Genetic variants in the KIF6 region and coronary event reduction from statin therapy
| Autor: | James J. Devlin, Todd G. Kirchgessner, Yonghong Li, Michele Robertson, Chris J. Packard, Marc S. Sabatine, Charles M. Rowland, Ian Ford, Olga Iakoubova, Lance A. Bare, Carmen H. Tong, James Shepherd |
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| Jazyk: | angličtina |
| Rok vydání: | 2010 |
| Předmět: |
Oncology
Male medicine.medical_specialty Linkage disequilibrium Kinesins Single-nucleotide polymorphism Coronary Disease 030204 cardiovascular system & hematology Biology Polymorphism Single Nucleotide Linkage Disequilibrium law.invention Pathogenesis 03 medical and health sciences 0302 clinical medicine Randomized controlled trial Meta-Analysis as Topic Polymorphism (computer science) law Internal medicine Genetics medicine SNP Humans Genetics(clinical) cardiovascular diseases Prospective cohort study Genetics (clinical) 030304 developmental biology Original Investigation Randomized Controlled Trials as Topic 0303 health sciences Chromosome Mapping Middle Aged 3. Good health KIF6 lipids (amino acids peptides and proteins) Female Hydroxymethylglutaryl-CoA Reductase Inhibitors |
| Zdroj: | Human Genetics |
| ISSN: | 1432-1203 0340-6717 |
| Popis: | A single nucleotide polymorphism (SNP) in KIF6, a member of the KIF9 family of kinesins, is associated with differential coronary event reduction from statin therapy in four randomized controlled trials; this SNP (rs20455) is also associated with the risk for coronary heart disease (CHD) in multiple prospective studies. We investigated whether other common SNPs in the KIF6 region were associated with event reduction from statin therapy. Of the 170 SNPs in the KIF6 region investigated in the Cholesterol and Recurrent Events trial (CARE), 28 were associated with differential event reduction from statin therapy (Pinteraction 0.4) in non-carriers. These three SNPs are in high linkage disequilibrium with one another (r2 > 0.84). Functional studies of these variants may help to understand the role of KIF6 in the pathogenesis of CHD and differential response to statin therapy. Electronic supplementary material The online version of this article (doi:10.1007/s00439-010-0892-6) contains supplementary material, which is available to authorized users. |
| Databáze: | OpenAIRE |
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