Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
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. dans Structure (London, England : 1993) 2011
Show all 5 Pubmed References
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 ... dans Genomics 1995
Show all 5 Pubmed References
a significant association between RAGE gene rs1800624 and rs1800625 polymorphisms and Age-related macular degeneration risk, is reported.
HMGB1 (Montrer HMGB1 Protéines) mediates fibroblast activity via RAGE-MAPK (Montrer MAPK1 Protéines) and NF-kappaB (Montrer NFKB1 Protéines) signaling in keloid scar formation.
Data revealed that hESC accumulates CML (Montrer BCR Protéines) and RAGE under oxidative stress conditions in different ways than somatic cells, being the accumulation of CML (Montrer BCR Protéines) statistically significant only in somatic cells and, conversely, the RAGE increase exclusively appreciated in hESC.
In women with Polycystic ovary syndrome(PCOS), the low ovarian levels of the anti-inflammatory sRAGE suggest that sRAGE could represent a biomarker and a potential therapeutic target for ovarian dysfunction in PCOS. Whether there is a direct causal relationship between sRAGE and vit (Montrer VIT Protéines) D in the ovaries remains to be determined
current research highlighted the Glo-I/AGE/RAGE system as an interesting therapeutic target in chronic liver diseases. These findings need further elucidation in preclinical and clinical studies.
Our findings suggested that polymorphisms in the RAGE gene are involved in genetic susceptibility to Alzheimer disease but did not modify the risk of lewy body disease.
Findings suggest soluble Receptor (Montrer IFNAR1 Protéines) for Advanced Glycation End products (sRAGE) protein from sRAGE-mesenchymal stem cells (MSC (Montrer MSC Protéines)) has better protection against neuronal cell death than sRAGE protein or single MSC (Montrer MSC Protéines) treatment by inhibiting the RAGE cell death cascade and RAGE-induce inflammation.
Protection against diabetic nephropathy in RAGE knockout mice is likely to be due in part to the decreased responsiveness to TGF beta (Montrer TGFB1 Protéines) stimulation and an antiapoptotic phenotype in mesangial cells.
the A allele of RAGE -374T/A polymorphism probably increase diabetic retinopathy risk (Meta-Analysis)
Advanced glycation end products decrease collagen I levels in fibroblasts from the vaginal wall of patients with pelvic organ prolapse via the RAGE, MAPK (Montrer MAPK1 Protéines) and NF-kappaB (Montrer NFKB1 Protéines) pathways.
Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 (Montrer HMGB1 Protéines) messenger RNA in enriched hippocampal microglia and robust and persistent upregulation of RAGE messenger RNA. CUS increased surface expression of RAGE protein on hippocampal microglia and anhedonic behavior. RAGE knockout mice were resilient to stress-induced anhedonia.
study found that diabetes predisposes to more severe infections because of additional inflammatory output through dual activation of MyD88 (Montrer MYD88 Protéines) by not only TLR4 (Montrer TLR4 Protéines) but also RAGE
RAGE controls myocardial dysfunction and oxidative stress in high-fat fed mice by sustaining mitochondrial dynamics and autophagy-lysosome pathway.
these data provide a previously uncharacterized in vivo mechanism contingent on oligodeoxy-nucleotide -administered dose, where TLR9 (Montrer TLR9 Protéines) governs the primary response and RAGE plays a distinct and cooperative function in providing a pivotal role in balancing the immune response.
data demonstrate that under the diabetic condition, DRG neurons are directly affected by elevated levels of glucose, independent of vascular or glial signals, and dependent on RAGE expression.
findings suggest that HMGB1 (Montrer HMGB1 Protéines) induces the transcytosis of albumin (Montrer ALB Protéines) via RAGE-dependent Src (Montrer SRC Protéines) phosphorylation and Cav-1 (Montrer CAV1 Protéines) phosphorylation. These studies revealed a new mechanism of HMGB1 (Montrer HMGB1 Protéines)-induced endothelial hyperpermeability.
data suggest that S100A8 (Montrer S100A8 Protéines)/A9 acts directly on BV-2 microglial cells via binding to TLR4 (Montrer TLR4 Protéines) and RAGE on the membrane and then stimulates the secretion of proinflammatory cytokines through ERK (Montrer EPHB2 Protéines) and JNK (Montrer MAPK8 Protéines)-mediated NF-kappaB (Montrer NFKB1 Protéines) activity in BV-2 microglial cells.
Activation of RAGE facilitates the development of hypoxia-induced pulmonary hypertension by increasing ECM (Montrer MMRN1 Protéines) 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 (Montrer HMGB1 Protéines)) which triggered airway smooth muscle remodelling in early-life.
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan (Montrer ACAN Protéines) content in nucleus pulposus.
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).
RAGE isoform NtRAGE-delta
, RAGE isoform sRAGE-delta
, advanced glycation end-products receptor
, receptor for advanced glycosylation end products
, advanced glycosylation end product-specific receptor variant 2
, 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 1
, advanced glycosylation end product-specific receptor variant 6
, advanced glycosylation end product-specific receptor variant 7
, advanced glycosylation end product-specific receptor variant 8
, advanced glycation end product receptor
, advanced glycosylation end product-specific receptor
, MAPK/MAK/MRK overlapping kinase
, renal tumor antigen