Simple Plex Human RAGE Cartridge

Simple Plex Human RAGE Cartridge Summary

*The Sample Volume represented is based on the amount of sample incorporated into the reaction after taking into account the assay’s minimum required dilution for a given matrix. Serial dilution may be necessary to achieve some of the final sample volumes represented.

Product Summary

Precision

Cell Culture Supernates, Serum, EDTA Plasma, Heparin Plasma

Recovery

Linearity

Product Datasheets

Preparation and Storage

Background: RAGE/AGER

RAGE (Receptor for Advanced Glycation End product) is a transmembrane glycoprotein that binds advanced glycation end products (AGEs), beta-amyloid peptides, HMGB1/Amphoterin, and several S100 family proteins. AGEs are adducts formed by the non-enzymatic glycation and oxidation of proteins and lipids. A soluble form can also be generated by MMP-mediated shedding. RAGE is expressed in the CNS during development as well as in adult endothelial cells, smooth muscle cells, pericytes, monocytes, and neurons. It is locally upregulated in vascular inflammation (e.g. diabetes, atherosclerosis, vascular injury, Alzheimer’s disease). At these sites, RAGE binding to S100A1, EN-RAGE/S100A12, or S100B induces inflammatory immune cell adhesion and infiltration as well as vascular smooth muscle proliferation, neointimal expansion, atherosclerotic plaque development, and transport of A-beta into the cerebrospinal fluid. In cancer, RAGE binding to HMGB1, S100A8, or S100A9 promotes tumor growth and metastasis in addition to inflammatory cell infiltration.

To view our complete solutions for RAGE research, visit bio-techne.com.

Related Research Areas

• Adhesion Molecules in Angiogenesis
• Blood-brain Barrier Transporters
• Cell Structure and Signaling Molecules
• Cytokine and Growth Factor Receptors on VSMC
• Diabetes
• Diabetic Peripheral Neuropathy
• Glucose Homeostasis
• Immune Regulatory Molecules on Endothelial Cells
• Inflammatory Mediators
• Integrins and Associated Molecules
• Microglia Activation
• Neurodegenerative Disease
• Platelet Immune Receptors
• ROS and Stress Resistance
• Uptake of Amyloid beta by Glia Cells