Circulating high-molecular-weight RAGE ligands activate pathways implicated in the development of diabetic nephropathy.
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Merlin C. Thomas | Merlin C Thomas | R. MacIsaac | G. Jerums | M. Cooper | K. Sourris | J. Forbes | L. Burrell | M. Coughlan | D. Webster | D. Steer | Sheila K. Patel | P. Srivastava | S. Penfold | S. Patel | M. Thomas | M. Cooper
[1] J. Golledge,et al. Serum carboxymethyllysine concentrations are reduced in diabetic men with abdominal aortic aneurysms: Health In Men Study. , 2009, Journal of vascular surgery.
[2] S. Devaraj,et al. Increased levels of ligands of Toll-like receptors 2 and 4 in type 1 diabetes , 2009, Diabetologia.
[3] M. Cooper,et al. RAGE-induced cytosolic ROS promote mitochondrial superoxide generation in diabetes. , 2009, Journal of the American Society of Nephrology : JASN.
[4] L. Audoly,et al. Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE , 2007, Nature Immunology.
[5] P. Nawroth,et al. Soluble RAGE but not endogenous secretory RAGE is associated with albuminuria in patients with type 2 diabetes , 2007, Cardiovascular diabetology.
[6] I. Lednev,et al. Hexameric Calgranulin C (S100A12) Binds to the Receptor for Advanced Glycated End Products (RAGE) Using Symmetric Hydrophobic Target-binding Patches* , 2006, Journal of Biological Chemistry.
[7] C. Heizmann,et al. Pathologies involving the S100 proteins and RAGE. , 2007, Sub-cellular biochemistry.
[8] L. Leng,et al. Association between serum levels of soluble receptor for advanced glycation end products and circulating advanced glycation end products in type 2 diabetes , 2006, Diabetologia.
[9] E. Abraham,et al. High mobility group box 1 protein interacts with multiple Toll-like receptors. , 2006, American journal of physiology. Cell physiology.
[10] D. Stern,et al. Understanding RAGE, the receptor for advanced glycation end products , 2005, Journal of Molecular Medicine.
[11] Merlin C. Thomas,et al. Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy. , 2005, Journal of the American Society of Nephrology : JASN.
[12] G. Jerums,et al. The breakdown of pre‐existing advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[13] Ann Marie Schmidt,et al. RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain , 2003, Nature Medicine.
[14] V. D’Agati,et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. , 2003, The American journal of pathology.
[15] Merlin C. Thomas,et al. Reduction of the accumulation of advanced glycation end products by ACE inhibition in experimental diabetic nephropathy. , 2002, Diabetes.
[16] J. Nagy,et al. N(epsilon)-(carboxymethyl)lysine levels in patients with type 2 diabetes: role of renal function. , 2001, American journal of kidney diseases : the official journal of the National Kidney Foundation.
[17] S. Takasawa,et al. Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice. , 2001, The Journal of clinical investigation.
[18] G. Jerums,et al. Renoprotective effects of a novel inhibitor of advanced glycation , 2001, Diabetologia.
[19] A. Dawnay,et al. Mass spectrometric monitoring of albumin in uremia. , 2000, Kidney international.
[20] T. Miyata,et al. Mechanism of the inhibitory effect of OPB-9195 [(+/-)-2-isopropylidenehydrazono-4-oxo-thiazolidin-5-yla cetanilide] on advanced glycation end product and advanced lipoxidation end product formation. , 2000, Journal of the American Society of Nephrology : JASN.
[21] M. Neurath,et al. RAGE Mediates a Novel Proinflammatory Axis A Central Cell Surface Receptor for S100/Calgranulin Polypeptides , 1999, Cell.
[22] S. Genuth,et al. Skin collagen glycation, glycoxidation, and crosslinking are lower in subjects with long-term intensive versus conventional therapy of type 1 diabetes: relevance of glycated collagen products versus HbA1c as markers of diabetic complications. DCCT Skin Collagen Ancillary Study Group. Diabetes Contro , 1999, Diabetes.
[23] J. Baynes,et al. Role of oxidative stress in diabetic complications: a new perspective on an old paradigm. , 1999, Diabetes.
[24] E. Schleicher,et al. Increased accumulation of the glycoxidation product N(epsilon)-(carboxymethyl)lysine in human tissues in diabetes and aging. , 1997, The Journal of clinical investigation.
[25] J. Chen,et al. The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin , 1995, The Journal of Biological Chemistry.
[26] F N Ziyadeh,et al. Prevention of diabetic nephropathy in db/db mice with glycated albumin antagonists. A novel treatment strategy. , 1995, The Journal of clinical investigation.
[27] A. McElduff,et al. Diabetes Control and Complications Trial , 1993 .
[28] G. Jerums,et al. Retardation by Aminoguanidine of Development of Albuminuria, Mesangial Expansion, and Tissue Fluorescence in Streptozocin-Induced Diabetic Rat , 1991, Diabetes.
[29] J. Baynes,et al. Nonenzymatic Glucosylation of Serum Proteins in Diabetes Mellitus , 1979, Diabetes.
[30] L. Maillard,et al. Action des acides amines sur les sucres : formation des melanoidines par voie methodique , 1912 .