protein_function: Mediates interactions of advanced glycosylation endproducts (AGE). These are nonenzymatically glycosylated proteinswhich accumulate in vascular tissue in aging and at an acceleratedrate in diabetes. Acts as a mediator of both acute and chronicvascular inflammation in conditions such as atherosclerosis and inparticular as a complication of diabetes. AGE,RAGE signaling playsan important role in regulating the production,expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2diabetes. Interaction with S100A12 on endothelium, mononuclearphagocytes, and lymphocytes triggers cellular activation, withgeneration of key proinflammatory mediators. Interaction withS100B after myocardial infarction may play a role in myocyteapoptosis by activating ERK1,2 and p53,TP53 signaling. Can alsobind oligonucleotides. Receptor for amyloid beta peptide.Contributes to the translocation of amyloid-beta peptide (ABPP)across the cell membrane from the extracellular to theintracellular space in cortical neurons. ABPP-initiated RAGEsignaling, especially stimulation of p38 mitogen-activated proteinkinase (MAPK), has the capacity to drive a transport systemdelivering ABPP as a complex with RAGE to the intraneuronal space.RAGE-dependent signaling in microglia contributes toneuroinflammation, amyloid accumulation, and impairedlearning,memory in a mouse model of Alzheimer disease..
RAGE, the Receptor for Advanced Glycation Endproducts, is a 35kD transmembrane receptor of the immunoglobulin super family. It is also known as ??AGER??. AGER gene is mapped to chromosome 6p21.3 by mapping by contiguous cosmids and YAC clones and by fluorescence in situ hybridization. The expression of RAGE is particularly increased in neurons close to deposits of amyloid beta peptide and to neurofibrillary tangles. RAGE has been linked to several chronic diseases, which are thought to result from vascular damage. The pathogenesis is hypothesized to include ligand binding upon which RAGE signals activation of the nuclear factor kappa B(NF-kappaB).