流行病學所WANG, RUEY-YUNRUEY-YUNWANGCHEN, CHIEN-CHUNG et al.CHIEN-CHUNG et al.CHEN2009-11-242018-06-292009-11-242018-06-292008http://ntur.lib.ntu.edu.tw//handle/246246/173144Objectives: Angiotensin converting enzyme ( ACE) plays major roles in the pathogenesis of cardiovascular diseases ( CVD) . However, findings on the relations between ACE variants and CVD have not been consistent. The purpose of this study was to map quantitative trait loci ( QTL) for serum ACE activity, a heritable endophenotype of cardiovascular diseases ( estimated heritability = 0.58). Methods: With 1, 271 individuals from 373 young- onset ( age <= 40) hypertension pedigrees, 479 deCODE microsatellite markers were genotyped. Results: We identified a previously unknown loci on chromosomes 9 at 149.4 cM ( LOD = 3.00) in addition to a strong linkage peak near the ACE structural locus on chromosome 17 at 89.6 cM ( LOD = 4.60). Conclusions: These results not only indicate that the ACE gene or nearby loci on 17q was among the strongest QTL influencing ACE activity, but also reveal a potential ACE QTL in human genome, pointing to the complexity of ACE regulation.en-USgenome-wide scanhypertensionangiotensin converting enzymequantitative trait lociChineseTaiwan[SDGs]SDG3dipeptidyl carboxypeptidase; adult; article; cardiovascular disease; chromosome 17q; chromosome 9; enzyme activity; enzyme regulation; female; gene identification; genome; genotype; human; hypertension; major clinical study; male; pedigree; phenotype; quantitative trait locus; Age of Onset; Cardiovascular Diseases; Female; Genome, Human; Genotype; Humans; Hypertension; Linkage Disequilibrium; Male; Pedigree; Peptidyl-Dipeptidase A; Phenotype; Taiwanjournal article10.1159/000108940WOS:000250096600004