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Rabbit Anti-RAGE/FITC Conjugated antibody
background:
Advanced glycosylation end product-specific receptor (AGER; RAGE) is a member of the immunoglobulin superfamily of cell surface molecules that binds molecules that have been irreversibly modified by non-enzymatic glycation and oxidation, and are know as advanced glycation end products (AGEs). It is expressed by endothelium, mononuclear phagocytes, neurons and smooth muscle cells. Whereas RAGE is present at high levels during development, especially in the central nervous system, its levels decline during maturity.The increased expression of RAGE is associated with several pathological states, such as diabetic vasculopathy, neuropathy, retinopathy and other disorders, including Alzheimer's disease and immune/inflammatory reactions of the vessel walls. In diabetic tissues, the production of RAGE is due to the overproduction of AGEs that eventually overwhelm the protective properties of RAGE. This results in oxidative stress and endothelial cell dysfunction that leads to vascular disease in diabetics. In the brain, RAGE also binds amyloid beta (Ab). Because Ab is overproduced in neurons and vessels in the brains of Alzheimer disease, this leads to the hyperstimulation of RAGE. The RAGE-Ab interaction is thought to result in oxidative stress leading to neuronal degeneration.
Function:
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. 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. Interaction with S100B after myocardial infarction may play a role in myocyte apoptosis by activating ERK1/2 and p53/TP53 signaling.
Subunit:
Interacts with S100B, S100A1 and APP. Interacts with S100A12.
Subcellular Location:
Isoform 1: Cell membrane; Single-pass type I membrane protein.
Isoform 2: Secreted.
Tissue Specificity:
Endothelial cells and cardiomyocytes.
Similarity:
Contains 2 Ig-like C2-type (immunoglobulin-like) domains.
Contains 1 Ig-like SLVtype (immunoglobulin-like) domain.
Database links:
Entrez Gene: 177 Human
Entrez Gene: 11596 Mouse
Entrez Gene: 81722 Rat
Omim: 600214 Human
SwissProt: Q15109 Human
SwissProt: Q62151 Mouse
SwissProt: Q63495 Rat
Unigene: 534342 Human
Unigene: 3383 Mouse
Unigene: 9829 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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