TY - JOUR
T1 - No association between the Bcl2-interacting killer (BIK) gene and schizophrenia
AU - Ohi, Kazutaka
AU - Hashimoto, Ryota
AU - Yasuda, Yuka
AU - Yamamori, Hidenaga
AU - Hori, Hiroaki
AU - Saitoh, Osamu
AU - Tatsumi, Masahiko
AU - Takeda, Masatoshi
AU - Iwata, Nakao
AU - Ozaki, Norio
AU - Kamijima, Kunitoshi
AU - Kunugi, Hiroshi
N1 - Funding Information:
This work was funded in part by Grants-in-Aid from the Japanese Ministry of Health, Labor and Welfare (H18-kokoro-005, H19-kokoro-002), the Japanese Ministry of Education, Culture, Sports, Science and Technology (18689030), CREST of JST, Grant-aid for Scientific Research on Priority Areas -Research on Pathomechanisms of Brain Disorders- from the MEXT (18023045) and Japan Foundation for Neuroscience and Mental Health. We thank all individuals who participated in this study.
PY - 2009/9/29
Y1 - 2009/9/29
N2 - 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.
AB - 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.
KW - Apoptosis
KW - BIK gene
KW - Bcl2 related protein family
KW - Schizophrenia
KW - Single nucleotide polymorphism
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U2 - 10.1016/j.neulet.2009.07.063
DO - 10.1016/j.neulet.2009.07.063
M3 - Article
C2 - 19632297
AN - SCOPUS:68149156376
SN - 0304-3940
VL - 463
SP - 60
EP - 63
JO - Neuroscience Letters
JF - Neuroscience Letters
IS - 1
ER -