http://purl.uniprot.org/citations/20855565 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/20855565 | http://www.w3.org/2000/01/rdf-schema#comment | "A low level of HDL-C is the most common plasma lipid abnormality observed in men with established coronary heart disease (CHD). To identify allelic variants associated with susceptibility to low HDL-C and CHD, we examined 60 candidate genes with key roles in HDL metabolism, insulin resistance, and inflammation using samples from the Veterans Affairs HDL Intervention Trial (VA-HIT; cases, n = 699) and the Framingham Offspring Study (FOS; controls, n = 705). VA-HIT was designed to examine the benefits of HDL-raising with gemfibrozil in men with low HDL-C (≤40 mg/dl) and established CHD. After adjustment for multiple testing within each gene, single-nucleotide polymorphisms (SNP) significantly associated with case status were identified in the genes encoding LIPC (rs4775065, P < 0.0001); CETP (rs5882, P = 0.0002); RXRA (rs11185660, P = 0.0021); ABCA1 (rs2249891, P = 0.0126); ABCC6 (rs150468, P = 0.0206; rs212077, P = 0.0443); CUBN (rs7893395, P = 0.0246); APOA2 (rs3813627, P = 0.0324); SELP (rs732314, P = 0.0376); and APOC4 (rs10413089, P = 0.0425). Included among the novel findings of this study are the identification of susceptibility alleles for low HDL-C/CHD risk in the genes encoding CUBN and RXRA, and the observation that genetic variation in SELP may influence CHD risk through its effects on HDL."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.org/dc/terms/identifier | "doi:10.1194/jlr.p008268"xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Gabriel S.B."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Brousseau M.E."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Collins D."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Peloso G.M."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Robins S.J."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Schaefer E.J."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Mirel D.B."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Cupples L.A."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/author | "Demissie S."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/name | "J Lipid Res"xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/pages | "3524-3532"xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/title | "Common genetic variation in multiple metabolic pathways influences susceptibility to low HDL-cholesterol and coronary heart disease."xsd:string |
http://purl.uniprot.org/citations/20855565 | http://purl.uniprot.org/core/volume | "51"xsd:string |
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