ArticleScientific reports2017
Genome-Wide Linkage Analysis of Large Multiple Multigenerational Families Identifies Novel Genetic Loci for Coronary Artery Disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 23 citations in OpenAlex.
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- Monocyte-Derived miRNA-1914-5p Attenuates IL-1β-Induced Monocyte Adhesion and Transmigration.International journal of molecular sciences · 2023Article
- Genome-wide linkage analysis combined with genome sequencing in large families with intracranial aneurysms.European journal of human genetics : EJHG · 2022Article
- Shared genetic etiology and causality between body fat percentage and cardiovascular diseases: a large-scale genome-wide cross-trait analysis.BMC medicine · 2021Article
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- UBA6 and Its Bispecific Pathways for Ubiquitin and FAT10.International journal of molecular sciences · 2019Review
- Analysis of causal effect of APOA5 variants on premature coronary artery disease.Annals of human genetics · 2018Article
- Genetic Risk in Coronary Artery Disease.Arquivos brasileiros de cardiologia · 2018Article
- CYP2C19 and ABCB1 genetic polymorphisms correlate with the recurrence of ischemic cardiovascular adverse events after clopidogrel treatment.Journal of clinical laboratory analysis · 2018Article
- Metabolic Pathway Genes Associated with Susceptibility Genes to Coronary Artery Disease.International journal of genomics · 2018Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Coronary artery disease (CAD) is the leading cause of death, and genetic factors contribute significantly to risk of CAD. This study aims to identify new CAD genetic loci through a large-scale linkage analysis of 24 large and multigenerational families with 433 family members (GeneQuest II). All family members were genotyped with markers spaced by every 10 cM and a model-free nonparametric linkage (NPL-all) analysis was carried out. Two highly significant CAD loci were identified on chromosome 17q21.2 (NPL score of 6.20) and 7p22.2 (NPL score of 5.19). We also identified four loci with significant NPL scores between 4.09 and 4.99 on 2q33.3, 3q29, 5q13.2 and 9q22.33. Similar analyses in individual families confirmed the six significant CAD loci and identified seven new highly significant linkages on 9p24.2, 9q34.2, 12q13.13, 15q26.1, 17q22, 20p12.3, and 22q12.1, and two significant loci on 2q11.2 and 11q14.1. Two loci on 3q29 and 9q22.33 were also successfully replicated in our previous linkage analysis of 428 nuclear families. Moreover, two published risk variants, SNP rs46522 in UBE2Z and SNP rs6725887 in WDR12 by GWAS, were found within the 17q21.2 and 2q33.3 loci. These studies lay a foundation for future identification of causative variants and genes for CAD.
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