Human AGER Protein expressed in HEK-293 Cells - ABIN2180572
Xue, Rai, Singer, Chabierski, Xie, Reverdatto, Burz, Schmidt, Hoffmann, Shekhtman: Advanced glycation end product recognition by the receptor for AGEs. in Structure (London, England : 1993) 2011
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Human AGER Protein expressed in Human Cells - ABIN2004453
Sugaya, Fukagawa, Matsumoto, Mita, Takahashi, Ando, Inoko, Ikemura et al.: Three genes in the human MHC class III region near the junction with the class II: gene for receptor of advanced glycosylation end products, PBX2 homeobox gene and a notch homolog, human counterpart ... in Genomics 1995
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Human AGER Protein expressed in HEK-293 Cells - ABIN621037
Amir, Waite, Tobler, Catalfamo, Koutouzis, Katz, Wallet: The role of hyperglycemia in mechanisms of exacerbated inflammatory responses within the oral cavity. in Cellular immunology 2011
RAGE has a role in binding preamyloid IAPP intermediates and mediates pancreatic beta cell proteotoxicity
contributory role of the RAGE gene, especially its two functional variants -429T > C and 82Gly > Ser, in susceptibility to T2DM in primary hypertensive patients
High expression of RAGE is associated with development and progression of prostate cancer.
sRAGE seems to be useful in the identification of frequent exacerbator phenotype in COPD patients.
High RAGE expression is associated with colorectal cancer stemness and development.
Study found that RAGE G82S gene polymorphism confers susceptibility to generalized chronic periodontitis in type II diabetic subjects of South Indian Tamilian ethnicity.
sRAGE could play a potential role in the control of inflammatory response in HTLV-1 carriers through the inhibition of HMGB1 signaling and potentially could be used as an indicator for evaluation of HTLV-1-associated myelopathy/tropical spastic paraparesis developing in HTLV-1-infected individuals.
In a population of mild hypertensives, low circulating sRAGE may be a very early marker of initial target organ damage, suggesting the possible participation of oxidative stress in initial cardiac changes in human hypertension.
RAGE sustains muscle inflammation and necrosis in Duchenne muscular dystrophy (DMD) muscles and that reducing RAGE activity might represent a potential therapeutic tool to counteract muscle inflammation and rescue muscle morphology in DMD conditions.
the G-A-T-G haplotype containing minor allele at position -374 A and major allele at position -429T, 1704G, and G82S G could be regarded as a marker for non-alcoholic steatohepatitis.
Particulate matter 2.5 induces the expression of TGF-beta1, PDGF-AB, and PDGF-BB in vitro via HMGB1-RAGE signaling, suggesting that this pathway may contribute to the airway remodeling observed in patients with chronic obstructive pulmonary disease.
Low expression of AGER was specifically associated with poor survival in lung adenocarcinoma.
Improvements in body composition are related to increased sRAGE isoforms in obese subjects participating in intermittent fasting.
The ratio of advanced glycation end products to sRAGE was independently associated with the existence of albuminuria in hypertensive patients.
review the vast array of information supporting a detrimental role of RAGE/NF-kappaB axis areview the vast array of information supporting a detrimental rolectivation in Alzheimer Disease brain and discuss those data in the context of recent findings pointing to an unexpected effect elicited by this signaling pathway which may rather contribute to reparative mechanisms in AD, namely positive modulation of adult neuroge...
Hepatocyte and Kupffer cell-derived HMGB1 participates in the pathogenesis of liver fibrosis by signaling through RAGE in hepatic stellate cells to activate the pMEK1/2, pERK1/2 and pcJun pathway and increase Collagen type I deposition.
Increased glycated albumin levels and decreased RAGE levels in serum are associated with negative coronary artery remodeling in patients with type 2 diabetes mellitus.
The soluble receptor for advanced glycation end-products (sRAGE) may act as a decoy for capturing advanced glycation end-products (AGEs) and inhibits the activation of the oxidative stress and apoptotic pathways. Lung AGEs/sRAGE is increased in idiopathic pulmonary fibrosis (IPF).
RAGE, S100A8 and S100A9 were overexpressed in pulmonary arterial hypertension pulmonary artery smooth muscle cells (PAH-PASMCs) in the absence of any external growth stimulus. PDGF-BB up-regulated the expression of RAGE in PAH-PASMCs. AS-1, an inhibitor of RAGE signaling, significantly inhibited overgrowth under a condition of no growth stimulation and PDGF-stimulated proliferation of PAH-PASMCs.
These results demonstrated a potential role of monocyte adhesion, chemotaxis, and macrophage polarization in the development cardiovascular diseases induced by IH and identified that RAGE could be a promising therapeutic target to prevent atherosclerosis in patients with OSA.
this study shows that the RAGE signaling pathway is involved in intestinal inflammation and represents a promising therapeutic target for Inflammatory Bowel Diseases
receptor for advanced glycation end-products does not have an effect on bone mineral density and synovitis in mice with intra-articular fractures
AGEs and RAGE interaction increases podocyte heparanase expression by activating NF-kappaB signal pathway.
data, suggests that the dimeric state of RAGE controls its function and ligand mediated signaling which may play important role in RAGE mediated various diseases.
These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE(-/-) mice via inhibition of endoplasmic reticulum stress.
microglial RAGE activation in presence of amyloid beta-enriched environment contributes to the entorhinal cortex vulnerability.
Established a murine model of myocardial ischemia-reperfusion injury; investigated and found remote ischemic postconditioning protects against IR injury thru RAGE-HMGB1 Pathway.
In this study, we found that the wnt co-receptor Lrp6 was a potent positive regulator of beta-catenin signaling in TDI-induced asthma models, both in vivo and in vitro. Additionally, for the first time, we demonstrated that RAGE could mediate phosphorylation of Lrp6, suggesting a functional cross talk between RAGE and the canonical wnt/beta-catenin signaling pathway involved in mediating beta-catenin activation.
Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 messenger RNA in enriched hippocampal microglia and robust and persistent upregulation of RAGE messenger RNA. CUS increased surface expression of RAGE protein on hippocampal microglia and anhedonic behavior. RAGE knockout mice were resilient to stress-induced anhedonia.
study found that diabetes predisposes to more severe infections because of additional inflammatory output through dual activation of MyD88 by not only TLR4 but also RAGE
RAGE controls myocardial dysfunction and oxidative stress in high-fat fed mice by sustaining mitochondrial dynamics and autophagy-lysosome pathway.
these data provide a previously uncharacterized in vivo mechanism contingent on oligodeoxy-nucleotide -administered dose, where TLR9 governs the primary response and RAGE plays a distinct and cooperative function in providing a pivotal role in balancing the immune response.
data demonstrate that under the diabetic condition, DRG neurons are directly affected by elevated levels of glucose, independent of vascular or glial signals, and dependent on RAGE expression.
findings suggest that HMGB1 induces the transcytosis of albumin via RAGE-dependent Src phosphorylation and Cav-1 phosphorylation. These studies revealed a new mechanism of HMGB1-induced endothelial hyperpermeability.
data suggest that S100A8/A9 acts directly on BV-2 microglial cells via binding to TLR4 and RAGE on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK and JNK-mediated NF-kappaB activity in BV-2 microglial cells.
Activation of RAGE facilitates the development of hypoxia-induced pulmonary hypertension by increasing ECM deposition in pulmonary arteries.
knockout of RAGE significantly ameliorates mainstream cigarette smoke-induced airway inflammation in mice
Here, the authors show that RAGE deficiency impairs anti-viral immunity during an early-life infection with pneumonia virus of mice (PVM; a murine analogue of RSV). The elevated viral load was associated with the release of high mobility group box-1 (HMGB1) which triggered airway smooth muscle remodelling in early-life.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan content in nucleus pulposus.
The advanced glycosylation end product (AGE) receptor encoded by this gene is a member of the immunoglobulin superfamily of cell surface receptors. It is a multiligand receptor, and besides AGE, interacts with other molecules implicated in homeostasis, development, and inflammation, and certain diseases, such as diabetes and Alzheimer's disease. Many alternatively spliced transcript variants encoding different isoforms, as well as non-protein-coding variants, have been described for this gene (PMID:18089847).
RAGE isoform NtRAGE-delta
, RAGE isoform sRAGE-delta
, advanced glycation end-products receptor
, receptor for advanced glycosylation end products
, advanced glycosylation end product-specific receptor variant 2
, advanced glycosylation end product-specific receptor variant 3
, advanced glycosylation end product-specific receptor variant 4
, advanced glycosylation end product-specific receptor variant 5
, advanced glycosylation end product-specific receptor variant 1
, advanced glycosylation end product-specific receptor variant 6
, advanced glycosylation end product-specific receptor variant 7
, advanced glycosylation end product-specific receptor variant 8
, advanced glycation end product receptor
, advanced glycosylation end product-specific receptor
, MAPK/MAK/MRK overlapping kinase
, renal tumor antigen