Assimes, Themistocles L. and Holm, Hilma and Kathiresan, Sekar and Reilly, Muredach P. and Thorleifsson, Gudmar and Voight, Benjamin F. and Erdmann, Jeanette and Willenborg, Christina and Vaidya, Dhananjay and Xie, Changchun and Patterson, Chris C. and Morgan, Thomas M. and Burnett, Mary Susan and Li, Mingyao and Hlatky, Mark A. and Knowles, Joshua W. and Thompson, John R. and Absher, Devin and Iribarren, Carlos and Go, Alan and Fortmann, Stephen P. and Sidney, Stephen and Risch, Neil and Tang, Hua and Myers, Richard M. and Berger, Klaus and Stoll, Monika and Shah, Svati H. and Thorgeirsson, Gudmundur and Andersen, Karl and Havulinna, Aki S. and Herrera, J. Enrique and Faraday, Nauder and Kim, Yoonhee and Kral, Brian G. and Mathias, Rasika A. and Ruczinski, Ingo and Suktitipat, Bhoom and Wilson, Alexander F. and Yanek, Lisa R. and Becker, Lewis C. and Linsel-Nitschke, Patrick and Lieb, Wolfgang and Koenig, Inke R. and Hengstenberg, Christian and Fischer, Marcus and Stark, Klaus and Reinhard, Wibke and Winogradow, Janina and Grassl, Martina and Grosshennig, Anika and Preuss, Michael and Schreiber, Stefan and Wichmann, H-Erich and Meisinger, Christa and Yee, Jean and Friedlander, Yechiel and Do, Ron and Meigs, James B. and Williams, Gordon and Nathan, David M. and MacRae, Calum A. and Qu, Liming and Wilensky, Robert L. and Matthai, William H. and Qasim, Atif N. and Hakonarson, Hakon and Pichard, Augusto D. and Kent, Kenneth M. and Satler, Lowell and Lindsay, Joseph M. and Waksman, Ron and Knouff, Christopher W. and Waterworth, Dawn M. and Walker, Max C. and Mooser, Vincent E. and Marrugat, Jaume and Lucas, Gavin and Subirana, Isaac and Sala, Joan and Ramos, Rafael and Martinelli, Nicola and Olivieri, Oliviero and Trabetti, Elisabetta and Malerba, Giovanni and Pignatti, Pier Franco and Guiducci, Candace and Mirel, Daniel and Parkin, Melissa and Hirschhorn, Joel N. and Asselta, Rosanna and Duga, Stefano and Musunuru, Kiran and Daly, Mark J. and Purcell, Shaun and Eifert, Sandra and Braund, Peter S. and Wright, Benjamin J. and Balmforth, Anthony J. and Ball, Stephen G. and Ouwehand, Willem H. and Deloukas, Panos and Scholz, Michael and Cambien, Francois and Huge, Andreas and Scheffold, Thomas and Salomaa, Veikko and Girelli, Domenico and Granger, Christopher B. and Peltonen, Leena and McKeown, Pascal P. and Altshuler, David and Melander, Olle and Devaney, Joseph M. and Epstein, Stephen E. and Rader, Daniel J. and Elosua, Roberto and Engert, James C. and Anand, Sonia S. and Hall, Alistair S. and Ziegler, Andreas and O'Donnell, Christopher J. and Spertus, John A. and Siscovick, David and Schwartz, Stephen M. and Becker, Diane and Thorsteinsdottir, Unnur and Stefansson, Kari and Schunkert, Heribert and Samani, Nilesh J. and Quertermous, Thomas (2010) Lack of Association Between the Trp719Arg Polymorphism in Kinesin-Like Protein-6 and Coronary Artery Disease in 19 Case-Control Studies. JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 56 (19). pp. 1552-1563. ISSN 0735-1097,
Full text not available from this repository. (Request a copy)Abstract
Objectives We sought to replicate the association between the kinesin-like protein 6 (KIF6) Trp719Arg polymorphism (rs20455), and clinical coronary artery disease (CAD). Background Recent prospective studies suggest that carriers of the 719Arg allele in KIF6 are at increased risk of clinical CAD compared with noncarriers. Methods The KIF6 Trp719Arg polymorphism (rs20455) was genotyped in 19 case-control studies of nonfatal CAD either as part of a genome-wide association study or in a formal attempt to replicate the initial positive reports. Results A total of 17,000 cases and 39,369 controls of European descent as well as a modest number of South Asians, African Americans, Hispanics, East Asians, and admixed cases and controls were successfully genotyped. None of the 19 studies demonstrated an increased risk of CAD in carriers of the 719Arg allele compared with noncarriers. Regression analyses and fixed-effects meta-analyses ruled out with high degree of confidence an increase of >= 2% in the risk of CAD among European 719Arg carriers. We also observed no increase in the risk of CAD among 719Arg carriers in the subset of Europeans with early-onset disease (younger than 50 years of age for men and younger than 60 years of age for women) compared with similarly aged controls as well as all non-European subgroups. Conclusions The KIF6 Trp719Arg polymorphism was not associated with the risk of clinical CAD in this large replication study. (J Am Coll Cardiol 2010;56:1552-63) (C) 2010 by the American College of Cardiology Foundation
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | NONFATAL MYOCARDIAL-INFARCTION; HEART-DISEASE; CARDIOVASCULAR-DISEASE; GENE VARIANTS; RISK-FACTORS; GENOMEWIDE ASSOCIATION; CHROMOSOME 9P21.3; GENOTYPE DATA; POPULATION; HEALTH; coronary artery disease; KIF6; kinesin-like protein 6; myocardial infarction; polymorphism |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 07 Jul 2020 06:14 |
| Last Modified: | 07 Jul 2020 06:14 |
| URI: | https://pred.uni-regensburg.de/id/eprint/23894 |
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