Mediates interactions of advanced glycosylation end products (AGE). These are nonenzymatically glycosylated proteins which accumulate in vascular tissue in aging and at an accelerated rate in diabetes. Acts as a mediator of both acute and chronic vascular inflammation in conditions such as atherosclerosis and in particular as a complication of diabetes. AGE/RAGE signaling plays an important role in regulating the production/expression of TNF- alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes. Interaction with S100A12 on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling. Receptor for amyloid beta peptide. Contributes to the translocation of amyloid-beta peptide (ABPP) across the cell membrane from the extracellular to the intracellular space in cortical neurons. ABPP-initiated RAGE signaling, especially stimulation of p38 mitogen-activated protein kinase (MAPK), has the capacity to drive a transport system delivering ABPP as a complex with RAGE to the intraneuronal space. Interacts with S100B, S100A1 and APP. Interacts with S100A12. Endothelial cells. 4 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Cellular Component: axon; basal plasma membrane; cell soma; cell surface; cytosol; extracellular space; integral to plasma membrane; plasma membrane
Molecular Function: advanced glycation end-product receptor activity; heparin binding; identical protein binding; protein binding; receptor activity; transmembrane receptor activity
Biological Process: activation of NF-kappaB transcription factor; astrocyte development; brain development; calcium ion homeostasis; cell surface receptor linked signal transduction; glycoprotein metabolic process; induction of positive chemotaxis; inflammatory response; innate immune response; JAK-STAT cascade; lung development; negative regulation of cell adhesion; negative regulation of collagen biosynthetic process; negative regulation of endothelial cell proliferation; negative regulation of interleukin-10 production; negative regulation of osteoblast proliferation; negative regulation of protein amino acid phosphorylation; neurite development; positive regulation of activated T cell proliferation; positive regulation of autophagy; positive regulation of fibroblast proliferation; positive regulation of inflammatory response; positive regulation of interleukin-12 production; positive regulation of JNK activity; positive regulation of neuron apoptosis; positive regulation of phagocytosis, engulfment; positive regulation of smooth muscle cell migration; positive regulation of smooth muscle cell proliferation; regulation of DNA binding; regulation of T cell mediated cytotoxicity; response to activity; response to fructose stimulus; response to genistein; response to hyperoxia; response to hypoxia; response to methylglyoxal; response to vitamin A; response to wounding
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.