No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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
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 ... in Genomics 1995
Show all 5 Pubmed References
Human AGER Protein expressed in HEK-293 Cells - ABIN621037
Amir, Waite, Tobler, Catalfamo, Koutouzis, Katz, Wallet: The role of hyperglycemia in mechanisms of exacerbated inflammatory responses within the oral cavity. in Cellular immunology 2011
these results indicated that miR-5591-5p targeting AGEs/AGER/JNK signaling axis possibly regulates the effect of ADSCs in repairing diabetic wound.
melanocytes expressing small hairpin RNA selective for the HMGB1 receptor, receptor for advanced glycosylation end product (RAGE), exhibited decreased expression of both HMGB1 and MX1 after UVB exposure
These results demonstrate that high glucose induces C3 up-regulation via RAGE- p38MAPK-NF-kappaB signalling in vivo and in vitro, which might be associated with synaptic protein loss.
The authors found an inverse association between prediagnostic sRAGE blood concentrations and risk of incident pancreatic cancer in postmenopausal women.
Vitamin D regulates AGE/RAGE signaling and its downstream effects. (Review)
The RAGE receptor is a multiligand pattern recognition receptor that is mainly expressed by type I alveolar epithelial cells.
Glycemia associates positively with plasma N-carboxymethyllysine (CML) and reciprocally with endogenous secretory receptor for advanced glycation end products (esRAGE) in older men. Circulating esRAGE modulates bone turnover in older men, whereas CML predicts incidence of hip fracture.
RAGE induces hepatocellular carcinoma proliferation and sorafenib resistance by modulating autophagy.
Diaph1 has a role in affecting RAGE clusters and diffusion
Smokers have lower lung AGER expression, but the portion of AGER, that leads to the production of anti-inflammatory esRAGE protein is increased.
RAGE has a role in binding preamyloid IAPP intermediates and mediates pancreatic beta cell proteotoxicity
contributory role of the RAGE gene, especially its two functional variants -429T > C and 82Gly > Ser, in susceptibility to T2DM in primary hypertensive patients
High expression of RAGE is associated with development and progression of prostate cancer.
sRAGE seems to be useful in the identification of frequent exacerbator phenotype in COPD patients.
High RAGE expression is associated with colorectal cancer stemness and development.
Study found that RAGE G82S gene polymorphism confers susceptibility to generalized chronic periodontitis in type II diabetic subjects of South Indian Tamilian ethnicity.
sRAGE could play a potential role in the control of inflammatory response in HTLV-1 carriers through the inhibition of HMGB1 signaling and potentially could be used as an indicator for evaluation of HTLV-1-associated myelopathy/tropical spastic paraparesis developing in HTLV-1-infected individuals.
In a population of mild hypertensives, low circulating sRAGE may be a very early marker of initial target organ damage, suggesting the possible participation of oxidative stress in initial cardiac changes in human hypertension.
RAGE sustains muscle inflammation and necrosis in Duchenne muscular dystrophy (DMD) muscles and that reducing RAGE activity might represent a potential therapeutic tool to counteract muscle inflammation and rescue muscle morphology in DMD conditions.
the G-A-T-G haplotype containing minor allele at position -374 A and major allele at position -429T, 1704G, and G82S G could be regarded as a marker for non-alcoholic steatohepatitis.
Transactivation of RAGE mediates angiotensin-induced inflammation and atherogenesis.
We hypothesise that AGEs play a key role in NASH development by activating their proinflammatory receptor, RAGE. RAGE-deficient mice and wildtype littermates, both on Ldlr(-/-) background, were fed a Western type diet (WTD) for 3 or 12 weeks. Flow cytometry, histology, gene expression and AGE measurements were performed to evaluate the effects of RAGE deficiency
Given that the receptor of advanced glycation end-products (RAGE) is a pivotal receptor that mediates amyloid-Abeta toxicity, RAGE siRNA was utilized to identify the involvement of RAGE in amyloid Abeta1-42 oligo induced autophagy in brain capillary endothelial cells.
Radiation could activate MAPK signaling pathway through promoting the expression of HMGB1 and RAGE.
RAGE deficiency up-regulates phagocytic capacity of phagocytes, resulting in lower bacterial burden in local skin and milder skin lesions in mice with staphylococcal skin infection.
Taken together, data demonstrated that MG induced angiogenic impairment in endothelial progenitor cells via alterations in the AGE/RAGE-VEGFR-2 pathway which may be utilized in the development of potential therapeutic and preventive targets for diabetic vascular complications.
The findings of the present study indicated that soluble RAGE protected the heart from ischemia/reperfusion injuries, which might be mediated by promoting infiltration and the differentiation of macrophages into M1, which would then synthesize and secrete IFNgamma through activating the NFkappaappa B signaling pathway.
Our data suggest a novel mechanism for sRAGE in preventing myocardial ischemia/reperfusion (MI/R)-induced apoptosis in heart: sRAGE inhibits MI/R-induced apoptosis in cardiomyocytes by degrading p53 by beta5i subunit that is increased via upregulation of IFN-gamma.
this study shows that the RAGE signaling pathway is involved in intestinal inflammation and represents a promising therapeutic target for Inflammatory Bowel Diseases
receptor for advanced glycation end-products does not have an effect on bone mineral density and synovitis in mice with intra-articular fractures
AGEs and RAGE interaction increases podocyte heparanase expression by activating NF-kappaB signal pathway.
Hepatocyte and Kupffer cell-derived HMGB1 participates in the pathogenesis of liver fibrosis by signaling through RAGE in hepatic stellate cells to activate the pMEK1/2, pERK1/2 and pcJun pathway and increase Collagen type I deposition.
data, suggests that the dimeric state of RAGE controls its function and ligand mediated signaling which may play important role in RAGE mediated various diseases.
These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE(-/-) mice via inhibition of endoplasmic reticulum stress.
microglial RAGE activation in presence of amyloid beta-enriched environment contributes to the entorhinal cortex vulnerability.
Established a murine model of myocardial ischemia-reperfusion injury; investigated and found remote ischemic postconditioning protects against IR injury thru RAGE-HMGB1 Pathway.
In this study, we found that the wnt co-receptor Lrp6 was a potent positive regulator of beta-catenin signaling in TDI-induced asthma models, both in vivo and in vitro. Additionally, for the first time, we demonstrated that RAGE could mediate phosphorylation of Lrp6, suggesting a functional cross talk between RAGE and the canonical wnt/beta-catenin signaling pathway involved in mediating beta-catenin activation.
Chronic unpredictable stress (CUS) promotes significant morphological changes and causes robust upregulation of HMGB1 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 by not only TLR4 but also RAGE
Our results suggested that the increased RAGE expression in inflammatory circumstances and interaction with AGEs are risk factors in decreasing of aggrecan 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