PCR detection of the insertion/deletion polymorphism of the human angiotensin converting enzyme gene (DCP1) (dipeptidyl carboxypeptidase 1)
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This article is published in Nucleic Acids Research.The article was published on 1992-03-25 and is currently open access. It has received 1194 citations till now. The article focuses on the topics: Angiotensin-converting enzyme.read more
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Journal ArticleDOI
Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction.
François Cambien,Odette Poirier,Laure Lecerf,Alun Evans,Jean-Pierre Cambou,Dominique Arveiler,Gérald Luc,Jean-Marie Bard,L Bara,Sylvain Ricard +9 more
TL;DR: It is reported that the DD genotype, which is associated with higher levels of circulating ACE than the ID and II genotypes, is significantly more frequent in patients with myocardial infarction than in controls, especially among subjects with low body-mass index and low plasma levels of ApoB.
Journal ArticleDOI
Genetic associations with human longevity at the APOE and ACE loci.
François Schächter,Laurence Faure-Delanef,Frédérique Guénot,Hervé Rouger,Philippe Froguel,Laurence Lesueur-Ginot,Daniel Cohen +6 more
TL;DR: Results on two genes, chosen for their impact on cardiovascular risk, encoding apolipoprotein E (ApoE), angiotensin–converting enzyme (ACE) are reported, finding that the ε4 allele of APOE, which promotes premature atherosclerosis, is significantly less frequent in centenarians than in controls.
Journal ArticleDOI
A Prospective Evaluation of an Angiotensin-Converting-Enzyme Gene Polymorphism and the Risk of Ischemic Heart Disease
Klaus Lindpaintner,Marc A. Pfeffer,Reinhold Kreutz,Meir J. Stampfer,Francine Grodstein,Fran LaMotte,Julie E. Buring,Charles H. Hennekens +7 more
TL;DR: The presence of the D allele of the ACE gene conferred no appreciable increase in the risk of ischemic heart disease or myocardial infarction in a large, prospectively followed population of U.S. male physicians.
Journal ArticleDOI
Angiotensin II type 1 receptor gene polymorphisms in human essential hypertension.
Alain Bonnardeaux,Eleanor Davies,Xavier Jeunemaitre,Isabelle Féry,Anne Charru,Eric Clauser,Laurence Tiret,François Cambien,Pierre Corvol,Florent Soubrier +9 more
TL;DR: Findings would be compatible with a common variant of the AT1 receptor imparting a small effect on blood pressure; further studies will be needed to address this possibility.
Journal ArticleDOI
Association between a deletion polymorphism of the angiotensin-converting-enzyme gene and left ventricular hypertrophy.
Heribert Schunkert,Hans-Werner Hense,Stephan R. Holmer,Monica Stender,Siegfried Perz,Ulrich Keil,Beverly H. Lorell,Günter A.J. Riegger +7 more
TL;DR: The findings suggest thatleft ventricular hypertrophy is partially determined by genetic disposition and identifies the DD genotype of ACE as a potential genetic marker associated with an elevated risk of left ventricularhypertrophy in middle-aged men.
References
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Journal ArticleDOI
Primer-directed enzymatic amplification of DNA with a thermostable DNA polymerase
Randall Keichi Saiki,David H. Gelfand,Susanne Stoffel,Stephen J. Scharf,Russell Higuchi,Glenn Thomas Horn,Kary B. Mullis,Henry A. Erlich +7 more
TL;DR: A thermostable DNA polymerase was used in an in vitro DNA amplification procedure, the polymerase chain reaction, which significantly improves the specificity, yield, sensitivity, and length of products that can be amplified.
Journal ArticleDOI
An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels.
TL;DR: The insertion/deletion polymorphism accounted for 47% of the total phenotypic variance of serum ACE, showing that the ACE gene locus is the major locus that determines serum ACE concentration.
Journal ArticleDOI
Structure of the angiotensin I-converting enzyme gene. Two alternate promoters correspond to evolutionary steps of a duplicated gene.
TL;DR: The gene duplication suggested by the internal homology of the endothelial ACE mRNA is now confirmed by the presence of two homologous clusters of eight exons having similar sizes and codon phases at exon-intron boundaries.