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Resequencing and Association Analysis of the KALRN and EPHB1 Genes And Their Contribution to Schizophrenia Susceptibility
Our genome-wide association study of schizophrenia found association signals at the Kalirin gene (KALRN) and EPH receptor B1 gene (EPHB1) in a Japanese population. The importance of these synaptogenic pathway genes in schizophrenia is gaining independent supports. Although there has been growing int...
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| Published in: | Schizophrenia bulletin 2012-05, Vol.38 (3), p.552-560 |
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| container_title | Schizophrenia bulletin |
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| creator | KUSHIMA, Itaru NAKAMURA, Yukako INADA, Toshiya HASHIMOTO, Ryota TAKEDA, Masatoshi KAIBUCHI, Kozo IWATA, Nakao OZAKI, Norio ALEKSIC, Branko IKEDA, Masashi ITO, Yoshihito SHIINO, Tomoko OKOCHI, Tomo FUKUO, Yasuhisa UJIKE, Hiroshi SUZUKI, Michio |
| description | Our genome-wide association study of schizophrenia found association signals at the Kalirin gene (KALRN) and EPH receptor B1 gene (EPHB1) in a Japanese population. The importance of these synaptogenic pathway genes in schizophrenia is gaining independent supports. Although there has been growing interest in rare ( |
| doi_str_mv | 10.1093/schbul/sbq118 |
| format | article |
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The present study design consisted of 3 phases. At the discovery phase, we conducted resequencing analyses for all exon regions of KALRN and EPHB1 using a DNA microarray-based method. Seventeen rare (<1%) missense mutations were discovered in the first sample set (320 schizophrenic patients). After the prioritization phase based on frequencies in the second sample set (729 cases and 562 controls), we performed association analyses for each selected mutation using the third sample set (1511 cases and 1517 controls), along with a combined association analysis across all selected mutations. In KALRN, we detected a significant association between schizophrenia and P2255T (OR = 2.09, corrected P = .048, 1 tailed); this was supported in the combined association analysis (OR = 2.07, corrected P = .006, 1 tailed). We found no evidence of association of EPHB1 with schizophrenia. In silico analysis indicated the functional relevance of these rare missense mutations.
We provide evidence that multiple rare (<1%) missense mutations in KALRN may be genetic risk factors for schizophrenia.</description><identifier>ISSN: 0586-7614</identifier><identifier>EISSN: 1745-1701</identifier><identifier>DOI: 10.1093/schbul/sbq118</identifier><identifier>PMID: 21041834</identifier><identifier>CODEN: SCZBB3</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult ; Adult and adolescent clinical studies ; Association analysis ; Biological and medical sciences ; Exons - genetics ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study - methods ; Genotype ; Guanine Nucleotide Exchange Factors - genetics ; Humans ; Japan - epidemiology ; Male ; Medical sciences ; Middle Aged ; Mutation, Missense - genetics ; Protein Serine-Threonine Kinases - genetics ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Psychoses ; Receptor, EphB1 - genetics ; Regular ; Risk Factors ; Schizophrenia ; Schizophrenia - epidemiology ; Schizophrenia - genetics</subject><ispartof>Schizophrenia bulletin, 2012-05, Vol.38 (3), p.552-560</ispartof><rights>2015 INIST-CNRS</rights><rights>The Author 2010. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-d9ef48202226a28218d3c6a4dfd30e9ff9a5ed23b8d49d014ad2572194610fc93</citedby><cites>FETCH-LOGICAL-c450t-d9ef48202226a28218d3c6a4dfd30e9ff9a5ed23b8d49d014ad2572194610fc93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329972/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329972/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25855469$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21041834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>KUSHIMA, Itaru</creatorcontrib><creatorcontrib>NAKAMURA, Yukako</creatorcontrib><creatorcontrib>INADA, Toshiya</creatorcontrib><creatorcontrib>HASHIMOTO, Ryota</creatorcontrib><creatorcontrib>TAKEDA, Masatoshi</creatorcontrib><creatorcontrib>KAIBUCHI, Kozo</creatorcontrib><creatorcontrib>IWATA, Nakao</creatorcontrib><creatorcontrib>OZAKI, Norio</creatorcontrib><creatorcontrib>ALEKSIC, Branko</creatorcontrib><creatorcontrib>IKEDA, Masashi</creatorcontrib><creatorcontrib>ITO, Yoshihito</creatorcontrib><creatorcontrib>SHIINO, Tomoko</creatorcontrib><creatorcontrib>OKOCHI, Tomo</creatorcontrib><creatorcontrib>FUKUO, Yasuhisa</creatorcontrib><creatorcontrib>UJIKE, Hiroshi</creatorcontrib><creatorcontrib>SUZUKI, Michio</creatorcontrib><title>Resequencing and Association Analysis of the KALRN and EPHB1 Genes And Their Contribution to Schizophrenia Susceptibility</title><title>Schizophrenia bulletin</title><addtitle>Schizophr Bull</addtitle><description>Our genome-wide association study of schizophrenia found association signals at the Kalirin gene (KALRN) and EPH receptor B1 gene (EPHB1) in a Japanese population. The importance of these synaptogenic pathway genes in schizophrenia is gaining independent supports. Although there has been growing interest in rare (<1%) missense mutations as potential contributors to the unexplained heritability of schizophrenia, there are no population-based studies targeting rare (<1%) coding mutations with a larger effect size (eg, OR >1.5) in KALRN or EPHB1.
The present study design consisted of 3 phases. At the discovery phase, we conducted resequencing analyses for all exon regions of KALRN and EPHB1 using a DNA microarray-based method. Seventeen rare (<1%) missense mutations were discovered in the first sample set (320 schizophrenic patients). After the prioritization phase based on frequencies in the second sample set (729 cases and 562 controls), we performed association analyses for each selected mutation using the third sample set (1511 cases and 1517 controls), along with a combined association analysis across all selected mutations. In KALRN, we detected a significant association between schizophrenia and P2255T (OR = 2.09, corrected P = .048, 1 tailed); this was supported in the combined association analysis (OR = 2.07, corrected P = .006, 1 tailed). We found no evidence of association of EPHB1 with schizophrenia. In silico analysis indicated the functional relevance of these rare missense mutations.
We provide evidence that multiple rare (<1%) missense mutations in KALRN may be genetic risk factors for schizophrenia.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Association analysis</subject><subject>Biological and medical sciences</subject><subject>Exons - genetics</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Genome-Wide Association Study - methods</subject><subject>Genotype</subject><subject>Guanine Nucleotide Exchange Factors - genetics</subject><subject>Humans</subject><subject>Japan - epidemiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mutation, Missense - genetics</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Psychoses</subject><subject>Receptor, EphB1 - genetics</subject><subject>Regular</subject><subject>Risk Factors</subject><subject>Schizophrenia</subject><subject>Schizophrenia - epidemiology</subject><subject>Schizophrenia - genetics</subject><issn>0586-7614</issn><issn>1745-1701</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqN0b1vEzEYBnALgWhaGFmRFySWo_68sxekNCotIgLUltny-aNndLFT-w4p_PU1TSiwMXnwz4_e1w8ArzB6h5Gkp8UM_Tyelv4OY_EELHDHeIM7hJ-CBeKibboWsyNwXMp3hDCTLXkOjghGDAvKFmB35Yq7m100Id5CHS1clpJM0FNIES6jHnclFJg8nAYHPy3XV58f1PnXyzMML1x0pSoLbwYXMlylOOXQzw-PpwSvzRB-pu2QXQwaXs_FuO0U-jCGafcCPPN6LO7l4TwB3z6c36wum_WXi4-r5boxjKOpsdJ5JggihLSaCIKFpabVzHpLkZPeS82dJbQXlklbN9SW8I5gyVqMvJH0BLzf527nfuOscXVEPaptDhuddyrpoP69iWFQt-mHopRI2ZEa8PYQkFP9qTKpTaiLjKOOLs1FYUYlqZb_B0VICMKEZJU2e2pyKiU7_zgRRupXs2rfrNo3W_3rv9d41L-rrODNAehi9Oizrp2WP44Lzlkr6T1cw69j</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>KUSHIMA, Itaru</creator><creator>NAKAMURA, Yukako</creator><creator>INADA, Toshiya</creator><creator>HASHIMOTO, Ryota</creator><creator>TAKEDA, Masatoshi</creator><creator>KAIBUCHI, Kozo</creator><creator>IWATA, Nakao</creator><creator>OZAKI, Norio</creator><creator>ALEKSIC, Branko</creator><creator>IKEDA, Masashi</creator><creator>ITO, Yoshihito</creator><creator>SHIINO, Tomoko</creator><creator>OKOCHI, Tomo</creator><creator>FUKUO, Yasuhisa</creator><creator>UJIKE, Hiroshi</creator><creator>SUZUKI, Michio</creator><general>Oxford University Press</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><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20120501</creationdate><title>Resequencing and Association Analysis of the KALRN and EPHB1 Genes And Their Contribution to Schizophrenia Susceptibility</title><author>KUSHIMA, Itaru ; NAKAMURA, Yukako ; INADA, Toshiya ; HASHIMOTO, Ryota ; TAKEDA, Masatoshi ; KAIBUCHI, Kozo ; IWATA, Nakao ; OZAKI, Norio ; ALEKSIC, Branko ; IKEDA, Masashi ; ITO, Yoshihito ; SHIINO, Tomoko ; OKOCHI, Tomo ; FUKUO, Yasuhisa ; UJIKE, Hiroshi ; SUZUKI, Michio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-d9ef48202226a28218d3c6a4dfd30e9ff9a5ed23b8d49d014ad2572194610fc93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Association analysis</topic><topic>Biological and medical sciences</topic><topic>Exons - genetics</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Genome-Wide Association Study - methods</topic><topic>Genotype</topic><topic>Guanine Nucleotide Exchange Factors - genetics</topic><topic>Humans</topic><topic>Japan - epidemiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mutation, Missense - genetics</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Psychoses</topic><topic>Receptor, EphB1 - genetics</topic><topic>Regular</topic><topic>Risk Factors</topic><topic>Schizophrenia</topic><topic>Schizophrenia - epidemiology</topic><topic>Schizophrenia - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>KUSHIMA, Itaru</creatorcontrib><creatorcontrib>NAKAMURA, Yukako</creatorcontrib><creatorcontrib>INADA, Toshiya</creatorcontrib><creatorcontrib>HASHIMOTO, Ryota</creatorcontrib><creatorcontrib>TAKEDA, Masatoshi</creatorcontrib><creatorcontrib>KAIBUCHI, Kozo</creatorcontrib><creatorcontrib>IWATA, Nakao</creatorcontrib><creatorcontrib>OZAKI, Norio</creatorcontrib><creatorcontrib>ALEKSIC, Branko</creatorcontrib><creatorcontrib>IKEDA, Masashi</creatorcontrib><creatorcontrib>ITO, Yoshihito</creatorcontrib><creatorcontrib>SHIINO, Tomoko</creatorcontrib><creatorcontrib>OKOCHI, Tomo</creatorcontrib><creatorcontrib>FUKUO, Yasuhisa</creatorcontrib><creatorcontrib>UJIKE, Hiroshi</creatorcontrib><creatorcontrib>SUZUKI, Michio</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><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Schizophrenia bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>KUSHIMA, Itaru</au><au>NAKAMURA, Yukako</au><au>INADA, Toshiya</au><au>HASHIMOTO, Ryota</au><au>TAKEDA, Masatoshi</au><au>KAIBUCHI, Kozo</au><au>IWATA, Nakao</au><au>OZAKI, Norio</au><au>ALEKSIC, Branko</au><au>IKEDA, Masashi</au><au>ITO, Yoshihito</au><au>SHIINO, Tomoko</au><au>OKOCHI, Tomo</au><au>FUKUO, Yasuhisa</au><au>UJIKE, Hiroshi</au><au>SUZUKI, Michio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resequencing and Association Analysis of the KALRN and EPHB1 Genes And Their Contribution to Schizophrenia Susceptibility</atitle><jtitle>Schizophrenia bulletin</jtitle><addtitle>Schizophr Bull</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>38</volume><issue>3</issue><spage>552</spage><epage>560</epage><pages>552-560</pages><issn>0586-7614</issn><eissn>1745-1701</eissn><coden>SCZBB3</coden><abstract>Our genome-wide association study of schizophrenia found association signals at the Kalirin gene (KALRN) and EPH receptor B1 gene (EPHB1) in a Japanese population. The importance of these synaptogenic pathway genes in schizophrenia is gaining independent supports. Although there has been growing interest in rare (<1%) missense mutations as potential contributors to the unexplained heritability of schizophrenia, there are no population-based studies targeting rare (<1%) coding mutations with a larger effect size (eg, OR >1.5) in KALRN or EPHB1.
The present study design consisted of 3 phases. At the discovery phase, we conducted resequencing analyses for all exon regions of KALRN and EPHB1 using a DNA microarray-based method. Seventeen rare (<1%) missense mutations were discovered in the first sample set (320 schizophrenic patients). After the prioritization phase based on frequencies in the second sample set (729 cases and 562 controls), we performed association analyses for each selected mutation using the third sample set (1511 cases and 1517 controls), along with a combined association analysis across all selected mutations. In KALRN, we detected a significant association between schizophrenia and P2255T (OR = 2.09, corrected P = .048, 1 tailed); this was supported in the combined association analysis (OR = 2.07, corrected P = .006, 1 tailed). We found no evidence of association of EPHB1 with schizophrenia. In silico analysis indicated the functional relevance of these rare missense mutations.
We provide evidence that multiple rare (<1%) missense mutations in KALRN may be genetic risk factors for schizophrenia.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>21041834</pmid><doi>10.1093/schbul/sbq118</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | PubMed; Oxford University Press:Jisc Collections:OUP Read and Publish 2024-2025 (2024 collection) (Reading list) |
| subjects | Adult Adult and adolescent clinical studies Association analysis Biological and medical sciences Exons - genetics Female Genetic Predisposition to Disease Genome-Wide Association Study - methods Genotype Guanine Nucleotide Exchange Factors - genetics Humans Japan - epidemiology Male Medical sciences Middle Aged Mutation, Missense - genetics Protein Serine-Threonine Kinases - genetics Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Psychoses Receptor, EphB1 - genetics Regular Risk Factors Schizophrenia Schizophrenia - epidemiology Schizophrenia - genetics |
| title | Resequencing and Association Analysis of the KALRN and EPHB1 Genes And Their Contribution to Schizophrenia Susceptibility |
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