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The association of CLOCK gene T3111C polymorphism and hPER3 gene 54-nucleotide repeat polymorphism with Chinese Han people schizophrenics

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Abstract

Many reports have shown that the biologic rhythm could be altered due to mutations of circadian gene hClock or hPeriod, and the mutations of circadian genes have some relationship with psychosis according to recent studies. A preliminary study has been conducted to examine wether the T3111C single nucleotide polymorphism of the hClock gene or the length polymorphism of the hPer3 gene is associated with the development of schizophrenia. The samples from schizophrenics (n = 148, male: 57.4%, female: 42.6%) and normal controls (n = 199, male: 59.3%, female: 40.7%) were examined. Allele frequencies of T3111C SNP of hClock were significantly different between schizophrenics and controls (χ2 = 19.738, P < 0.05). Schizophrenics had a significantly higher frequency of the C allele compared with controls (OR = 2.613, 95% CI = 1.693–4.034). On the other hand, there is no significant difference of allele frequencies of 18 exon of hper3 between schizophrenics and controls (χ2 = 0.192, P > 0.05). Our results suggest that the T3111C (RS1801260) polymorphism of hClock gene is associated with schizophrenia, but it seems that the length polymorphism of 18 exon of hPer3 may not be associated with schizophrenia. It is important to address of the relationship between circadian gene polymorphisms and dopamine functions in further study.

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Acknowledgments

This study was supported by the National Nature Science Foundation of China, by CMB, by the Youth Foundation of SCU and by Open Fund of State Key Laboratory of Oral Diseases (Nos. 30470623 and 30070288 to ZW, no. 30700393 to YW, no. 88-486 to ZW, and no. 2008063 to ZJ).

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Correspondence to Zhengrong Wang.

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Jing Zhang and Ga Liao contributed equally to this work.

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Zhang, J., Liao, G., Liu, C. et al. The association of CLOCK gene T3111C polymorphism and hPER3 gene 54-nucleotide repeat polymorphism with Chinese Han people schizophrenics. Mol Biol Rep 38, 349–354 (2011). https://doi.org/10.1007/s11033-010-0114-2

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  • DOI: https://doi.org/10.1007/s11033-010-0114-2

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