DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was LDL cholesterol. The EFO term low density lipoprotein cholesterol measurement was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: low density lipoprotein cholesterol measurement

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2020-05-06

SPECIES:

AUTHORS:

S Kathiresan, CJ Willer, GM Peloso, S Demissie, K Musunuru, EE Schadt, L Kaplan, D Bennett, Y Li, T Tanaka, BF Voight, LL Bonnycastle, AU Jackson, G Crawford, A Surti, C Guiducci, NP Burtt, S Parish, R Clarke, D Zelenika, KA Kubalanza, MA Morken, LJ Scott, HM Stringham, P Galan, AJ Swift, J Kuusisto, RN Bergman, J Sundvall, M Laakso, L Ferrucci, P Scheet, S Sanna, M Uda, Q Yang, KL Lunetta, J Dupuis, PI de Bakker, CJ O'Donnell, JC Chambers, JS Kooner, S Hercberg, P Meneton, EG Lakatta, A Scuteri, D Schlessinger, J Tuomilehto, FS Collins, L Groop, D Altshuler, R Collins, GM Lathrop, O Melander, V Salomaa, L Peltonen, M Orho-Melander, JM Ordovas, M Boehnke, GR Abecasis, KL Mohlke, LA Cupples

TITLE:

Common variants at 30 loci contribute to polygenic dyslipidemia.

JOURNAL:

Nature genetics Jan 2009, Vol 41, pp. 56-65

ABSTRACT:

Blood low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol and triglyceride levels are risk factors for cardiovascular disease. To dissect the polygenic basis of these traits, we conducted genome-wide association screens in 19,840 individuals and replication in up to 20,623 individuals. We identified 30 distinct loci associated with lipoprotein concentrations (each with P < 5 x 10(-8)), including 11 loci that reached genome-wide significance for the first time. The 11 newly defined loci include common variants associated with LDL cholesterol near ABCG8, MAFB, HNF1A and TIMD4; with HDL cholesterol near ANGPTL4, FADS1-FADS2-FADS3, HNF4A, LCAT, PLTP and TTC39B; and with triglycerides near AMAC1L2, FADS1-FADS2-FADS3 and PLTP. The proportion of individuals exceeding clinical cut points for high LDL cholesterol, low HDL cholesterol and high triglycerides varied according to an allelic dosage score (P < 10(-15) for each trend). These results suggest that the cumulative effect of multiple common variants contributes to polygenic dyslipidemia. PUBMED: 19060906
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