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Rat (Rattus) AGER ELISA Kit für 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 für 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 für 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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results imply that the interaction of matrix AGEs with RAGE plays a role in the TGFbeta2-mediated EMT (zeige 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 (zeige HMGB1 ELISA Kits) triggered EPC (zeige TCF21 ELISA Kits) apoptosis in a manner of RAGE-mediated activation of the PERK (zeige EIF2AK3 ELISA Kits)/eIF2alpha (zeige 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 (zeige 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 (zeige HMGB1 ELISA Kits) attenuates TGF-beta (zeige 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 (zeige AOC3 ELISA Kits) (sVAP-1 (zeige SNAP47 ELISA Kits)) and cardiometabolic risk markers in apparently healthy adolescents: a cross-sectional study.
RAGE location was present at the cell membrane of alveolar epithelial cellss in control lungs, while it was almost missing in pulmonary fibrotic tissue.
A capture method based on the VC1 domain reveals new binding properties of the AGER.
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.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan (zeige ACAN ELISA Kits) content in nucleus pulposus.
RAGE is phosphorylated by the ATM (zeige 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 (zeige 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 (zeige 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 (zeige BEST1 ELISA Kits) compared to WT mice, which coincided with lower IL-17A (zeige IL17A ELISA Kits) in RAGE-/- mice. In sepsis, RAGE deficiency impairs bacterial kidney clearance.
SAA (zeige 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.
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