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http://purl.uniprot.org/citations/19878569http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19878569http://www.w3.org/2000/01/rdf-schema#comment"

Background

Plasma level of high-density lipoprotein-cholesterol (HDL-C), a heritable trait, is an important determinant of susceptibility to atherosclerosis. Non-synonymous and regulatory single nucleotide polymorphisms (SNPs) in genes implicated in HDL-C synthesis and metabolism are likely to influence plasma HDL-C, apolipoprotein A-I (apo A-I) levels and severity of coronary atherosclerosis.

Methods

We genotyped 784 unrelated Caucasian individuals from two sets of populations (Lipoprotein and Coronary Atherosclerosis Study-LCAS, N = 333 and TexGen, N = 451) for 94 SNPs in 42 candidate genes by 5' nuclease assays. We tested the distribution of the phenotypes by the Shapiro-Wilk normality test. We used Box-Cox regression to analyze associations of the non-normally distributed phenotypes (plasma HDL-C and apo A-I levels) with the genotypes. We included sex, age, body mass index (BMI), diabetes mellitus (DM), and cigarette smoking as covariates. We calculated the q values as indicators of the false positive discovery rate (FDR).

Results

Plasma HDL-C levels were associated with sex (higher in females), BMI (inversely), smoking (lower in smokers), DM (lower in those with DM) and SNPs in APOA5, APOC2, CETP, LPL and LIPC (each q ConclusionPutatively functional variants of APOA2, APOA5, APOC2, CETP, LPL, LIPC and SOAT2 are independent genetic determinants of plasma HDL-C levels. The non-synonymous S19W SNP in APOA5 is also an independent determinant of plasma apo A-I level, severity of coronary atherosclerosis and its progression."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.org/dc/terms/identifier"doi:10.1186/1471-2350-10-111"xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Marian A.J."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Willerson J.T."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Todd J."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Lombardi R."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Gotto A.M. Jr."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Ballantyne C.M."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Chen S.N."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/author"Cilingiroglu M."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/name"BMC Med Genet"xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/pages"111"xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/title"Candidate genetic analysis of plasma high-density lipoprotein-cholesterol and severity of coronary atherosclerosis."xsd:string
http://purl.uniprot.org/citations/19878569http://purl.uniprot.org/core/volume"10"xsd:string
http://purl.uniprot.org/citations/19878569http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/19878569
http://purl.uniprot.org/citations/19878569http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/19878569
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