No association between the Bcl2-interacting killer (BIK) gene and schizophrenia

Kazutaka Ohi, Ryota Hashimoto, Yuka Yasuda, Hidenaga Yamamori, Hiroaki Hori, Osamu Saitoh, Masahiko Tatsumi, Masatoshi Takeda, Nakao Iwata, Norio Ozaki, Kunitoshi Kamijima, Hiroshi Kunugi

研究成果: ジャーナルへの寄稿学術論文査読

1 被引用数 (Scopus)

抄録

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.

本文言語英語
ページ(範囲)60-63
ページ数4
ジャーナルNeuroscience Letters
463
1
DOI
出版ステータス出版済み - 29-09-2009
外部発表はい

All Science Journal Classification (ASJC) codes

  • 神経科学一般

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