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

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1 Citation (Scopus)


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.

Original languageEnglish
Pages (from-to)60-63
Number of pages4
JournalNeuroscience Letters
Issue number1
Publication statusPublished - 29-09-2009

All Science Journal Classification (ASJC) codes

  • General Neuroscience


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