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 By similarity. 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.
AGER Polyclonal Antibody, FITC Conjugated. FITC. Raised in: Rabbit.
Liquid. 0.03% Proclin 300, 50% Glycerol, 0.01M PBS, PH 7.4.
>95%, Protein G purified
Recombinant Human Advanced glycosylation end product-specific receptor protein (23-342AA)
Shipped at 4°C. Upon delivery aliquot and store at -20°C (short-term) or -80°C (long-term). Avoid repeated freeze.
Receptor for advanced glycosylation end products, AGER, RAGE