Lack of association between sigma receptor gene variants and schizophrenia
Several pharmacological studies suggest the possible involvement of sigma(1) receptors in the pathogenesis of schizophrenia. An association has been reported between schizophrenia and two variants (GC-241-240TT and Gln2Pro) in the sigma(1) receptor gene (SIGMAR1). We also previously reported that, a...
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Veröffentlicht in: | Psychiatry and clinical neurosciences 2004-08, Vol.58 (4), p.359-363 |
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creator | Satoh, Fumiaki Miyatake, Ryosuke Furukawa, Aizo Suwaki, Hiroshi |
description | Several pharmacological studies suggest the possible involvement of sigma(1) receptors in the pathogenesis of schizophrenia. An association has been reported between schizophrenia and two variants (GC-241-240TT and Gln2Pro) in the sigma(1) receptor gene (SIGMAR1). We also previously reported that, along with T-485 A, these two variants alter SIGMAR1 function. To investigate the role of SIGMAR1 in conveying susceptibility to schizophrenia, we performed a case-control study. We initially screened for polymorphisms in the SIGMAR1 coding region using PCR-single strand conformation polymorphism analysis. The distribution of SIGMAR1 polymorphisms was analyzed in 100 schizophrenic and 104 control subjects. A novel G620A variant was detected in exon4. G620A was predicted to alter the amino acid represented by codon 211 from arginine to glutamine. Our case-control study showed no significant association between the T-485 A, GC-241-240TT, Gln2Pro, and G620A (Arg211Gln) variants and schizophrenia and clinical characteristics. These findings suggest that these SIGMAR1 variants may not affect susceptibility to schizophrenia. |
doi_str_mv | 10.1111/j.1440-1819.2004.01268.x |
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An association has been reported between schizophrenia and two variants (GC-241-240TT and Gln2Pro) in the sigma(1) receptor gene (SIGMAR1). We also previously reported that, along with T-485 A, these two variants alter SIGMAR1 function. To investigate the role of SIGMAR1 in conveying susceptibility to schizophrenia, we performed a case-control study. We initially screened for polymorphisms in the SIGMAR1 coding region using PCR-single strand conformation polymorphism analysis. The distribution of SIGMAR1 polymorphisms was analyzed in 100 schizophrenic and 104 control subjects. A novel G620A variant was detected in exon4. G620A was predicted to alter the amino acid represented by codon 211 from arginine to glutamine. Our case-control study showed no significant association between the T-485 A, GC-241-240TT, Gln2Pro, and G620A (Arg211Gln) variants and schizophrenia and clinical characteristics. 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An association has been reported between schizophrenia and two variants (GC-241-240TT and Gln2Pro) in the sigma(1) receptor gene (SIGMAR1). We also previously reported that, along with T-485 A, these two variants alter SIGMAR1 function. To investigate the role of SIGMAR1 in conveying susceptibility to schizophrenia, we performed a case-control study. We initially screened for polymorphisms in the SIGMAR1 coding region using PCR-single strand conformation polymorphism analysis. The distribution of SIGMAR1 polymorphisms was analyzed in 100 schizophrenic and 104 control subjects. A novel G620A variant was detected in exon4. G620A was predicted to alter the amino acid represented by codon 211 from arginine to glutamine. Our case-control study showed no significant association between the T-485 A, GC-241-240TT, Gln2Pro, and G620A (Arg211Gln) variants and schizophrenia and clinical characteristics. These findings suggest that these SIGMAR1 variants may not affect susceptibility to schizophrenia.</description><subject>Adult</subject><subject>Amino Acid Substitution - genetics</subject><subject>Case controlled studies</subject><subject>Case-Control Studies</subject><subject>Codon - genetics</subject><subject>Exons - genetics</subject><subject>Female</subject><subject>Genetic factors</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic Variation - genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>Japan</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Phenotype</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Single-Stranded Conformational</subject><subject>Receptors, sigma - genetics</subject><subject>Schizophrenia</subject><subject>Schizophrenia - diagnosis</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenic Psychology</subject><subject>Sigma-1 Receptor</subject><subject>Statistics as Topic</subject><issn>1323-1316</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>7QJ</sourceid><recordid>eNo1j71OwzAYRT2AaCm8AvLEluB_JyOqgIIqscAcfXa-ti6NE-yUv6enEuUsdzm60iGEclbyAzfbkivFCl7xuhSMqZJxYary64RMuRSy4JKbCTnPecsYk9LwMzLhWtSVUXZKnpbg32i_opBz7wOMoY_U4fiJGGkO6w5oQo_D2Ce6xoj0A1KAOGYKsaXZb8JPP2wSxgAX5HQFu4yXx52R1_u7l_miWD4_PM5vl8XALRsLySVqCcoprTRg1cLKgpDeOqhbwb0W6L1xoE3lBJq21a6yQmoGktW6FnJGrv9-h9S_7zGPTReyx90OIvb73GjLjGXSHMSro7h3HbbNkEIH6bv5r5e_6eZcig</recordid><startdate>200408</startdate><enddate>200408</enddate><creator>Satoh, Fumiaki</creator><creator>Miyatake, Ryosuke</creator><creator>Furukawa, Aizo</creator><creator>Suwaki, Hiroshi</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QJ</scope></search><sort><creationdate>200408</creationdate><title>Lack of association between sigma receptor gene variants and schizophrenia</title><author>Satoh, Fumiaki ; Miyatake, Ryosuke ; Furukawa, Aizo ; Suwaki, Hiroshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p170t-313e53a4b4545ae8daf7a23c7ba9d21c52ecc6ba568b2e6dd5b872350a3095923</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Amino Acid Substitution - genetics</topic><topic>Case controlled studies</topic><topic>Case-Control Studies</topic><topic>Codon - genetics</topic><topic>Exons - genetics</topic><topic>Female</topic><topic>Genetic factors</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic Variation - genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>Japan</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Phenotype</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Single-Stranded Conformational</topic><topic>Receptors, sigma - genetics</topic><topic>Schizophrenia</topic><topic>Schizophrenia - diagnosis</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenic Psychology</topic><topic>Sigma-1 Receptor</topic><topic>Statistics as Topic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Satoh, Fumiaki</creatorcontrib><creatorcontrib>Miyatake, Ryosuke</creatorcontrib><creatorcontrib>Furukawa, Aizo</creatorcontrib><creatorcontrib>Suwaki, Hiroshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Applied Social Sciences Index & Abstracts (ASSIA)</collection><jtitle>Psychiatry and clinical neurosciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Satoh, Fumiaki</au><au>Miyatake, Ryosuke</au><au>Furukawa, Aizo</au><au>Suwaki, Hiroshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of association between sigma receptor gene variants and schizophrenia</atitle><jtitle>Psychiatry and clinical neurosciences</jtitle><addtitle>Psychiatry Clin Neurosci</addtitle><date>2004-08</date><risdate>2004</risdate><volume>58</volume><issue>4</issue><spage>359</spage><epage>363</epage><pages>359-363</pages><issn>1323-1316</issn><abstract>Several pharmacological studies suggest the possible involvement of sigma(1) receptors in the pathogenesis of schizophrenia. An association has been reported between schizophrenia and two variants (GC-241-240TT and Gln2Pro) in the sigma(1) receptor gene (SIGMAR1). We also previously reported that, along with T-485 A, these two variants alter SIGMAR1 function. To investigate the role of SIGMAR1 in conveying susceptibility to schizophrenia, we performed a case-control study. We initially screened for polymorphisms in the SIGMAR1 coding region using PCR-single strand conformation polymorphism analysis. The distribution of SIGMAR1 polymorphisms was analyzed in 100 schizophrenic and 104 control subjects. A novel G620A variant was detected in exon4. G620A was predicted to alter the amino acid represented by codon 211 from arginine to glutamine. Our case-control study showed no significant association between the T-485 A, GC-241-240TT, Gln2Pro, and G620A (Arg211Gln) variants and schizophrenia and clinical characteristics. These findings suggest that these SIGMAR1 variants may not affect susceptibility to schizophrenia.</abstract><cop>Australia</cop><pmid>15298647</pmid><doi>10.1111/j.1440-1819.2004.01268.x</doi><tpages>5</tpages></addata></record> |
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subjects | Adult Amino Acid Substitution - genetics Case controlled studies Case-Control Studies Codon - genetics Exons - genetics Female Genetic factors Genetic Predisposition to Disease - genetics Genetic Variation - genetics Genotype Humans Japan Male Middle Aged Phenotype Polymerase Chain Reaction Polymorphism, Single-Stranded Conformational Receptors, sigma - genetics Schizophrenia Schizophrenia - diagnosis Schizophrenia - genetics Schizophrenic Psychology Sigma-1 Receptor Statistics as Topic |
title | Lack of association between sigma receptor gene variants and schizophrenia |
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