Genetic and expression analyses of the STOP ( MAP6) gene in schizophrenia
Accumulating evidence suggests that the pathologic lesions of schizophrenia may in part be due to the altered cytoskeletal architecture of neurons. Microtubule-associated proteins (MAPs) that bind to cytoskeletal microtubules to stabilize their assembly are prominently expressed in neurons. Of the M...
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| Veröffentlicht in: | Schizophrenia research 2006-06, Vol.84 (2), p.244-252 |
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| creator | Shimizu, Hiromitsu Iwayama, Yoshimi Yamada, Kazuo Toyota, Tomoko Minabe, Yoshio Nakamura, Kauhiko Nakajima, Mizuho Hattori, Eiji Mori, Norio Osumi, Noriko Yoshikawa, Takeo |
| description | Accumulating evidence suggests that the pathologic lesions of schizophrenia may in part be due to the altered cytoskeletal architecture of neurons. Microtubule-associated proteins (MAPs) that bind to cytoskeletal microtubules to stabilize their assembly are prominently expressed in neurons. Of the MAPs, MAP6 (STOP) has a particular relevance to schizophrenia pathology, since mice deficient in the gene display neuroleptic-responsive behavioral defects. Here we examined the genetic contribution of
MAP6 to schizophrenia in a case (
n
=
570) –control (
n
=
570) study, using dense single nucleotide polymorphism (SNP) markers. We detected nominal allelic (
p
=
0.0291) and haplotypic (global
p
=
0.0343 for 2 SNP-window, global
p
=
0.0138 for 3 SNP-window) associations between the 3′ genomic interval of the gene and schizophrenia.
MAP6 transcripts are expressed as two isoforms. A postmortem brain expression study showed up-regulation of mRNA isoform 2 in the prefrontal cortex (Brodmann's area 46) of patients with schizophrenia. These data suggest that the contribution of
MAP6 to the processes that lead to schizophrenia should be further investigated. |
| doi_str_mv | 10.1016/j.schres.2006.03.017 |
| format | Article |
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MAP6 to schizophrenia in a case (
n
=
570) –control (
n
=
570) study, using dense single nucleotide polymorphism (SNP) markers. We detected nominal allelic (
p
=
0.0291) and haplotypic (global
p
=
0.0343 for 2 SNP-window, global
p
=
0.0138 for 3 SNP-window) associations between the 3′ genomic interval of the gene and schizophrenia.
MAP6 transcripts are expressed as two isoforms. A postmortem brain expression study showed up-regulation of mRNA isoform 2 in the prefrontal cortex (Brodmann's area 46) of patients with schizophrenia. These data suggest that the contribution of
MAP6 to the processes that lead to schizophrenia should be further investigated.</description><identifier>ISSN: 0920-9964</identifier><identifier>EISSN: 1573-2509</identifier><identifier>DOI: 10.1016/j.schres.2006.03.017</identifier><identifier>PMID: 16624526</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Adult ; Adult and adolescent clinical studies ; Biological and medical sciences ; Brain - pathology ; Case-Control Studies ; Cytoskeleton ; Female ; Gene Expression ; Gene Frequency ; Genotype ; Haplotype ; Haplotypes ; Humans ; Isoform ; Male ; Medical sciences ; Microtubule-associated protein ; Microtubule-Associated Proteins - genetics ; Middle Aged ; Polymorphism, Single Nucleotide ; Postmortem brain ; Protein Isoforms ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger ; Schizophrenia ; Schizophrenia - genetics ; Schizophrenia - pathology</subject><ispartof>Schizophrenia research, 2006-06, Vol.84 (2), p.244-252</ispartof><rights>2006 Elsevier B.V.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-f6de1fc127f418f9bb4ecd5591045b6d438045660d98dbc1ba0cd00ed69fb003</citedby><cites>FETCH-LOGICAL-c390t-f6de1fc127f418f9bb4ecd5591045b6d438045660d98dbc1ba0cd00ed69fb003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.schres.2006.03.017$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17799848$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16624526$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shimizu, Hiromitsu</creatorcontrib><creatorcontrib>Iwayama, Yoshimi</creatorcontrib><creatorcontrib>Yamada, Kazuo</creatorcontrib><creatorcontrib>Toyota, Tomoko</creatorcontrib><creatorcontrib>Minabe, Yoshio</creatorcontrib><creatorcontrib>Nakamura, Kauhiko</creatorcontrib><creatorcontrib>Nakajima, Mizuho</creatorcontrib><creatorcontrib>Hattori, Eiji</creatorcontrib><creatorcontrib>Mori, Norio</creatorcontrib><creatorcontrib>Osumi, Noriko</creatorcontrib><creatorcontrib>Yoshikawa, Takeo</creatorcontrib><title>Genetic and expression analyses of the STOP ( MAP6) gene in schizophrenia</title><title>Schizophrenia research</title><addtitle>Schizophr Res</addtitle><description>Accumulating evidence suggests that the pathologic lesions of schizophrenia may in part be due to the altered cytoskeletal architecture of neurons. Microtubule-associated proteins (MAPs) that bind to cytoskeletal microtubules to stabilize their assembly are prominently expressed in neurons. Of the MAPs, MAP6 (STOP) has a particular relevance to schizophrenia pathology, since mice deficient in the gene display neuroleptic-responsive behavioral defects. Here we examined the genetic contribution of
MAP6 to schizophrenia in a case (
n
=
570) –control (
n
=
570) study, using dense single nucleotide polymorphism (SNP) markers. We detected nominal allelic (
p
=
0.0291) and haplotypic (global
p
=
0.0343 for 2 SNP-window, global
p
=
0.0138 for 3 SNP-window) associations between the 3′ genomic interval of the gene and schizophrenia.
MAP6 transcripts are expressed as two isoforms. A postmortem brain expression study showed up-regulation of mRNA isoform 2 in the prefrontal cortex (Brodmann's area 46) of patients with schizophrenia. These data suggest that the contribution of
MAP6 to the processes that lead to schizophrenia should be further investigated.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Case-Control Studies</subject><subject>Cytoskeleton</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Frequency</subject><subject>Genotype</subject><subject>Haplotype</subject><subject>Haplotypes</subject><subject>Humans</subject><subject>Isoform</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microtubule-associated protein</subject><subject>Microtubule-Associated Proteins - genetics</subject><subject>Middle Aged</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Postmortem brain</subject><subject>Protein Isoforms</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger</subject><subject>Schizophrenia</subject><subject>Schizophrenia - genetics</subject><subject>Schizophrenia - pathology</subject><issn>0920-9964</issn><issn>1573-2509</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMtKAzEUhoMoWi9vIJKNoosZT-aSmWyEUryB0oLdh0xyoinTmZpMRX16Iy24c5UEvv_kPx8hpwxSBoxfL9Kg3zyGNAPgKeQpsGqHjFhZ5UlWgtglIxAZJELw4oAchrAAAFZCtU8OGOdZUWZ8RB7vscPBaao6Q_FzFQcG13fxqdqvgIH2lg5vSF_m0xm9pM_jGb-irzFDXUdjAffdr2KLzqljsmdVG_Bkex6R-d3tfPKQPE3vHyfjp0TnAobEcoPMapZVtmC1FU1ToDZlKRgUZcNNkdfxwjkYUZtGs0aBNgBouLANQH5ELjZjV75_X2MY5NIFjW2rOuzXQfJKxI1FFcFiA2rfh-DRypV3S-W_JAP5a1Au5Mag_DUoIZfRYIydbeevmyWav9BWWQTOt4AKWrXWq0678MdVsUBd1JG72XAYZXw49PE3h51G4zzqQZre_d_kB0Mbj5U</recordid><startdate>20060601</startdate><enddate>20060601</enddate><creator>Shimizu, Hiromitsu</creator><creator>Iwayama, Yoshimi</creator><creator>Yamada, Kazuo</creator><creator>Toyota, Tomoko</creator><creator>Minabe, Yoshio</creator><creator>Nakamura, Kauhiko</creator><creator>Nakajima, Mizuho</creator><creator>Hattori, Eiji</creator><creator>Mori, Norio</creator><creator>Osumi, Noriko</creator><creator>Yoshikawa, Takeo</creator><general>Elsevier B.V</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20060601</creationdate><title>Genetic and expression analyses of the STOP ( MAP6) gene in schizophrenia</title><author>Shimizu, Hiromitsu ; Iwayama, Yoshimi ; Yamada, Kazuo ; Toyota, Tomoko ; Minabe, Yoshio ; Nakamura, Kauhiko ; Nakajima, Mizuho ; Hattori, Eiji ; Mori, Norio ; Osumi, Noriko ; Yoshikawa, Takeo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-f6de1fc127f418f9bb4ecd5591045b6d438045660d98dbc1ba0cd00ed69fb003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Case-Control Studies</topic><topic>Cytoskeleton</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Frequency</topic><topic>Genotype</topic><topic>Haplotype</topic><topic>Haplotypes</topic><topic>Humans</topic><topic>Isoform</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microtubule-associated protein</topic><topic>Microtubule-Associated Proteins - genetics</topic><topic>Middle Aged</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Postmortem brain</topic><topic>Protein Isoforms</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger</topic><topic>Schizophrenia</topic><topic>Schizophrenia - genetics</topic><topic>Schizophrenia - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimizu, Hiromitsu</creatorcontrib><creatorcontrib>Iwayama, Yoshimi</creatorcontrib><creatorcontrib>Yamada, Kazuo</creatorcontrib><creatorcontrib>Toyota, Tomoko</creatorcontrib><creatorcontrib>Minabe, Yoshio</creatorcontrib><creatorcontrib>Nakamura, Kauhiko</creatorcontrib><creatorcontrib>Nakajima, Mizuho</creatorcontrib><creatorcontrib>Hattori, Eiji</creatorcontrib><creatorcontrib>Mori, Norio</creatorcontrib><creatorcontrib>Osumi, Noriko</creatorcontrib><creatorcontrib>Yoshikawa, Takeo</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Schizophrenia research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimizu, Hiromitsu</au><au>Iwayama, Yoshimi</au><au>Yamada, Kazuo</au><au>Toyota, Tomoko</au><au>Minabe, Yoshio</au><au>Nakamura, Kauhiko</au><au>Nakajima, Mizuho</au><au>Hattori, Eiji</au><au>Mori, Norio</au><au>Osumi, Noriko</au><au>Yoshikawa, Takeo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic and expression analyses of the STOP ( MAP6) gene in schizophrenia</atitle><jtitle>Schizophrenia research</jtitle><addtitle>Schizophr Res</addtitle><date>2006-06-01</date><risdate>2006</risdate><volume>84</volume><issue>2</issue><spage>244</spage><epage>252</epage><pages>244-252</pages><issn>0920-9964</issn><eissn>1573-2509</eissn><abstract>Accumulating evidence suggests that the pathologic lesions of schizophrenia may in part be due to the altered cytoskeletal architecture of neurons. Microtubule-associated proteins (MAPs) that bind to cytoskeletal microtubules to stabilize their assembly are prominently expressed in neurons. Of the MAPs, MAP6 (STOP) has a particular relevance to schizophrenia pathology, since mice deficient in the gene display neuroleptic-responsive behavioral defects. Here we examined the genetic contribution of
MAP6 to schizophrenia in a case (
n
=
570) –control (
n
=
570) study, using dense single nucleotide polymorphism (SNP) markers. We detected nominal allelic (
p
=
0.0291) and haplotypic (global
p
=
0.0343 for 2 SNP-window, global
p
=
0.0138 for 3 SNP-window) associations between the 3′ genomic interval of the gene and schizophrenia.
MAP6 transcripts are expressed as two isoforms. A postmortem brain expression study showed up-regulation of mRNA isoform 2 in the prefrontal cortex (Brodmann's area 46) of patients with schizophrenia. These data suggest that the contribution of
MAP6 to the processes that lead to schizophrenia should be further investigated.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>16624526</pmid><doi>10.1016/j.schres.2006.03.017</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Schizophrenia research, 2006-06, Vol.84 (2), p.244-252 |
| issn | 0920-9964 1573-2509 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Adult Adult and adolescent clinical studies Biological and medical sciences Brain - pathology Case-Control Studies Cytoskeleton Female Gene Expression Gene Frequency Genotype Haplotype Haplotypes Humans Isoform Male Medical sciences Microtubule-associated protein Microtubule-Associated Proteins - genetics Middle Aged Polymorphism, Single Nucleotide Postmortem brain Protein Isoforms Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger Schizophrenia Schizophrenia - genetics Schizophrenia - pathology |
| title | Genetic and expression analyses of the STOP ( MAP6) gene in schizophrenia |
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