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No evidence for an association between G protein beta 3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia

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dc.contributor.authorLee, Heon-Jeong-
dc.contributor.authorKang, Seung-Gul-
dc.contributor.authorPaik, Jong-Woo-
dc.contributor.authorLee, Moon-Soo-
dc.contributor.authorCho, Bang-Hyun-
dc.contributor.authorPark, Young-Min-
dc.contributor.authorKim, Won-
dc.contributor.authorChoi, Jung-Eun-
dc.contributor.authorJung, In-Kwa-
dc.contributor.authorKim, Leen-
dc.contributor.authorLee, Min-Soo-
dc.date.available2020-11-03T11:46:21Z-
dc.date.issued2007-12-
dc.identifier.issn0885-6222-
dc.identifier.issn1099-1077-
dc.identifier.urihttps://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/17589-
dc.description.abstractObjective Tardive dyskinesia (TD) is a long-term adverse effect of antipsychotic. We evaluated candidate functional polymorphism of the G protein beta 3 subunit (GNB3) gene for association with drug-induced TD in the Korean schizophrenic patients. Methods We investigated whether the C825T polymorphism of the GNB3 gene is associated with the TD in a Korean sample of schizophrenic patients with (n=83) and without TD (n=126), matched for antipsychotic drug exposure and other relevant variables. Results The distribution of genotypes and allele frequencies of GNB3 were not different between schizophrenic patients with TD and without TD (p>0.05). Conclusion Within the limitations imposed by the size of the clinical sample, these findings suggest that the GNB3 825 C/T single nucleotide polymorphism (SNP) does not contribute significantly to risk for TD. Copyright (C) 2007 John Wiley & Sons, Ltd.-
dc.format.extent4-
dc.language영어-
dc.language.isoENG-
dc.publisherWILEY-BLACKWELL-
dc.titleNo evidence for an association between G protein beta 3 subunit gene C825T polymorphism and tardive dyskinesia in schizophrenia-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1002/hup.875-
dc.identifier.scopusid2-s2.0-35348957329-
dc.identifier.wosid000252305600001-
dc.identifier.bibliographicCitationHUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL, v.22, no.8, pp 501 - 504-
dc.citation.titleHUMAN PSYCHOPHARMACOLOGY-CLINICAL AND EXPERIMENTAL-
dc.citation.volume22-
dc.citation.number8-
dc.citation.startPage501-
dc.citation.endPage504-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalResearchAreaPsychiatry-
dc.relation.journalResearchAreaPsychology-
dc.relation.journalWebOfScienceCategoryClinical Neurology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryPsychiatry-
dc.relation.journalWebOfScienceCategoryPsychology-
dc.subject.keywordPlusSUBUNIT GENE-
dc.subject.keywordPlusRECEPTOR GENE-
dc.subject.keywordPlusVARIANT-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusDISORDERS-
dc.subject.keywordAuthorschizophrenia-
dc.subject.keywordAuthortardive dyskinesia-
dc.subject.keywordAuthorG protein-
dc.subject.keywordAuthorpolymorphism-
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Anam Hospital (Department of Psychiatry, Anam Hospital)
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