Human apolipoprotein A-I gene promoter mutation influences plasma low density lipoprotein cholesterol response to dietary fat saturation.

[1]  J. Davignon,et al.  G-->A substitution at position -75 of the apolipoprotein A-I gene promoter. Evidence against a direct effect on HDL cholesterol levels. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[2]  N. Miller,et al.  Pathophysiology of reverse cholesterol transport. Insights from inherited disorders of lipoprotein metabolism. , 1989, Arteriosclerosis.

[3]  D. Jacobs,et al.  Variability in Individual Serum Cholesterol Response to Change in Diet , 1983, Arteriosclerosis.

[4]  P. Talmud,et al.  Polymorphism in the promoter region of the apolipoprotein AI gene associated with differences in apolipoprotein AI levels: The European Atherosclerosis Research Study , 1994, Genetic epidemiology.

[5]  N. Tuteja,et al.  Transcription efficiency of human apolipoprotein A‐I promoter varies with naturally occurring A to G transition , 1992, FEBS letters.

[6]  C. Fielding,et al.  A protein cofactor of lecithin:cholesterol acyltransferase. , 1972, Biochemical and biophysical research communications.

[7]  R. Lauer,et al.  Childhood prevention of atherosclerosis and hypertension , 1980 .

[8]  C. Bouchard,et al.  Apolipoprotein E polymorphism alters the association between body fatness and plasma lipoproteins in women. , 1990, Journal of lipid research.

[9]  M. Denke.  Review of human studies evaluating individual dietary responsiveness in patients with hypercholesterolemia. , 1995, The American journal of clinical nutrition.

[10]  S. Humphries,et al.  Guanidine to adenine (G/A) substitution in the promoter region of the apolipoprotein AI gene is associated with elevated serum apolipoprotein AI levels in chinese non‐smokers , 1994, Genetic epidemiology.

[11]  A. Kessling,et al.  G to A substitution in the promoter region of the apolipoprotein AI gene is associated with elevated serum apolipoprotein AI and high density lipoprotein cholesterol concentrations. , 1990, Molecular biology & medicine.

[12]  E. Avvedimento,et al.  A polymorphism (G-->A transition) in the -78 position of the apolipoprotein A-I promoter increases transcription efficiency. , 1994, The Journal of biological chemistry.

[13]  G E Dallal,et al.  Dietary fat and serum lipids: an evaluation of the experimental data. , 1993, The American journal of clinical nutrition.

[14]  J. Breslow,et al.  Polymorphism in the human apolipoprotein A-I gene promoter region. Association of the minor allele with decreased production rate in vivo and promoter activity in vitro. , 1992, The Journal of clinical investigation.

[15]  H. Tenkanen.  Genotyping of apolipoprotein A-IV by digestion of amplified DNA with restriction endonuclease Fnu4HI: use of a tailored primer to abolish additional recognition sites during the gene amplification. , 1991, Journal of lipid research.

[16]  J. Ordovás,et al.  Influence of mutation in human apolipoprotein A-1 gene promoter on plasma LDL cholesterol response to dietary fat , 1994, The Lancet.

[17]  C. Garcés,et al.  Adenine for guanine substitution — pairs 5‘ to the apolipoprotein (APO) A4 gene: relation with hgh density lipoprotein cholesterol and APO A‐I concentrations , 1993 .

[18]  M. Farrall,et al.  Familial combined hyperlipidaemia linked to the apolipoprotein AI–CIII–AIV gene cluster on chromosome 11q23q–q24 , 1991, Nature.

[19]  K. Jablonski,et al.  Effects of sex and ethnicity on responses to a low-fat diet: a study of African Americans and whites. , 1995, The American journal of clinical nutrition.

[20]  S. Grundy,et al.  Genetic analysis of a polymorphism in the human apolipoprotein A-I gene promoter: effect on plasma HDL-cholesterol levels. , 1994, Journal of lipid research.

[21]  S. Humphries,et al.  Genetic markers in the apo AI-CIII-AIV gene cluster for combined hyperlipidemia, hypertriglyceridemia, and predisposition to atherosclerosis. , 1993, Atherosclerosis.

[22]  A. Lichtenstein,et al.  ApoA-IV phenotype affects diet-induced plasma LDL cholesterol lowering. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[23]  R. Krauss,et al.  Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[24]  P. Clifton,et al.  Influence of gender, body mass index, and age on response of plasma lipids to dietary fat plus cholesterol. , 1992, Arteriosclerosis and thrombosis : a journal of vascular biology.

[25]  S. Grundy.  Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. , 1986, The New England journal of medicine.

[26]  J. Ordovás,et al.  Effect of 347-serine mutation in apoprotein A-IV on plasma LDL cholesterol response to dietary fat. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[27]  F. Baralle,et al.  Human apolipoprotein A-I gene promoter polymorphism: association with hyperalphalipoproteinemia. , 1990, Journal of lipid research.

[28]  T. Read,et al.  Cigarette smoke alters chylomicron metabolism in rats. , 1993, Journal of vascular surgery.

[29]  D. T. Vernier,et al.  Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. , 1990, Journal of lipid research.

[30]  A. Lichtenstein,et al.  Gene-diet interaction in determining plasma lipid response to dietary intervention. , 1995, Atherosclerosis.

[31]  P. Monaci,et al.  Promoter elements and factors involved in hepatic transcription of the human ApoA-I gene positive and negative regulators bind to overlapping sites. , 1991, The Journal of biological chemistry.

[32]  A. von Eckardstein,et al.  Nonsynonymous polymorphic sites in the apolipoprotein (apo) A-IV gene are associated with changes in the concentration of apo B- and apo A-I-containing lipoproteins in a normal population. , 1992, American journal of human genetics.

[33]  R. Weinberg,et al.  Attenuated hypercholesterolemic response to a high-cholesterol diet in subjects heterozygous for the apolipoprotein A-IV-2 allele. , 1994, The New England journal of medicine.

[34]  J. Mckenney,et al.  Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II) , 1993, JAMA.

[35]  V. Gudnason,et al.  Interaction between a polymorphism of the apo A-I promoter region and smoking determines plasma levels of HDL and apo A-I. , 1992, Arteriosclerosis and thrombosis : a journal of vascular biology.

[36]  E. Boerwinkle,et al.  Genetic variation at the apolipoprotein gene loci contribute to response of plasma lipids to dietary change , 1990, Genetic epidemiology.

[37]  M. de Oya,et al.  Effect of dietary monounsaturated fatty acids on plasma lipoproteins and apolipoproteins in women. , 1992, The American journal of clinical nutrition.

[38]  J. Blangero,et al.  Genetic analysis of apolipoprotein A-I in two dietary environments. , 1990, American journal of human genetics.

[39]  R. Krauss,et al.  Apolipoprotein E isoform phenotype and LDL subclass response to a reduced-fat diet. , 1995, Arteriosclerosis, thrombosis, and vascular biology.