinant Human Rage standard: 2 vials

 2. One 96-well plate coated with Human Rage  Ab

 3. Sample diluent buffer: 12 mL - 1

 4. Detection antibody: 130 µL, dilution 1:100

 5. Streptavidin-HRP: 130 µL, dilution 1:100

 6. Antibody diluent buffer: 12 mL x1   

 7. Streptavidin-HRP diluent buffer: 12 mL x1

 8. TMB developing agent: 10 mL x1

9. Stop solution: 10 mL x1

10. Washing solution (20x): 25 mL x1

Background

Receptor for Advanced Glycation End product (RAGE) is a multi-ligand type I transmembrane glycoprotein belonging to the immunoglobulin (Ig) superfamily. Naturally occurring soluble RAGE (sRAGE) spliced variants have been identified and could potentially act as endogenous inhibitors of RAGE activity. RAGE is highly expressed in the central nervous system (CNS) during development. It is also expressed at lower levels in adult cells including endothelial and smooth muscle cells, mononuclear phagocytes, pericytes, neurons, cardiac myocytes, and hepatocytes.

Interactions of RAGE with its ligands such as advanced glycation end products (AGEs), amyloid-β (Aβ) peptide, HMG-1 (also known as Amphoterin), and several members of the S100 protein superfamily have been associated with a series of physiological and pathological processes. Increasing evidence supports a role for AGE/RAGE interactions in the pathophysiology of diabetes. Both AGEs and RAGE are upregulated in diabetic blood vessels, monocytes, and podocytes. Blockade of RAGE activation by recombinant sRAGE or function-blocking antibodies suppresses vascular hyperpermeability, atherosclerotic lesion development, and enhances wound healing in diabetic rodents. Aβ is a primary component of neurodegenerative plaques associated with Alzheimer’s disease (AD). Elevated levels of RAGE have been found to be co-localized with Aβ in AD brain. Interaction of Aβ with RAGE expressed on endothelial cells, neurons, and microglia leads to the generation of reactive oxygen species and the production of proinflammatory factors, potential mechanisms underlying AD-related neurodegeneration. It is shown that RAGE interactions with HMG-1 regulate cell motility. For instance, HMG-1/RAGE stimulates neurite outgrowth in neuroblastoma cell. Blockage of HMG-1/RAGE activation has also been shown to suppress tumor growth and metastasis in animal models of cancer. Binding of EN-RAGE/S100A12 or S100B initiates several signaling pathways mediated by NFκB, leading to induction of pro-inflammatory cytokines. In addition, it is reported that both RAGE and S100 proteins are upregulated in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), and the induction of EAE is suppressed when a dominant-negative form of RAGE is over-expressed.