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Rat (Rattus) AGER ELISA Kit for Sandwich ELISA - ABIN625213
Greco, Tassorelli, Mangione, Levandis, Certo, Nappi, Bagetta, Blandini, Amantea: Neuroprotection by the PARP inhibitor PJ34 modulates cerebral and circulating RAGE levels in rats exposed to focal brain ischemia. in European journal of pharmacology 2014
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Human AGER ELISA Kit for Sandwich ELISA - ABIN625349
Bala, Gohil: Interaction of glycated protein and DFO mimicked hypoxia in cellular responses of HUVECs. in Molecular bioSystems 2012
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Mouse (Murine) AGER ELISA Kit for Sandwich ELISA - ABIN1672810
Neeper, Schmidt, Brett, Yan, Wang, Pan, Elliston, Stern, Shaw: Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. in The Journal of biological chemistry 1992
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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 ELISA Kits) and beta5i expression mediated by STAT3 (show STAT3 ELISA Kits) 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 ELISA Kits) mouse livers, together with impaired proteolytic, antioxidant and mitochondrial respiratory activities. In parallel, acute exposure of HepG2 cells to glycated albumin (show ALB ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) triggered EPC (show TCF21 ELISA Kits) apoptosis in a manner of RAGE-mediated activation of the PERK (show EIF2AK3 ELISA Kits)/eIF2alpha (show EIF2A ELISA Kits) pathway.
Activation of RAGE by AGEs causes up regulation of the transcription factor nuclear factor-kappaB and its target genes. of the RAGE engagement stimulates oxidative stress, evokes inflammatory and fibrotic reactions, which all contribute to the development and progression of devastating cardiovascular disorders.
The lowering of glycative stress via modulation of RAGE-AGE axis or glyoxalase 1 (show GLO1 ELISA Kits) activity is beneficial for tubular homeostasis and the subsequent prevention and treatment of kidney disease, suggesting the possibility of novel therapeutic approaches which target glycative stress.
HMGB1 (show HMGB1 ELISA Kits) attenuates TGF-beta (show TGFB1 ELISA Kits)-induced epithelial-mesenchymal transition of FaDu hypopharyngeal carcinoma cells through regulation of RAGE expression
Correlation among soluble receptors for advanced glycation end-products, soluble vascular adhesion protein-1/semicarbazide-sensitive amine oxidase (show AOC3 ELISA Kits) (sVAP-1 (show SNAP47 ELISA Kits)) and cardiometabolic risk markers in apparently healthy adolescents: a cross-sectional study.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan (show ACAN ELISA Kits) content in nucleus pulposus.
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 ELISA Kits) 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 ELISA Kits) 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.
Ager deletion enhances ischemic muscle inflammation, angiogenesis, and blood flow recovery in diabetic mice.
HMGB1 (show HMGB1 ELISA Kits) neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition
Our results indicate that lack of RAGE has no significant impact on septic arthritis. However, RAGE-/- mice had significantly higher BMD (show BEST1 ELISA Kits) compared to WT mice, which coincided with lower IL-17A (show IL17A ELISA Kits) in RAGE-/- mice. In sepsis, RAGE deficiency impairs bacterial kidney clearance.
SAA (show SAA1 ELISA Kits) is a potential new uremic toxin involved in uremia-related atherosclerosis through interaction with RAGE.
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