No association between a polymorphic CAG repeat in the human potassium channel gene hKCa3 and bipolar disorder
A recent case‐control study suggested that modest enlargements of a CAG repeat in the hKCa3 potassium channel may be associated with bipolar disorder. We tried to replicate this result in a UK Caucasian sample of 203 DSM‐IV bipolar I disorder patients and 206 controls group‐matched for age and sex....
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Veröffentlicht in: | American journal of medical genetics 1999-02, Vol.88 (1), p.57-60 |
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container_title | American journal of medical genetics |
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creator | Guy, C.A. Bowen, T. Williams, N. Jones, I.R. McCandless, F. McGuffin, P. Owen, M.J. Craddock, N. O'Donovan, M.C. |
description | A recent case‐control study suggested that modest enlargements of a CAG repeat in the hKCa3 potassium channel may be associated with bipolar disorder. We tried to replicate this result in a UK Caucasian sample of 203 DSM‐IV bipolar I disorder patients and 206 controls group‐matched for age and sex. Using the same model of analysis as the earlier study, bipolar probands did not have a higher frequency of alleles with greater than 19 repeats than controls (χ2 = 1.44, 1 df, P = 0.23). Similarly, comparison of the distributions of repeat sizes between probands and controls did not approach statistical significance (Mann‐Whitney U test, P = 0.35). We conclude that our data provide no support for the hypothesis that variation at the hKCa3 gene contributes to susceptibility to bipolar disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:57–60, 1999. © 1999 Wiley‐Liss, Inc. |
doi_str_mv | 10.1002/(SICI)1096-8628(19990205)88:1<57::AID-AJMG10>3.0.CO;2-6 |
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We tried to replicate this result in a UK Caucasian sample of 203 DSM‐IV bipolar I disorder patients and 206 controls group‐matched for age and sex. Using the same model of analysis as the earlier study, bipolar probands did not have a higher frequency of alleles with greater than 19 repeats than controls (χ2 = 1.44, 1 df, P = 0.23). Similarly, comparison of the distributions of repeat sizes between probands and controls did not approach statistical significance (Mann‐Whitney U test, P = 0.35). We conclude that our data provide no support for the hypothesis that variation at the hKCa3 gene contributes to susceptibility to bipolar disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:57–60, 1999. © 1999 Wiley‐Liss, Inc.</description><identifier>ISSN: 0148-7299</identifier><identifier>EISSN: 1096-8628</identifier><identifier>DOI: 10.1002/(SICI)1096-8628(19990205)88:1<57::AID-AJMG10>3.0.CO;2-6</identifier><identifier>PMID: 10050968</identifier><identifier>CODEN: AJMGDA</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Adult and adolescent clinical studies ; Alleles ; Biological and medical sciences ; bipolar disorder ; Bipolar Disorder - etiology ; Bipolar Disorder - genetics ; Bipolar disorders ; Case-Control Studies ; Female ; Genotype ; hKCa3 ; human potassium channel gene ; Humans ; Male ; Medical sciences ; Middle Aged ; Mood disorders ; polymorphic CAG repeat ; Polymorphism, Genetic ; Potassium Channels - genetics ; Potassium Channels, Calcium-Activated ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Small-Conductance Calcium-Activated Potassium Channels ; Trinucleotide Repeats - genetics</subject><ispartof>American journal of medical genetics, 1999-02, Vol.88 (1), p.57-60</ispartof><rights>Copyright © 1999 Wiley‐Liss, Inc.</rights><rights>1999 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4360-c1a55fa02e6e57f41e07bde933649aa51f8621db09d27c14912f48de922c2fa93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1674754$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10050968$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guy, C.A.</creatorcontrib><creatorcontrib>Bowen, T.</creatorcontrib><creatorcontrib>Williams, N.</creatorcontrib><creatorcontrib>Jones, I.R.</creatorcontrib><creatorcontrib>McCandless, F.</creatorcontrib><creatorcontrib>McGuffin, P.</creatorcontrib><creatorcontrib>Owen, M.J.</creatorcontrib><creatorcontrib>Craddock, N.</creatorcontrib><creatorcontrib>O'Donovan, M.C.</creatorcontrib><title>No association between a polymorphic CAG repeat in the human potassium channel gene hKCa3 and bipolar disorder</title><title>American journal of medical genetics</title><addtitle>Am. J. Med. Genet</addtitle><description>A recent case‐control study suggested that modest enlargements of a CAG repeat in the hKCa3 potassium channel may be associated with bipolar disorder. We tried to replicate this result in a UK Caucasian sample of 203 DSM‐IV bipolar I disorder patients and 206 controls group‐matched for age and sex. Using the same model of analysis as the earlier study, bipolar probands did not have a higher frequency of alleles with greater than 19 repeats than controls (χ2 = 1.44, 1 df, P = 0.23). Similarly, comparison of the distributions of repeat sizes between probands and controls did not approach statistical significance (Mann‐Whitney U test, P = 0.35). We conclude that our data provide no support for the hypothesis that variation at the hKCa3 gene contributes to susceptibility to bipolar disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:57–60, 1999. © 1999 Wiley‐Liss, Inc.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>bipolar disorder</subject><subject>Bipolar Disorder - etiology</subject><subject>Bipolar Disorder - genetics</subject><subject>Bipolar disorders</subject><subject>Case-Control Studies</subject><subject>Female</subject><subject>Genotype</subject><subject>hKCa3</subject><subject>human potassium channel gene</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mood disorders</subject><subject>polymorphic CAG repeat</subject><subject>Polymorphism, Genetic</subject><subject>Potassium Channels - genetics</subject><subject>Potassium Channels, Calcium-Activated</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Small-Conductance Calcium-Activated Potassium Channels</subject><subject>Trinucleotide Repeats - genetics</subject><issn>0148-7299</issn><issn>1096-8628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkVFv0zAUhSMEYmXwF5AfENoeUmwnduKCNpVAS2GsQoAmnq4cx1kNiRPsVKP_HlcpAwkknmxdf_fc43ui6JzgKcGYPjv5uCpWpwQLHuec5idECIEpZqd5PiMvWDabzVev4vnb90uCz5Ipnhbr5zTmd6LJbc_daIJJmscZFeIoeuD9V4xJKND70VGYwQKXTyJ72SHpfaeMHExnUamHG60tkqjvml3buX5jFCrmS-R0r-WAjEXDRqPNtpU2MENoNtsWqY20VjfoWtvw-K6QCZK2QqUJMtKhyvjOVdo9jO7VsvH60eE8jj4vXn8q3sQX6-WqmF_EKk04jhWRjNUSU801y-qUaJyVlRZJwlMhJSN1-CGpSiwqmimSCkLrNA8ApYrWUiTH0dNRt3fd9632A7TGK9000upu64ELJlKe8wBejaBynfdO19A700q3A4JhHwXAPgrYrxX2a4VfUUAe7sAygBAFjFFAAhiKNVDYKz8-WNiWra7-0B13H4AnB0B6JZvaSauM_83xLM1YGrAvI3ZjGr37y97_3P3T3KEStONR2_hB_7jVlu4b8CzJGFxdLgEvkg8pXbyEPPkJG6LAaA</recordid><startdate>19990205</startdate><enddate>19990205</enddate><creator>Guy, C.A.</creator><creator>Bowen, T.</creator><creator>Williams, N.</creator><creator>Jones, I.R.</creator><creator>McCandless, F.</creator><creator>McGuffin, P.</creator><creator>Owen, M.J.</creator><creator>Craddock, N.</creator><creator>O'Donovan, M.C.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><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>19990205</creationdate><title>No association between a polymorphic CAG repeat in the human potassium channel gene hKCa3 and bipolar disorder</title><author>Guy, C.A. ; Bowen, T. ; Williams, N. ; Jones, I.R. ; McCandless, F. ; McGuffin, P. ; Owen, M.J. ; Craddock, N. ; O'Donovan, M.C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4360-c1a55fa02e6e57f41e07bde933649aa51f8621db09d27c14912f48de922c2fa93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>bipolar disorder</topic><topic>Bipolar Disorder - etiology</topic><topic>Bipolar Disorder - genetics</topic><topic>Bipolar disorders</topic><topic>Case-Control Studies</topic><topic>Female</topic><topic>Genotype</topic><topic>hKCa3</topic><topic>human potassium channel gene</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Mood disorders</topic><topic>polymorphic CAG repeat</topic><topic>Polymorphism, Genetic</topic><topic>Potassium Channels - genetics</topic><topic>Potassium Channels, Calcium-Activated</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Small-Conductance Calcium-Activated Potassium Channels</topic><topic>Trinucleotide Repeats - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guy, C.A.</creatorcontrib><creatorcontrib>Bowen, T.</creatorcontrib><creatorcontrib>Williams, N.</creatorcontrib><creatorcontrib>Jones, I.R.</creatorcontrib><creatorcontrib>McCandless, F.</creatorcontrib><creatorcontrib>McGuffin, P.</creatorcontrib><creatorcontrib>Owen, M.J.</creatorcontrib><creatorcontrib>Craddock, N.</creatorcontrib><creatorcontrib>O'Donovan, M.C.</creatorcontrib><collection>Istex</collection><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>American journal of medical genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guy, C.A.</au><au>Bowen, T.</au><au>Williams, N.</au><au>Jones, I.R.</au><au>McCandless, F.</au><au>McGuffin, P.</au><au>Owen, M.J.</au><au>Craddock, N.</au><au>O'Donovan, M.C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>No association between a polymorphic CAG repeat in the human potassium channel gene hKCa3 and bipolar disorder</atitle><jtitle>American journal of medical genetics</jtitle><addtitle>Am. J. Med. Genet</addtitle><date>1999-02-05</date><risdate>1999</risdate><volume>88</volume><issue>1</issue><spage>57</spage><epage>60</epage><pages>57-60</pages><issn>0148-7299</issn><eissn>1096-8628</eissn><coden>AJMGDA</coden><abstract>A recent case‐control study suggested that modest enlargements of a CAG repeat in the hKCa3 potassium channel may be associated with bipolar disorder. We tried to replicate this result in a UK Caucasian sample of 203 DSM‐IV bipolar I disorder patients and 206 controls group‐matched for age and sex. Using the same model of analysis as the earlier study, bipolar probands did not have a higher frequency of alleles with greater than 19 repeats than controls (χ2 = 1.44, 1 df, P = 0.23). Similarly, comparison of the distributions of repeat sizes between probands and controls did not approach statistical significance (Mann‐Whitney U test, P = 0.35). We conclude that our data provide no support for the hypothesis that variation at the hKCa3 gene contributes to susceptibility to bipolar disorder. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:57–60, 1999. © 1999 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>10050968</pmid><doi>10.1002/(SICI)1096-8628(19990205)88:1<57::AID-AJMG10>3.0.CO;2-6</doi><tpages>4</tpages></addata></record> |
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subjects | Adult Adult and adolescent clinical studies Alleles Biological and medical sciences bipolar disorder Bipolar Disorder - etiology Bipolar Disorder - genetics Bipolar disorders Case-Control Studies Female Genotype hKCa3 human potassium channel gene Humans Male Medical sciences Middle Aged Mood disorders polymorphic CAG repeat Polymorphism, Genetic Potassium Channels - genetics Potassium Channels, Calcium-Activated Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Small-Conductance Calcium-Activated Potassium Channels Trinucleotide Repeats - genetics |
title | No association between a polymorphic CAG repeat in the human potassium channel gene hKCa3 and bipolar disorder |
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