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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Advanced glycosylation end product-specific receptor

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). [provided by RefSeq, May 2011] (from NCBI)
Top mentioned proteins: AGE, V1a, HMGB1, CAN, HAD
Papers using RAGE antibodies
Non-enzymatic glycation of bone collagen modifies osteoclastic activity and differention
Wolf Gunter et al., In Arthritis Research & Therapy, 2006
... anti-imidazolone (kindly provided by Toshumitsu Niwa, Japan); anti-p27Kip1 (Cell Signaling Technology, Inc., Danvers, MA, USA); anti-RAGE (SP6366P, Acris Antibodies, Hiddenhausen, Germany); anti-NFκB ...
Papers on RAGE
High dietary advanced glycation end products are associated with poorer spatial learning and accelerated Aβ deposition in an Alzheimer mouse model.
Schnaider-Beeri et al., Ramat Gan, Israel. In Aging Cell, Feb 2016
We here examined the effect of a diet high in AGEs in the context of an irradiated diet on memory, insoluble Aβ42 , AGEs levels in hippocampus, on expression of the receptor for AGEs (RAGE), and on oxidative stress in the vasculature.
Perforin Promotes Amyloid Beta Internalisation in Neurons.
Behbahani et al., Huddinge, Sweden. In Mol Neurobiol, Feb 2016
We here investigated how extracellular Aβ peptides are internalised and focused on three different pathways: (i) via endocytic mechanisms, (ii) via the receptor for advanced glycation end products (RAGE) and (iii) via the pore-forming protein perforin.
Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression.
Yen et al., T'ai-chung-shih, Taiwan. In Mol Nutr Food Res, Feb 2016
AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species (ROS) that are an important regulator of the hallmarks of cancer.
Diabetes-associated cardiac fibrosis: Cellular effectors, molecular mechanisms and therapeutic opportunities.
Frangogiannis et al., United States. In J Mol Cell Cardiol, Jan 2016
Hyperglycemia directly activates a fibrogenic program, leading to accumulation of advanced glycation end-products (AGEs) that crosslink extracellular matrix proteins, and transduce fibrogenic signals through reactive oxygen species generation, or through activation of Receptor for AGEs (RAGE)-mediated pathways.
RAGE axis in neuroinflammation, neurodegeneration and its emerging role in the pathogenesis of amyotrophic lateral sclerosis.
Rai et al., Bhubaneshwar, India. In Neurosci Biobehav Rev, Jan 2016
UNASSIGNED: RAGE, the receptor of advanced glycation end-products, is thought to be one of the potential contributors to the neurodegeneration.
Advanced glycation End-products (AGEs): an emerging concern for processed food industries.
Raina et al., Ludhiāna, India. In J Food Sci Technol, Dec 2015
The concept of AGEs receptor - RAGE is mentioned.
Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease.
Corsi Romanelli et al., Milano, Italy. In J Diabetes Res, Dec 2015
Increased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal.
Inflammatory and Fibrotic Responses of Cardiac Fibroblasts to Myocardial Damage Associated Molecular Patterns (DAMPs).
Turner, Leeds, United Kingdom. In J Mol Cell Cardiol, Dec 2015
CF express a range of innate immunity pattern recognition receptors (TLRs, NLRs, IL-1R1, RAGE) that are stimulated by a host of different DAMPs that are evident in the injured or remodelling myocardium.
Toll-like receptor 2 (TLR2) is a marker of angiogenesis in the necrotic area of human medulloblastoma.
Szukiewicz et al., Warsaw, Poland. In Folia Neuropathol, 2014
In this context, the aim of our present study was to examine in medulloblastoma the distribution of Toll-like receptor 2 (TLR2) and receptor for advanced glycosylation end-product (RAGE), and mast cells associated with the tumor neovascularization process.
Association between RAGE gene polymorphisms and ulcerative colitis susceptibility: a case-control study in a Chinese Han population.
Zhong et al., Shanghai, China. In Genet Mol Res, 2014
The aim of this study was to investigate the association of three polymorphisms in the receptor for advanced glycation end-products (RAGE) gene with UC risk in a Chinese population.
Dendritic cells decide CD8(+) T cell fate.
Mowat, Glasgow, United Kingdom. In Immunity, 2014
(2014) propose that CD103(+) DCs in mouse lung selectively generate effector CD8(+) T cells by binding the alarmin HMGB1 via CD24 and presenting it to RAGE(+) T cells.
Distinct dendritic cell subsets dictate the fate decision between effector and memory CD8(+) T cell differentiation by a CD24-dependent mechanism.
Braciale et al., Charlottesville, United States. In Immunity, 2014
Mechanistically, CD24 was shown to regulate CD8(+) T cell activation through HMGB1-mediated engagement of T cell RAGE.
Tumor necrosis factor-α blocks differentiation and enhances suppressive activity of immature myeloid cells during chronic inflammation.
Baniyash et al., Canada. In Immunity, 2013
Here we showed that TNF-α exhibited a dual function during chronic inflammation: arresting differentiation of immature myeloid-derived suppressor cells (MDSCs) primarily via the S100A8 and S100A9 inflammatory proteins and their corresponding receptor (RAGE) and augmenting MDSC suppressive activity.
Receptor for advanced glycation end products is protective during murine tuberculosis.
van der Poll et al., Amsterdam, Netherlands. In Mol Immunol, 2012
these data suggest that RAGE plays a beneficial role in the host response to pulmonary tuberculosis.
Receptor for advanced glycation end products inhibits proliferation in osteoblast through suppression of Wnt, PI3K and ERK signaling.
Li et al., Shanghai, China. In Biochem Biophys Res Commun, 2012
these results suggest that RAGE inhibits osteoblast proliferation via suppression of Wnt, PI3K and ERK signaling, which provides novel mechanisms by which RAGE regulates osteoblast growth.
Hypertension induces brain β-amyloid accumulation, cognitive impairment, and memory deterioration through activation of receptor for advanced glycation end products in brain vasculature.
Lembo et al., Roma, Italy. In Hypertension, 2012
Data show that a chronic vascular insult can activate brain vascular receptor for advanced glycation end products (RAGE), favoring parenchymal amyloid beta protein deposition and the onset of cognitive deterioration.
Clinical chorioamnionitis is characterized by changes in the expression of the alarmin HMGB1 and one of its receptors, sRAGE.
Hassan et al., Detroit, United States. In J Matern Fetal Neonatal Med, 2012
An alarmin, HMGB1, and one of its receptors, sRAGE, are engaged in the process of clinical chorioamnionitis at term.
Glycer-AGEs-RAGE signaling enhances the angiogenic potential of hepatocellular carcinoma by upregulating VEGF expression.
Takeuchi et al., Hiroshima, Japan. In World J Gastroenterol, 2012
results suggest that Glycer-AGEs-RAGE signaling enhances the angiogenic potential of hepatocellular carcinoma cells by upregulating VEGF expression.
HMGB1 and RAGE in inflammation and cancer.
Coyle et al., Gaithersburg, United States. In Annu Rev Immunol, 2009
HMGB1 can associate with other molecules, including TLR ligands and cytokines, and activates cells through the differential engagement of multiple surface receptors including TLR2, TLR4, and RAGE.
Immune and inflammatory mechanisms of atherosclerosis (*).
Ley et al., Norfolk, United States. In Annu Rev Immunol, 2008
Incapacitating ROS-generating NADPH oxidase or the receptor for AGE (RAGE) has beneficial effects.
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