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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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Thus, hypoxia not only increases RAGE expression in THP (zeige UMOD Proteine)-1cells by promoting nuclear translocation of NF-kappa B (zeige NFKB1 Proteine) and HIF1alpha (zeige HIF1A Proteine), 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 (zeige IFNB1 Proteine) 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 (zeige PSMB9 Proteine) and beta5i expression mediated by STAT3 (zeige STAT3 Proteine) 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 (zeige LEPR Proteine) mouse livers, together with impaired proteolytic, antioxidant and mitochondrial respiratory activities. In parallel, acute exposure of HepG2 cells to glycated albumin (zeige ALB Proteine) 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 (zeige ITK Proteine) 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 Proteine) triggered EPC (zeige TCF21 Proteine) apoptosis in a manner of RAGE-mediated activation of the PERK (zeige EIF2AK3 Proteine)/eIF2alpha (zeige EIF2A Proteine) 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.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan (zeige ACAN Proteine) content in nucleus pulposus.
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 (zeige HMGB1 Proteine)) 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 (zeige ATM Proteine) 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 Proteine) 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.
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