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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
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.
In response to HMGB1 stimulation, human aortic endothelial cells rapidly undergo ectodomain shedding of RAGE and TLR4, and thereby become insensitive to further HMGB1 stimulation.
MiR-1915 exerted tumor-suppressive effects on cellular proliferation, invasion, and migration of helicobacter pylori-infected gastric cancer cells via targeting RAGE.
Report decreased sRAGE levels in patients with chronic plaque psoriasis.
Taken together, these observations suggest that Long non-coding RNA AGER-1 has an inhibitory effect on lung cancer development via AGER, which may serve as a target for lung cancer treatment.
In a candidate association study identified 2 polymorphisms (T-429C and G1704T) in RAGE, which were not only associated with increased MI risk but also interacted with metabolic risk factors to increase that risk.
High RAGE expression is associated with Breast Carcinoma.
AGEs increase IL-6 and ICAM-1 expression via the RAGE, MAPK and NF-kappaB pathways in HGFs and may exacerbate the progression of the pathogenesis of periodontal diseases.
Low serum sRAGE level is associated with Sarcopenia.
Results show that RAGE is activated by HMGB1 to induce EMT in prostate cancer cells.
Endogenous secretory receptor for advanced glycation end products protects endothelial cells from advanced glycosylation end-product associated apoptosis.
high mobility group box 1-receptor for advanced glycation end-products (HMGB1-RAGE) signaling pathway may be involved in the pathogenesis of preterm premature rupture of the membranes (pPROM).
Results show that RAGE is upregulated in breast cancer tissues, and confirmed that RAGE was a direct target of miR-328.
The results suggest that S100A12 does not participate in the induction of inflammation in dental pulp. However, RAGE can participate in the inflammation in the pulp of males.
The results show for the first time that RAGE is present in neuronally-derived plasma exosomes, and suggest that exosomal RAGE may be a novel biomarker that reflects pathophysiological processes in the brain.
Decreased soluble RAGE in neutrophilic asthma is correlated with disease severity and RAGE G82S variants.
Our study provides novel evidence for a potential role of AGER in bridging human papillomavirus (HPV)-induced inflammation and cervical cancer.
Plasmatic RAGE level is significantly lower in patients with prosthetic-joint-associated infections.
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.
We investigated the role of RAGE in postischaemic leukocyte adhesion after myocardial infarction and its effect on postischaemic myocardial function. RAGE represents an additional pro-inflammatory endothelial mediator of ischaemia-reperfusion injury.
The results indicate that cells respond to advanced glycation end products by increasing matrix assembly and that RAGE is involved in this response.
Receptor for AGE expression and reactive oxygen species production were upregulated in db/db mouse livers, together with impaired proteolytic, antioxidant and mitochondrial respiratory activities. In parallel, acute exposure of HepG2 cells to glycated albumin also elicited intracellular free radical formation
RAGE is phosphorylated by the ATM kinase and is recruited to the site of DNA-double-strand break via an early DNA damage response.
receptor for advanced glycation end products (RAGE) was required for stabilization of beta-catenin in toluene diisocyanate-induced asthma, identifying protective effects of RAGE blockade in this mouse model
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