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 Coronary artery disease. The EFO term coronary artery disease 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: coronary artery disease

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

M Nikpay, A Goel, HH Won, LM Hall, C Willenborg, S Kanoni, D Saleheen, T Kyriakou, CP Nelson, JC Hopewell, TR Webb, L Zeng, A Dehghan, M Alver, SM Armasu, K Auro, A Bjonnes, DI Chasman, S Chen, I Ford, N Franceschini, C Gieger, C Grace, S Gustafsson, J Huang, SJ Hwang, YK Kim, ME Kleber, KW Lau, X Lu, Y Lu, LP Lyytikäinen, E Mihailov, AC Morrison, N Pervjakova, L Qu, LM Rose, E Salfati, R Saxena, M Scholz, AV Smith, E Tikkanen, A Uitterlinden, X Yang, W Zhang, W Zhao, M de Andrade, PS de Vries, NR van Zuydam, SS Anand, L Bertram, F Beutner, G Dedoussis, P Frossard, D Gauguier, AH Goodall, O Gottesman, M Haber, BG Han, J Huang, S Jalilzadeh, T Kessler, IR König, L Lannfelt, W Lieb, L Lind, CM Lindgren, ML Lokki, PK Magnusson, NH Mallick, N Mehra, T Meitinger, FU Memon, AP Morris, MS Nieminen, NL Pedersen, A Peters, LS Rallidis, A Rasheed, M Samuel, SH Shah, J Sinisalo, KE Stirrups, S Trompet, L Wang, KS Zaman, D Ardissino, E Boerwinkle, IB Borecki, EP Bottinger, JE Buring, JC Chambers, R Collins, LA Cupples, J Danesh, I Demuth, R Elosua, SE Epstein, T Esko, MF Feitosa, OH Franco, MG Franzosi, CB Granger, D Gu, V Gudnason, AS Hall, A Hamsten, TB Harris, SL Hazen, C Hengstenberg, A Hofman, E Ingelsson, C Iribarren, JW Jukema, PJ Karhunen, BJ Kim, JS Kooner, IJ Kullo, T Lehtimäki, RJ Loos, O Melander, A Metspalu, W März, CN Palmer, M Perola, T Quertermous, DJ Rader, PM Ridker, S Ripatti, R Roberts, V Salomaa, DK Sanghera, SM Schwartz, U Seedorf, AF Stewart, DJ Stott, J Thiery, PA Zalloua, CJ O'Donnell, MP Reilly, TL Assimes, JR Thompson, J Erdmann, R Clarke, H Watkins, S Kathiresan, R McPherson, P Deloukas, H Schunkert, NJ Samani, M Farrall

TITLE:

A comprehensive 1,000 Genomes-based genome-wide association meta-analysis of coronary artery disease.

JOURNAL:

Nature genetics Oct 2015, Vol 47, pp. 1121-30

ABSTRACT:

Existing knowledge of genetic variants affecting risk of coronary artery disease (CAD) is largely based on genome-wide association study (GWAS) analysis of common SNPs. Leveraging phased haplotypes from the 1000 Genomes Project, we report a GWAS meta-analysis of ∼185,000 CAD cases and controls, interrogating 6.7 million common (minor allele frequency (MAF) > 0.05) and 2.7 million low-frequency (0.005 < MAF < 0.05) variants. In addition to confirming most known CAD-associated loci, we identified ten new loci (eight additive and two recessive) that contain candidate causal genes newly implicating biological processes in vessel walls. We observed intralocus allelic heterogeneity but little evidence of low-frequency variants with larger effects and no evidence of synthetic association. Our analysis provides a comprehensive survey of the fine genetic architecture of CAD, showing that genetic susceptibility to this common disease is largely determined by common SNPs of small effect size. PUBMED: 26343387
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