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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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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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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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These data indicate that RAGE plays a central role in maintaining inflammatory signaling in PDAC that benefits tumor growth.
In conclusion, RAGE is clearly involved in corneal re-epithelialization most probably mediated by signalling via S100 proteins.
RAGE binds to a diverse repertoire of ligands. DIAPH1 (show DIAPH1 ELISA Kits) interaction with the RAGE cytoplasmic domain. [review]
High RAGE expression is associated with mesothelioma.
There was no significant difference in plasma levels of sRAGE or HMGB1 (show HMGB1 ELISA Kits) between pAPS (show PAPSS1 ELISA Kits) patients and HCs (show HLCS ELISA Kits). Plasma levels of sRAGE/HMGB1 (show HMGB1 ELISA Kits) could not be utilized to differentiate between APA (show ENPEP ELISA Kits)+SLE and APS (show SH2B2 ELISA Kits)+SLE patients
Ligand-induced association of RAGE homodimers on the cell surface increases the molecular dimension of the receptor, recruiting DIAPH1 (show DIAPH1 ELISA Kits) and activating signaling pathways.
AGER polymorphisms showed no statistically significant difference between patients with primary open-angle glaucoma and healthy controls.
Our findings demonstrate how RAGE-PR3 interactions between human prostate cancer cells and the bone marrow microenvironment mediate bone metastasis during prostate cancer progression
The severity of acute respiratory distress syndrome in preterm infants seemed to be associated with the plasma level of sRAGE and AQP5 (show AQP5 ELISA Kits): the more severe the disease, the higher the plasma level of sRAGE and AQP5 (show AQP5 ELISA Kits)
Advanced glycation end products are capable of inducing VEGF (show VEGFA ELISA Kits) production and inflammatory responses via RAGE-NF-kappaB (show NFKB1 ELISA Kits) pathway activation in synoviocytes.
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.
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.
that selective RAGE regulation reflects a self-protective mechanism to maintain low levels of RAGE ligands
Data show that receptor for advanced glycation end products (RAGE) impairs collateral growth in a diabetic setting and also in a non-diabetic setting, indicting the importance of RAGE and alternate RAGE ligands in the setting of collateral vessel growth.
These findings demonstrate the role for RAGE-dependent IL-10 (show IL10 ELISA Kits) suppression as a key modulator of mortality from Gram-negative sepsis.
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