Polymorphisms in the Trace Amine Receptor 4 (TRAR4) gene on chromosome 6q23.2 are associated with susceptibility to schizophrenia
Identifieur interne : 004B51 ( PascalFrancis/Corpus ); précédent : 004B50; suivant : 004B52Polymorphisms in the Trace Amine Receptor 4 (TRAR4) gene on chromosome 6q23.2 are associated with susceptibility to schizophrenia
Auteurs : Jubao Duan ; Maria Martinez ; Alan R. Sanders ; CUIPING HOU ; Naruya Saitou ; Takashi Kitano ; Bryan J. Mowry ; Raymond R. Crowe ; Jeremy M. Silverman ; Douglas F. Levinson ; Pablo V. GejmanSource :
- American journal of human genetics [ 0002-9297 ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia-and, more recently, for bipolar disorder-on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples.
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Format Inist (serveur)
NO : | PASCAL 05-0039546 INIST |
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ET : | Polymorphisms in the Trace Amine Receptor 4 (TRAR4) gene on chromosome 6q23.2 are associated with susceptibility to schizophrenia |
AU : | DUAN (Jubao); MARTINEZ (Maria); SANDERS (Alan R.); CUIPING HOU; SAITOU (Naruya); KITANO (Takashi); MOWRY (Bryan J.); CROWE (Raymond R.); SILVERMAN (Jeremy M.); LEVINSON (Douglas F.); GEJMAN (Pablo V.) |
AF : | Center for Psychiatric Genetics, Department of Psychiatry and Behavioral Sciences, Evanston Northwestern Healthcare and Feinberg School of Medicine, Northwestern University/Evanston, IL/Etats-Unis (1 aut., 3 aut., 4 aut., 11 aut.); Méthodologie Statistique et Epidémiologie Génétique des Maladies Multifactorielles, INSERM/Evry/France (2 aut.); Division of Population Genetics, National Institute of Genetics/Mishima/Japon (5 aut., 6 aut.); Queensland Centre for Schizophrenia Research, The Park, Centre for Mental Health/Wacol/Australie (7 aut.); Department of Psychiatry, University of Queensland/Brisbane/Australie (7 aut.); Mental Health Clinical Research Center and Department of Psychiatry, University of Iowa College of Medicine/Iowa City/Etats-Unis (8 aut.); Department of Psychiatry, Mount Sinai School of Medicine/New York/Etats-Unis (9 aut.); Department of Psychiatry, University of Pennsylvania/Philadelphia/Etats-Unis (10 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | American journal of human genetics; ISSN 0002-9297; Coden AJHGAG; Etats-Unis; Da. 2004; Vol. 75; No. 4; Pp. 624-638; Bibl. 3 p.1/4 |
LA : | Anglais |
EA : | Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia-and, more recently, for bipolar disorder-on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples. |
CC : | 002B23A; 002A07C03; 002B18C06A |
FD : | Schizophrénie; Polymorphisme; Amine; Récepteur biologique; Chromosome 4; Chromosome B4; Gène; Chromosome C6; Carte génétique; Sensibilité; Pathogénie; Déterminisme génétique; Prédisposition; Génétique; Homme; Association génétique |
FG : | Psychose |
ED : | Schizophrenia; Polymorphism; Amine; Biological receptor; Chromosome 4; Chromosome B4; Gene; Chromosome C6; Genetic mapping; Sensitivity; Pathogenesis; Genetic determinism; Predisposition; Genetics; Human |
EG : | Psychosis |
SD : | Esquizofrenia; Polimorfismo; Amina; Receptor biológico; Cromosoma 4; Cromosoma B4; Gen; Cromosoma C6; Mapa genético; Sensibilidad; Patogenia; Determinismo genético; Predisposición; Genética; Hombre |
LO : | INIST-2610.354000122286160080 |
ID : | 05-0039546 |
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Pascal:05-0039546Le document en format XML
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<series><title level="j" type="main">American journal of human genetics</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amine</term>
<term>Biological receptor</term>
<term>Chromosome 4</term>
<term>Chromosome B4</term>
<term>Chromosome C6</term>
<term>Gene</term>
<term>Genetic determinism</term>
<term>Genetic mapping</term>
<term>Genetics</term>
<term>Human</term>
<term>Pathogenesis</term>
<term>Polymorphism</term>
<term>Predisposition</term>
<term>Schizophrenia</term>
<term>Sensitivity</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Schizophrénie</term>
<term>Polymorphisme</term>
<term>Amine</term>
<term>Récepteur biologique</term>
<term>Chromosome 4</term>
<term>Chromosome B4</term>
<term>Gène</term>
<term>Chromosome C6</term>
<term>Carte génétique</term>
<term>Sensibilité</term>
<term>Pathogénie</term>
<term>Déterminisme génétique</term>
<term>Prédisposition</term>
<term>Génétique</term>
<term>Homme</term>
<term>Association génétique</term>
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<front><div type="abstract" xml:lang="en">Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia-and, more recently, for bipolar disorder-on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples.</div>
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<fA14 i1="05"><s1>Department of Psychiatry, University of Queensland</s1>
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<fA14 i1="06"><s1>Mental Health Clinical Research Center and Department of Psychiatry, University of Iowa College of Medicine</s1>
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<fA14 i1="07"><s1>Department of Psychiatry, Mount Sinai School of Medicine</s1>
<s2>New York</s2>
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<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Department of Psychiatry, University of Pennsylvania</s1>
<s2>Philadelphia</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA20><s1>624-638</s1>
</fA20>
<fA21><s1>2004</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
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<fA47 i1="01" i2="1"><s0>05-0039546</s0>
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<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>American journal of human genetics</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia-and, more recently, for bipolar disorder-on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples.</s0>
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<fC03 i1="01" i2="X" l="FRE"><s0>Schizophrénie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Schizophrenia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Esquizofrenia</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Polymorphisme</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Polymorphism</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Polimorfismo</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Amine</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Amine</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Amina</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Récepteur biologique</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Biological receptor</s0>
<s5>05</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Receptor biológico</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Chromosome 4</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Chromosome 4</s0>
<s5>06</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Cromosoma 4</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Chromosome B4</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Chromosome B4</s0>
<s5>08</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Cromosoma B4</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Gène</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Gene</s0>
<s5>09</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Gen</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Chromosome C6</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Chromosome C6</s0>
<s5>11</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Cromosoma C6</s0>
<s5>11</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Carte génétique</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Genetic mapping</s0>
<s5>12</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Mapa genético</s0>
<s5>12</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Sensibilité</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Sensitivity</s0>
<s5>14</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Sensibilidad</s0>
<s5>14</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Pathogénie</s0>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Pathogenesis</s0>
<s5>15</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Patogenia</s0>
<s5>15</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Déterminisme génétique</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Genetic determinism</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Determinismo genético</s0>
<s5>17</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Prédisposition</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Predisposition</s0>
<s5>18</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Predisposición</s0>
<s5>18</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Génétique</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Genetics</s0>
<s5>19</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Genética</s0>
<s5>19</s5>
</fC03>
<fC03 i1="15" i2="X" l="FRE"><s0>Homme</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="ENG"><s0>Human</s0>
<s5>20</s5>
</fC03>
<fC03 i1="15" i2="X" l="SPA"><s0>Hombre</s0>
<s5>20</s5>
</fC03>
<fC03 i1="16" i2="X" l="FRE"><s0>Association génétique</s0>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Psychose</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Psychosis</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Psicosis</s0>
<s5>37</s5>
</fC07>
<fN21><s1>017</s1>
</fN21>
<fN44 i1="01"><s1>PSI</s1>
</fN44>
<fN82><s1>PSI</s1>
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<server><NO>PASCAL 05-0039546 INIST</NO>
<ET>Polymorphisms in the Trace Amine Receptor 4 (TRAR4) gene on chromosome 6q23.2 are associated with susceptibility to schizophrenia</ET>
<AU>DUAN (Jubao); MARTINEZ (Maria); SANDERS (Alan R.); CUIPING HOU; SAITOU (Naruya); KITANO (Takashi); MOWRY (Bryan J.); CROWE (Raymond R.); SILVERMAN (Jeremy M.); LEVINSON (Douglas F.); GEJMAN (Pablo V.)</AU>
<AF>Center for Psychiatric Genetics, Department of Psychiatry and Behavioral Sciences, Evanston Northwestern Healthcare and Feinberg School of Medicine, Northwestern University/Evanston, IL/Etats-Unis (1 aut., 3 aut., 4 aut., 11 aut.); Méthodologie Statistique et Epidémiologie Génétique des Maladies Multifactorielles, INSERM/Evry/France (2 aut.); Division of Population Genetics, National Institute of Genetics/Mishima/Japon (5 aut., 6 aut.); Queensland Centre for Schizophrenia Research, The Park, Centre for Mental Health/Wacol/Australie (7 aut.); Department of Psychiatry, University of Queensland/Brisbane/Australie (7 aut.); Mental Health Clinical Research Center and Department of Psychiatry, University of Iowa College of Medicine/Iowa City/Etats-Unis (8 aut.); Department of Psychiatry, Mount Sinai School of Medicine/New York/Etats-Unis (9 aut.); Department of Psychiatry, University of Pennsylvania/Philadelphia/Etats-Unis (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>American journal of human genetics; ISSN 0002-9297; Coden AJHGAG; Etats-Unis; Da. 2004; Vol. 75; No. 4; Pp. 624-638; Bibl. 3 p.1/4</SO>
<LA>Anglais</LA>
<EA>Several linkage studies across multiple population groups provide convergent support for a susceptibility locus for schizophrenia-and, more recently, for bipolar disorder-on chromosome 6q13-q26. We genotyped 192 European-ancestry and African American (AA) pedigrees with schizophrenia from samples that previously showed linkage evidence to 6q13-q26, focusing on the MOXD1-STX7-TRARs gene cluster at 6q23.2, which contains a number of prime candidate genes for schizophrenia. Thirty-one screening single-nucleotide polymorphisms (SNPs) were selected, providing a minimum coverage of at least 1 SNP/20 kb. The association observed with rs4305745 (P = .0014) within the TRAR4 (trace amine receptor 4) gene remained significant after correction for multiple testing. Evidence for association was proportionally stronger in the smaller AA sample. We performed database searches and sequenced genomic DNA in a 30-proband subsample to obtain a high-density map of 23 SNPs spanning 21.6 kb of this gene. Single-SNP analyses and also haplotype analyses revealed that rs4305745 and/or two other polymorphisms in perfect linkage disequilibrium (LD) with rs4305745 appear to be the most likely variants underlying the association of the TRAR4 region with schizophrenia. Comparative genomic analyses further revealed that rs4305745 and/or the associated polymorphisms in complete LD with rs4305745 could potentially affect gene expression. Moreover, RT-PCR studies of various human tissues, including brain, confirm that TRAR4 is preferentially expressed in those brain regions that have been implicated in the pathophysiology of schizophrenia. These data provide strong preliminary evidence that TRAR4 is a candidate gene for schizophrenia; replication is currently being attempted in additional clinical samples.</EA>
<CC>002B23A; 002A07C03; 002B18C06A</CC>
<FD>Schizophrénie; Polymorphisme; Amine; Récepteur biologique; Chromosome 4; Chromosome B4; Gène; Chromosome C6; Carte génétique; Sensibilité; Pathogénie; Déterminisme génétique; Prédisposition; Génétique; Homme; Association génétique</FD>
<FG>Psychose</FG>
<ED>Schizophrenia; Polymorphism; Amine; Biological receptor; Chromosome 4; Chromosome B4; Gene; Chromosome C6; Genetic mapping; Sensitivity; Pathogenesis; Genetic determinism; Predisposition; Genetics; Human</ED>
<EG>Psychosis</EG>
<SD>Esquizofrenia; Polimorfismo; Amina; Receptor biológico; Cromosoma 4; Cromosoma B4; Gen; Cromosoma C6; Mapa genético; Sensibilidad; Patogenia; Determinismo genético; Predisposición; Genética; Hombre</SD>
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