The biology of the receptor for advanced glycation end products and its ligands.

[1]  C. Soto,et al.  Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis , 2000, Nature Medicine.

[2]  T. Kislinger,et al.  Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases , 2000, Nature.

[3]  T. Kislinger,et al.  N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression* , 1999, The Journal of Biological Chemistry.

[4]  K. Tracey,et al.  HMG-1 as a late mediator of endotoxin lethality in mice. , 1999, Science.

[5]  H. Huttunen,et al.  Receptor for Advanced Glycation End Products (RAGE)-mediated Neurite Outgrowth and Activation of NF-κB Require the Cytoplasmic Domain of the Receptor but Different Downstream Signaling Pathways* , 1999, The Journal of Biological Chemistry.

[6]  M. Neurath,et al.  RAGE Mediates a Novel Proinflammatory Axis A Central Cell Surface Receptor for S100/Calgranulin Polypeptides , 1999, Cell.

[7]  A. Schmidt,et al.  Activation of receptor for advanced glycation end products: a mechanism for chronic vascular dysfunction in diabetic vasculopathy and atherosclerosis. , 1999, Circulation research.

[8]  J. Pober Immunobiology of human vascular endothelium , 1999, Immunologic research.

[9]  B. Vanhaesebroeck,et al.  A Redox-triggered Ras-Effector Interaction , 1998, The Journal of Biological Chemistry.

[10]  J. Baynes,et al.  Chemical modification of proteins by methylglyoxal. , 1998, Cellular and molecular biology.

[11]  A. Schmidt,et al.  Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts , 1998, Nature Medicine.

[12]  B. Zlokovic,et al.  Human blood-brain barrier receptors for Alzheimer's amyloid-beta 1- 40. Asymmetrical binding, endocytosis, and transcytosis at the apical side of brain microvascular endothelial cell monolayer. , 1998, The Journal of clinical investigation.

[13]  D. Rader,et al.  Reduction in amyloid A amyloid formation in apolipoprotein-E-deficient mice. , 1998, The American journal of pathology.

[14]  A. Schmidt,et al.  Activation of the Receptor for Advanced Glycation End Products Triggers a p21 ras -dependent Mitogen-activated Protein Kinase Pathway Regulated by Oxidant Stress* , 1997, The Journal of Biological Chemistry.

[15]  W. Tourtellotte,et al.  Amyloid-beta peptide-receptor for advanced glycation endproduct interaction elicits neuronal expression of macrophage-colony stimulating factor: a proinflammatory pathway in Alzheimer disease. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[16]  T. Miyata,et al.  The receptor for advanced glycation end products (RAGE) is a central mediator of the interaction of AGE-beta2microglobulin with human mononuclear phagocytes via an oxidant-sensitive pathway. Implications for the pathogenesis of dialysis-related amyloidosis. , 1996, The Journal of clinical investigation.

[17]  X. Chen,et al.  RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease , 1996, Nature.

[18]  G. King,et al.  The cellular and molecular mechanisms of diabetic complications. , 1996, Endocrinology and metabolism clinics of North America.

[19]  P. Guillausseau,et al.  Rapid Publication , 1971, Nature.

[20]  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.

[21]  A. Schmidt,et al.  The dark side of glucose , 1995, Nature Medicine.

[22]  K. Schmid,et al.  The myeloic related protein MRP8/14 (27E10 antigen)— usefulness as a potential marker for disease activity in ulcerative colitis and putative biological function , 1995, European journal of clinical investigation.

[23]  A. Schmidt,et al.  Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes. , 1995, The Journal of clinical investigation.

[24]  J. Baynes,et al.  N epsilon-(carboxymethyl)lysine is a dominant advanced glycation end product (AGE) antigen in tissue proteins. , 1995, Biochemistry.

[25]  M. Mattson Free radicals and disruption of neuronal ion homeostasis in AD: A role for amyloid β-peptide? , 1995, Neurobiology of Aging.

[26]  M. Mattson,et al.  Different amyloidogenic peptides share a similar mechanism of neurotoxicity involving reactive oxygen species and calcium , 1995, Brain Research.

[27]  T. Willnow,et al.  Lipoprotein and receptor interactions in vivo , 1995, Current opinion in lipidology.

[28]  P. Fraser,et al.  Arresting amyloidosis in vivo using small-molecule anionic sulphonates or sulphates: implications for Alzheimer's disease , 1995, Nature Medicine.

[29]  D. Selkoe,et al.  Alzheimer's Disease: A Central Role for Amyloid , 1994, Journal of neuropathology and experimental neurology.

[30]  A. Schmidt,et al.  Advanced glycation end products (AGEs) on the surface of diabetic erythrocytes bind to the vessel wall via a specific receptor inducing oxidant stress in the vasculature: a link between surface-associated AGEs and diabetic complications. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[31]  M. Mattson,et al.  A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[32]  Y. Zou,et al.  Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. , 1993, The American journal of pathology.

[33]  H. Rauvala,et al.  Amphoterin, the 30-kDa protein in a family of HMG1-type polypeptides. Enhanced expression in transformed cells, leading edge localization, and interactions with plasminogen activation. , 1993, The Journal of biological chemistry.

[34]  N. Taniguchi,et al.  beta 2-Microglobulin modified with advanced glycation end products is a major component of hemodialysis-associated amyloidosis. , 1993, The Journal of clinical investigation.

[35]  T. Lyons,et al.  Accumulation of Maillard reaction products in skin collagen in diabetes and aging. , 1993, The Journal of clinical investigation.

[36]  W. Hurley,et al.  Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface. , 1992, The Journal of biological chemistry.

[37]  K. O. Elliston,et al.  Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. , 1992, The Journal of biological chemistry.

[38]  V. Monnier,et al.  Structure elucidation of a senescence cross-link from human extracellular matrix. Implication of pentoses in the aging process. , 1989, The Journal of biological chemistry.

[39]  H. Rauvala,et al.  Isolation and some characteristics of an adhesive factor of brain that enhances neurite outgrowth in central neurons. , 1987, The Journal of biological chemistry.

[40]  S. V. van Duinen,et al.  Hereditary cerebral hemorrhage with amyloidosis in patients of Dutch origin is related to Alzheimer disease. , 1987, Proceedings of the National Academy of Sciences of the United States of America.

[41]  C. Kilo,et al.  Increased Vascular Permeability in Spontaneously Diabetic BB/W Rats and in Rats With Mild Versus Severe Streptozocin-Induced Diabetes: Prevention by Aldose Reductase Inhibitors and Castration , 1987, Diabetes.