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Megakaryoblastic leukemia factor-1 gene in the susceptibility to coronary artery disease |
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| Authors: | Kunihiko Hinohara Toshiaki Nakajima Michio Yasunami Shigeru Houda Taishi Sasaoka Ken Yamamoto Bok-Soo Lee Hiroki Shibata Yumiko Tanaka-Takahashi Megumi Takahashi Takuro Arimura Akinori Sato Taeko Naruse Jimin Ban Hidetoshi Inoko Yoshiji Yamada Motoji Sawabe Jeong-Euy Park Toru Izumi Akinori Kimura |
| Institution: | 1. Department of Molecular Pathogenesis, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan 2. Laboratory of Genome Diversity, School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, Japan 3. Department of Internal Medicine and Cardiology, Kitasato University School of Medicine, Sagamihara, Japan 4. Division of Molecular Population Genetics, Department of Molecular Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan 5. Division of Cardiology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea 6. Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Japan 7. Department of Human Functional Genomics, Mie University Graduate School of Medicine, Tsu, Japan 8. Department of Pathology, Tokyo Metropolitan Geriatric Medical Center, Tokyo, Japan |
| Abstract: | Coronary artery disease (CAD) is based on the atherosclerosis of coronary artery and may manifest with myocardial infarction or angina pectoris. Although it is widely accepted that genetic factors are linked to CAD and several disease-related genes have been reported, only a few could be replicated suggesting that there might be some other CAD-related genes. To identify novel susceptibility loci for CAD, we used microsatellite markers in the screening and found six different candidate CAD loci. Subsequent single nucleotide polymorphism (SNP) association studies revealed an association between CAD and megakaryoblastic leukemia factor-1 gene (MKL1). The association with a promoter SNP of MKL1, ?184C > T, was found in a Japanese population and the association was replicated in another Japanese population and a Korean population. Functional analysis of the MKL1 promoter SNP suggested that the higher MKL1 expression was associated with CAD. These findings suggest that MKL1 is involved in the pathogenesis of CAD. |
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