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: extracellular space; cell surface; cell soma; axon; integral to plasma membrane; plasma membrane; basal plasma membrane; cytosol
Molecular Function: identical protein binding; protein binding; advanced glycation end-product receptor activity; transmembrane receptor activity; receptor activity
Biological Process: positive regulation of JNK activity; glycoprotein metabolic process; negative regulation of collagen biosynthetic process; positive regulation of smooth muscle cell proliferation; negative regulation of cell adhesion; positive regulation of smooth muscle cell migration; activation of NF-kappaB transcription factor; response to vitamin A; induction of positive chemotaxis; calcium ion homeostasis; positive regulation of fibroblast proliferation; cell surface receptor linked signal transduction; negative regulation of protein amino acid phosphorylation; regulation of DNA binding; positive regulation of neuron apoptosis; response to methylglyoxal; response to wounding; inflammatory response; positive regulation of autophagy; response to fructose stimulus; neurite development; JAK-STAT cascade; response to genistein; response to hyperoxia; negative regulation of endothelial cell proliferation; response to hypoxia; innate immune response; negative regulation of osteoblast proliferation; response to activity; brain development; positive regulation of phagocytosis, engulfment; lung development; positive regulation of inflammatory response
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.