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anti-Mouse (Murine) Antibodies:
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Rat (Rattus) Polyclonal AGER Primary Antibody for FACS, IF (p) - ABIN725900
Huang, Yao, Zhang, Dong, Yu, Sheng: The effect of high-mobility group box 1 protein on activity of regulatory T cells after thermal injury in rats. in Shock (Augusta, Ga.) 2009
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Human Polyclonal AGER Primary Antibody for IHC (p), WB - ABIN3043529
Qin, Niu, Wang, Xu, Qiao, Gu: Heparanase induced by advanced glycation end products (AGEs) promotes macrophage migration involving RAGE and PI3K/AKT pathway. in Cardiovascular diabetology 2013
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Human Polyclonal AGER Primary Antibody for IHC (fro), IHC (p) - ABIN3044329
Wang, Zhang, Liu, Cui, Yang, Li, Du: Tanshinone II A down-regulates HMGB1, RAGE, TLR4, NF-kappaB expression, ameliorates BBB permeability and endothelial cell function, and protects rat brains against focal ischemia. in Brain research 2010
Show all 4 Pubmed References
Human Polyclonal AGER Primary Antibody for IF (p), IHC (p) - ABIN1386239
Durning, Preston-Hurlburt, Clark, Xu, Herold: The Receptor for Advanced Glycation Endproducts Drives T Cell Survival and Inflammation in Type 1 Diabetes Mellitus. in Journal of immunology (Baltimore, Md. : 1950) 2016
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Rat (Rattus) Polyclonal AGER Primary Antibody for FACS, IF (p) - ABIN725907
Zhu, Yao, Zhang, Dong, Yu, Sheng: Anti-RAGE antibody ameliorates severe thermal injury in rats through regulating cellular immune function. in Acta pharmacologica Sinica 2014
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Human Polyclonal AGER Primary Antibody for IHC (p), WB - ABIN1397268
Guan, Sheu, Wu, Chiang, Liu: ATP synthase subunit-β down-regulation aggravates diabetic nephropathy. in Scientific reports 2015
Human Polyclonal AGER Primary Antibody for ELISA, WB - ABIN1573995
Milutinovic, Alcorn, Englert, Crum, Oury: The receptor for advanced glycation end products is a central mediator of asthma pathogenesis. in The American journal of pathology 2012
Human Polyclonal AGER Primary Antibody for IHC, ELISA - ABIN1585839
Patche, Girard, Catan, Boyer, Dobi, Planesse, Diotel, Guerin-Dubourg, Baret, Bravo, Paradela-Dobarro, Álvarez, Essop, Meilhac, Bourdon, Rondeau: Diabetes-induced hepatic oxidative stress: a new pathogenic role for glycated albumin. in Free radical biology & medicine 2017
Human Polyclonal AGER Primary Antibody for ICC, IF - ABIN449216
Oztay, Sancar-Bas, Gezginci-Oktayoglu, Ercin, Bolkent: Exendin-4 partly ameliorates - hyperglycemia-mediated tissue damage in lungs of streptozotocin-induced diabetic mice. in Peptides 1970
Results suggest a possible association between a functional polymorphism in AGER and IPF disease susceptibility, and indicate a potential prognostic value of circulatory sRAGE.
Thus, hypoxia not only increases RAGE expression in THP (show UMOD Antibodies)-1cells by promoting nuclear translocation of NF-kappa B (show NFKB1 Antibodies) and HIF1alpha (show HIF1A Antibodies), but also regulates chemotaxis and pro-inflammatory cytokines release, which may be partially mediated through upregulation of RAGE expression.
This study demonstrated that RAGE mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-beta (show IFNB1 Antibodies) 1a therapy results in upregulation of RAGE in MS patients.
High RAGE expression is associated with lung cancer.
findings collectively demonstrate that fasting blood sRAGE and esRAGE may be causally implicated in IGM in primary hypertensive patients
Our data suggest that the inhibition of sRAGE on I/R-induced apoptosis is associated with activation and expression of proteasome, including improved proteasome activity and elevated beta1i (show PSMB9 Antibodies) and beta5i expression mediated by STAT3 (show STAT3 Antibodies) activation. We predict that sRAGE is a novel intervention to target UPS activation for preventing and treating myocardial apoptosis.
Receptor for AGE expression and reactive oxygen species production were upregulated in db/db (show LEPR Antibodies) mouse livers, together with impaired proteolytic, antioxidant and mitochondrial respiratory activities. In parallel, acute exposure of HepG2 cells to glycated albumin (show ALB Antibodies) also elicited intracellular free radical formation
Our data suggest that H2S reduces RAGE dimer formation and impairs its membrane stability. The lowered plasma membrane abundance of RAGE therefore helps to protect cells against various RAGE mediated pathological effects.
results imply that the interaction of matrix AGEs with RAGE plays a role in the TGFbeta2-mediated EMT (show ITK Antibodies) of lens epithelial cells and suggest that the blockade of RAGE could be a strategy to prevent PCO and other age-associated fibrosis.
novel findings suggest that HMGB1 (show HMGB1 Antibodies) triggered EPC (show TCF21 Antibodies) apoptosis in a manner of RAGE-mediated activation of the PERK (show EIF2AK3 Antibodies)/eIF2alpha (show EIF2A Antibodies) pathway.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan (show ACAN Antibodies) content in nucleus pulposus.
Activation of RAGE facilitates the development of hypoxia-induced pulmonary hypertension by increasing ECM (show MMRN1 Antibodies) 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 (show HMGB1 Antibodies)) 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.
RAGE is phosphorylated by the ATM (show ATM Antibodies) 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 (show CTNNB1 Antibodies) in toluene diisocyanate-induced asthma, identifying protective effects of RAGE blockade in this mouse model
perturbation of Bone marrow mesenchymal stromal cells in diabetes mellitus could be partially explained by chronic RAGE signaling.
RAGE mediates inflammation that contributes to lung damage, in cigarette smoke-induced lung pathology.
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).
advanced glycosylation end product-specific receptor
, RAGE isoform NtRAGE-delta
, RAGE isoform sRAGE-delta
, advanced glycation end product receptor
, advanced glycosylation end product-specific receptor variant 1
, 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 6
, advanced glycosylation end product-specific receptor variant 7
, advanced glycosylation end product-specific receptor variant 8
, receptor for advanced glycosylation end products
, advanced glycation end-products receptor
, advanced glycosylation end product-specific receptor variant 2