A link between diabetes and atherosclerosis: Glucose regulates expression of CD36 at the level of translation

[1]  Joseph,et al.  Regulated Expression of CD 36 During Monocyte-to-Macrophage Differentiation : Potential Role of CD 36 in Foam Cell Formation , 2002 .

[2]  Hiroyuki Arai,et al.  CD36, a Member of the Class B Scavenger Receptor Family, as a Receptor for Advanced Glycation End Products* , 2001, The Journal of Biological Chemistry.

[3]  D. Morris,et al.  Upstream Open Reading Frames as Regulators of mRNA Translation , 2000, Molecular and Cellular Biology.

[4]  Michael Ruogu Zhang,et al.  CART classification of human 5' UTR sequences. , 2000, Genome research.

[5]  S. Hazen,et al.  Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice. , 2000, The Journal of clinical investigation.

[6]  S. Hazen,et al.  Macrophage scavenger receptor CD36 is the major receptor for LDL modified by monocyte-generated reactive nitrogen species. , 2000, The Journal of clinical investigation.

[7]  A. Sachs,et al.  Glucose depletion rapidly inhibits translation initiation in yeast. , 2000, Molecular biology of the cell.

[8]  S. Hazen,et al.  Erratum: Macrophage scavenger receptor CD36 is the major receptor for LDL modified by monocyte-generated reactive nitrogen species (Journal of Clinical Investigation (2000) 105 (1095-1108)) , 2000 .

[9]  S. O’Rahilly,et al.  Dominant negative mutations in human PPARγ associated with severe insulin resistance, diabetes mellitus and hypertension , 1999, Nature.

[10]  K. Chien,et al.  PPARγ Is Required for Placental, Cardiac, and Adipose Tissue Development , 1999 .

[11]  R. Silverstein,et al.  A Null Mutation in Murine CD36 Reveals an Important Role in Fatty Acid and Lipoprotein Metabolism* , 1999, The Journal of Biological Chemistry.

[12]  J. Sabina,et al.  Expanded sequence dependence of thermodynamic parameters improves prediction of RNA secondary structure. , 1999, Journal of molecular biology.

[13]  P. Pilch,et al.  Reconstitution of Insulin-sensitive Glucose Transport in Fibroblasts Requires Expression of Both PPARγ and C/EBPα* , 1999, The Journal of Biological Chemistry.

[14]  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.

[15]  Jan Barciszewski,et al.  RNA Biochemistry and Biotechnology , 1999 .

[16]  James Scott,et al.  Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats , 1999, Nature Genetics.

[17]  Michael Zuker,et al.  Algorithms and Thermodynamics for RNA Secondary Structure Prediction: A Practical Guide , 1999 .

[18]  I. Charo,et al.  Decreased lesion formation in CCR2−/− mice reveals a role for chemokines in the initiation of atherosclerosis , 1998, Nature.

[19]  Olivier J. Blanchard The Basic Mechanisms , 1998 .

[20]  R. Evans,et al.  PPARγ Promotes Monocyte/Macrophage Differentiation and Uptake of Oxidized LDL , 1998, Cell.

[21]  R. Evans,et al.  Oxidized LDL Regulates Macrophage Gene Expression through Ligand Activation of PPARγ , 1998, Cell.

[22]  B. Spiegelman PPARγ in Monocytes: Less Pain, Any Gain? , 1998, Cell.

[23]  U. Sauer,et al.  High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. , 1998, The Journal of clinical investigation.

[24]  H. Vlassara Recent Progress in Advanced Glycation End Products and Diabetic Complications , 1997, Diabetes.

[25]  C. Semenkovich,et al.  The Mystery of Diabetes and Atherosclerosis: Time for a New Plot , 1997, Diabetes.

[26]  S Y Le,et al.  A common RNA structural motif involved in the internal initiation of translation of cellular mRNAs. , 1997, Nucleic acids research.

[27]  M. Matsumoto,et al.  Rage: A Novel Cellular Receptor for Advanced Glycation End Products , 1996, Diabetes.

[28]  L. Yesner,et al.  Regulated expression of CD36 during monocyte-to-macrophage differentiation: potential role of CD36 in foam cell formation. , 1996, Blood.

[29]  K. Docherty,et al.  Glucose Stimulates the Activity of the Guanine Nucleotide-exchange Factor eIF-2B in Isolated Rat Islets of Langerhans (*) , 1996, The Journal of Biological Chemistry.

[30]  Y. Oka,et al.  Glucose-Regulated Translational Control of Proinsulin Biosynthesis With That of the Proinsulin Endopeptidases PG2 and PC3 in the Insulin-Producing MIN6 Cell Line , 1996, Diabetes.

[31]  M. Laakso,et al.  Epidemiological evidence for the association of hyperglycaemia and atherosclerotic vascular disease in non-insulin-dependent diabetes mellitus. , 1996, Annals of medicine.

[32]  T. McCaffrey,et al.  Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1. , 1995, The Journal of clinical investigation.

[33]  C. Beaumont,et al.  Mutation in the iron responsive element of the L ferritin mRNA in a family with dominant hyperferritinaemia and cataract , 1995, Nature Genetics.

[34]  S. Yamashita,et al.  Reduced uptake of oxidized low density lipoproteins in monocyte-derived macrophages from CD36-deficient subjects. , 1995, The Journal of clinical investigation.

[35]  D. Greenwalt,et al.  Heart CD36 expression is increased in murine models of diabetes and in mice fed a high fat diet. , 1995, The Journal of clinical investigation.

[36]  C. Semenkovich,et al.  Human fatty acid synthase mRNA: tissue distribution, genetic mapping, and kinetics of decay after glucose deprivation. , 1995, Journal of lipid research.

[37]  P. Edwards,et al.  Atherosclerosis: basic mechanisms. Oxidation, inflammation, and genetics. , 1995, Circulation.

[38]  J. V. Hunt,et al.  Glucose oxidation and low-density lipoprotein-induced macrophage ceroid accumulation: possible implications for diabetic atherosclerosis. , 1994, The Biochemical journal.

[39]  L. Stanton,et al.  CD36 is a receptor for oxidized low density lipoprotein. , 1993, The Journal of biological chemistry.

[40]  D. Steinberg,et al.  Role of oxidized low density lipoprotein in atherogenesis. , 1991, The Journal of clinical investigation.

[41]  N. Sonenberg,et al.  mRNAs containing extensive secondary structure in their 5′ non‐coding region translate efficiently in cells overexpressing initiation factor eIF‐4E. , 1992, The EMBO journal.

[42]  M. Kozak,et al.  Regulation of translation in eukaryotic systems. , 1992, Annual review of cell biology.

[43]  P. Guest,et al.  Insulin secretory granule biogenesis. Co-ordinate regulation of the biosynthesis of the majority of constituent proteins. , 1991, The Biochemical journal.

[44]  B. M. Jackson,et al.  Suppression of ribosomal reinitiation at upstream open reading frames in amino acid-starved cells forms the basis for GCN4 translational control , 1991, Molecular and cellular biology.

[45]  D. Steinberg,et al.  Role of oxidised low density lipoprotein in atherogenesis. , 1993, British heart journal.

[46]  C. Ucla,et al.  Differential expression and regulation of the glucokinase gene in liver and islets of Langerhans. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[47]  S. Ho,et al.  Site-directed mutagenesis by overlap extension using the polymerase chain reaction. , 1989, Gene.

[48]  D. Morris,et al.  Isolation of a cDNA clone encoding S-adenosylmethionine decarboxylase. Expression of the gene in mitogen-activated lymphocytes. , 1986, The Journal of biological chemistry.

[49]  B. Jacotot [Atherosclerosis: basic mechanisms]. , 1983, La semaine des hopitaux : organe fonde par l'Association d'enseignement medical des hopitaux de Paris.