No association between the Bcl2-interacting killer (BIK) gene and schizophrenia |
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| Authors: | Kazutaka Ohi Ryota Hashimoto Yuka Yasuda Hidenaga Yamamori Hiroaki Hori Osamu Saitoh Masahiko Tatsumi Masatoshi Takeda Nakao Iwata Norio Ozaki Kunitoshi Kamijima Hiroshi Kunugi |
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| Affiliation: | 1. Department of Psychiatry, Osaka University Graduate School of Medicine, Suita, Osaka, Japan;2. The Osaka-Hamamatsu Joint Research Center for Child Mental Development, Graduate School of Medicine, Osaka University, Suita, Osaka, Japan;3. Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan;4. Japan Science and Technology Agency, CREST, Kawaguchi, Saitama, Japan;5. Department of Molecular Neuropsychiatry, Osaka University Graduate School of Medicine, Suita, Osaka, Japan;6. Department of Psychiatry, National Center Hospital, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan;g Yokohama Shinryo Clinic, Yokohama, Kanagawa, Japan;h Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan;i Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan;j Department of Psychiatry, Showa University School of Medicine, Shinagawaku, Tokyo, Japan |
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| Abstract: | The Bcl2-interacting killer (BIK) gene interacts with cellular and viral survival-promoting proteins, such as Bcl-2, to enhance apoptosis. The BIK protein promotes cell death in a manner analogous to Bcl-2-related death-promoting proteins, Bax and Bak. There have been lower Bcl-2 levels and increased Bax/Bcl-2 ratio in the temporal cortex of patients with schizophrenia compared with those in controls. Because the death-promoting activity of BIK was suppressed in the presence of the cellular and viral survival-promoting proteins, the BIK protein is suggested as a likely target for antiapoptotic proteins. The purpose of this study is to investigate the association between genetic variants in the BIK gene and schizophrenia in a large Japanese population (1181 patients with schizophrenia and 1243 healthy controls). We found nominal evidence for association of alleles, rs926328 (χ2 = 4.44, p = 0.035, odds ratio = 1.13) and rs2235316 (χ2 = 4.41, p = 0.036, odds ratio = 1.13), with schizophrenia. However, these associations were no longer positive after correction for multiple testing (rs926328: corrected p = 0.105, rs2235316: corrected p = 0.108). We conclude that BIK might not play a major role in the susceptibility of schizophrenia in Japanese population. |
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| Keywords: | Schizophrenia BIK gene Apoptosis Bcl2 related protein family Single nucleotide polymorphism |
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