Expressive

rs11107903 - FGD6

Magnitude 2.2 · 4 studies on file

Reported associations

  • Population-specific and trans-ancestry genome-wide analyses identify distinct and shared genetic risk loci for coronary artery disease. - Nature genetics (2020) · Koyama S, Ito K, Terao C, Akiyama M, Horikoshi M, Momozawa Y, Matsunaga H, Ieki H, Ozaki K, Onouchi Y, Takahashi A, Nomura S, Morita H, Akazawa H, Kim C, Seo JS, Higasa K, Iwasaki M, Yamaji T, Sawada N, Tsugane S, Koyama T, Ikezaki H, Takashima N, Tanaka K, Arisawa K, Kuriki K, Naito M, Wakai K, Suna S, Sakata Y, Sato H, Hori M, Sakata Y, Matsuda K, Murakami Y, Aburatani H, Kubo M, Matsuda F, Kamatani Y, Komuro I · PubMed 33020668

    To elucidate the genetics of coronary artery disease (CAD) in the Japanese population, we conducted a large-scale genome-wide association study of 168,228 individuals of Japanese ancestry (25,892 cases and 142,336 controls) with genotype imputation using a newly developed reference panel of Japanese haplotypes including 1,781 CAD cases and 2,636 controls. We detected eight new susceptibility loci and Japanese-specific rare variants contributing to disease severity and increased cardiovascular mortality. We then conducted a trans-ancestry meta-analysis and discovered 35 additional new loci. Using the meta-analysis results, we derived a polygenic risk score (PRS) for CAD, which outperformed those derived from either Japanese or European genome-wide association studies. The PRS prioritized ri

  • Identification of 64 Novel Genetic Loci Provides an Expanded View on the Genetic Architecture of Coronary Artery Disease - Unknown journal (n.d.) · Unknown authors · PubMed 29212778

    ABSTRACT: Supplemental Digital Content is available in the text. Rationale: Coronary artery disease (CAD) is a complex phenotype driven by genetic and environmental factors. Ninety-seven genetic risk loci have been identified to date, but the identification of additional susceptibility loci might be important to enhance our understanding of the genetic architecture of CAD. Objective: To expand the number of genome-wide significant loci, catalog functional insights, and enhance our understanding of the genetic architecture of CAD. Methods and Results: We performed a genome-wide association study in 34 541 CAD cases and 261 984 controls of UK Biobank resource followed by replication in 88 192 cases and 162 544 controls from CARDIoGRAMplusC4D. We identified 75 loci that replicated and

  • Genome-wide association studies in a large Korean cohort identify quantitative trait loci for 36 traits and illuminate their genetic architectures - Unknown journal (n.d.) · Unknown authors · PubMed 40436827

    ABSTRACT: Genome-wide association studies (GWAS) have predominantly focused on European ancestry populations, limiting biological discoveries across diverse populations. Here we report GWAS findings from 153,950 individuals across 36 quantitative traits in the Korean Cancer Prevention Study-II (KCPS2) Biobank. We discovered 301 previously unreported genetic loci in KCPS2, including an association between thyroid-stimulating hormone and CD36. Meta-analysis with the Korean Genome and Epidemiology Study, Biobank Japan, Taiwan Biobank, and UK Biobank identified 4588 loci that were not significant in any contributing GWAS. We describe differences in genetic architectures across these East Asian and European samples. We also highlight East Asian specific associations, including a known pleiotrop

  • Discovery and systematic characterization of risk variants and genes for coronary artery disease in over a million participants - Unknown journal (n.d.) · Unknown authors · PubMed 36474045

    ABSTRACT: The discovery of genetic loci associated with complex diseases has outpaced the elucidation of mechanisms of disease pathogenesis. Here we conducted a genome-wide association study (GWAS) for coronary artery disease (CAD) comprising 181,522 cases among 1,165,690 participants of predominantly European ancestry. We detected 241 associations, including 30 new loci. Cross-ancestry meta-analysis with a Japanese GWAS yielded 38 additional new loci. We prioritized likely causal variants using functionally informed fine-mapping, yielding 42 associations with less than five variants in the 95% credible set. Similarity-based clustering suggested roles for early developmental processes, cell cycle signaling and vascular cell migration and proliferation in the pathogenesis of CAD. We priorit

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