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Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate
The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, al...
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| Published in: | Journal of headache and pain 2011-12, Vol.12 (6), p.603-608 |
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| creator | Cox, Hannah C. Lea, Rod A. Bellis, Claire Carless, Melanie Dyer, Tom Blangero, John Griffiths, Lyn R. |
| description | The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (
P
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| doi_str_mv | 10.1007/s10194-011-0392-7 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3208049</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>902335341</sourcerecordid><originalsourceid>FETCH-LOGICAL-c501t-3b92d7fb031bca00db3c2d62615867f3a4c87ee0ab1d0a0a5e78616f72aa5b443</originalsourceid><addsrcrecordid>eNp9kU2P1SAUhonROOPoD3BjiBvHRfUApZSNibnxK07Gjbolp5S2jC29Qqvx30u94_Uj0RUnOc95OfAQcp_BEwagniYGTJcFMFaA0LxQN8gpY1wXXCh181hX-oTcSekKgIOo5W1ywnMBui5Pyf4jRo9hSdQHugyODuuEge7nBVPy60TtgCG4kfYuOHr-dnd5KR5TjI7m_mw9Lq6lX_0y0Mn3EX2GchDSwfcDjT59-jG4eEt9msdM3yW3OhyTu3d9npEPL1-8370uLt69erN7flFYCWwpRKN5q7oGBGssArSNsLyteMVkXalOYGlr5Rxgw1pAQOlUXbGqUxxRNmUpzsizQ-5-bSbXWheWiKPZRz9h_GZm9ObPTvCD6ecvRnCoodQ54NF1QJw_ry4tZvLJunHE4OY1GQ1cCClKlsnz_5JZg-SyLPUW-vAv9GpeY8gfseVlJVJuq7MDZOOcUnTdcWsGZhNvDuJNFm828UblmQe_P_c48dN0BvgBSLkVehd_3fzv1O8JVrjR</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>902098554</pqid></control><display><type>article</type><title>Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate</title><source>Publicly Available Content Database</source><source>Springer Nature - SpringerLink Journals - Fully Open Access </source><source>PubMed Central</source><creator>Cox, Hannah C. ; Lea, Rod A. ; Bellis, Claire ; Carless, Melanie ; Dyer, Tom ; Blangero, John ; Griffiths, Lyn R.</creator><creatorcontrib>Cox, Hannah C. ; Lea, Rod A. ; Bellis, Claire ; Carless, Melanie ; Dyer, Tom ; Blangero, John ; Griffiths, Lyn R.</creatorcontrib><description>The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (
P
< 0.05) with migraine. Two SNPs, rs73532286 and rs6426929, separated by approximately 0.1 kb, displayed complete LD (
r
2
= 1.00,
D
′ = 1.00,
D
′ 95% CI = 0.96–1.00). In all cases, the minor allele led to a decrease in migraine risk (beta coefficient = 0.286–0.315), suggesting that common gene variants confer an increased risk of migraine in the Norfolk pedigree. This effect may be explained by founder effect in this genetic isolate. This study provides evidence for association of variants in the KCNN3 ion channel gene with migraine susceptibility in the Norfolk genetic isolate with the rarer allelic variants conferring a possible protective role. This the first comprehensive analysis of this potential candidate gene in migraine and also the first study that has utilised the unique Norfolk Island large pedigree isolate to implicate a specific migraine gene. Studies of additional variants in KCNN3 in the Norfolk pedigree are now required (e.g. polyglutamine variants) and further analyses in other population data sets are required to clarify the association of the KCNN3 gene and migraine risk in the general outbred population.</description><identifier>ISSN: 1129-2369</identifier><identifier>EISSN: 1129-2377</identifier><identifier>DOI: 10.1007/s10194-011-0392-7</identifier><identifier>PMID: 22030984</identifier><identifier>CODEN: JHPOAT</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Adult ; Aged ; Female ; Genes ; Genetic Predisposition to Disease - genetics ; Genetic Variation - genetics ; Humans ; Indexing in process ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Migraine ; Migraine Disorders - genetics ; Migraine Disorders - metabolism ; Migraine Disorders - physiopathology ; Neurology ; Original ; Pain Medicine ; Pedigree ; Polymorphism, Single Nucleotide - genetics ; Small-Conductance Calcium-Activated Potassium Channels - genetics</subject><ispartof>Journal of headache and pain, 2011-12, Vol.12 (6), p.603-608</ispartof><rights>The Author(s) 2011</rights><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-3b92d7fb031bca00db3c2d62615867f3a4c87ee0ab1d0a0a5e78616f72aa5b443</citedby><cites>FETCH-LOGICAL-c501t-3b92d7fb031bca00db3c2d62615867f3a4c87ee0ab1d0a0a5e78616f72aa5b443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/902098554/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/902098554?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22030984$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cox, Hannah C.</creatorcontrib><creatorcontrib>Lea, Rod A.</creatorcontrib><creatorcontrib>Bellis, Claire</creatorcontrib><creatorcontrib>Carless, Melanie</creatorcontrib><creatorcontrib>Dyer, Tom</creatorcontrib><creatorcontrib>Blangero, John</creatorcontrib><creatorcontrib>Griffiths, Lyn R.</creatorcontrib><title>Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate</title><title>Journal of headache and pain</title><addtitle>J Headache Pain</addtitle><addtitle>J Headache Pain</addtitle><description>The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (
P
< 0.05) with migraine. Two SNPs, rs73532286 and rs6426929, separated by approximately 0.1 kb, displayed complete LD (
r
2
= 1.00,
D
′ = 1.00,
D
′ 95% CI = 0.96–1.00). In all cases, the minor allele led to a decrease in migraine risk (beta coefficient = 0.286–0.315), suggesting that common gene variants confer an increased risk of migraine in the Norfolk pedigree. This effect may be explained by founder effect in this genetic isolate. This study provides evidence for association of variants in the KCNN3 ion channel gene with migraine susceptibility in the Norfolk genetic isolate with the rarer allelic variants conferring a possible protective role. This the first comprehensive analysis of this potential candidate gene in migraine and also the first study that has utilised the unique Norfolk Island large pedigree isolate to implicate a specific migraine gene. Studies of additional variants in KCNN3 in the Norfolk pedigree are now required (e.g. polyglutamine variants) and further analyses in other population data sets are required to clarify the association of the KCNN3 gene and migraine risk in the general outbred population.</description><subject>Adult</subject><subject>Aged</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic Predisposition to Disease - genetics</subject><subject>Genetic Variation - genetics</subject><subject>Humans</subject><subject>Indexing in process</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Migraine</subject><subject>Migraine Disorders - genetics</subject><subject>Migraine Disorders - metabolism</subject><subject>Migraine Disorders - physiopathology</subject><subject>Neurology</subject><subject>Original</subject><subject>Pain Medicine</subject><subject>Pedigree</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Small-Conductance Calcium-Activated Potassium Channels - genetics</subject><issn>1129-2369</issn><issn>1129-2377</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNp9kU2P1SAUhonROOPoD3BjiBvHRfUApZSNibnxK07Gjbolp5S2jC29Qqvx30u94_Uj0RUnOc95OfAQcp_BEwagniYGTJcFMFaA0LxQN8gpY1wXXCh181hX-oTcSekKgIOo5W1ywnMBui5Pyf4jRo9hSdQHugyODuuEge7nBVPy60TtgCG4kfYuOHr-dnd5KR5TjI7m_mw9Lq6lX_0y0Mn3EX2GchDSwfcDjT59-jG4eEt9msdM3yW3OhyTu3d9npEPL1-8370uLt69erN7flFYCWwpRKN5q7oGBGssArSNsLyteMVkXalOYGlr5Rxgw1pAQOlUXbGqUxxRNmUpzsizQ-5-bSbXWheWiKPZRz9h_GZm9ObPTvCD6ecvRnCoodQ54NF1QJw_ry4tZvLJunHE4OY1GQ1cCClKlsnz_5JZg-SyLPUW-vAv9GpeY8gfseVlJVJuq7MDZOOcUnTdcWsGZhNvDuJNFm828UblmQe_P_c48dN0BvgBSLkVehd_3fzv1O8JVrjR</recordid><startdate>20111201</startdate><enddate>20111201</enddate><creator>Cox, Hannah C.</creator><creator>Lea, Rod A.</creator><creator>Bellis, Claire</creator><creator>Carless, Melanie</creator><creator>Dyer, Tom</creator><creator>Blangero, John</creator><creator>Griffiths, Lyn R.</creator><general>Springer Milan</general><general>Springer Nature B.V</general><scope>C6C</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>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20111201</creationdate><title>Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate</title><author>Cox, Hannah C. ; Lea, Rod A. ; Bellis, Claire ; Carless, Melanie ; Dyer, Tom ; Blangero, John ; Griffiths, Lyn R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-3b92d7fb031bca00db3c2d62615867f3a4c87ee0ab1d0a0a5e78616f72aa5b443</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic Predisposition to Disease - genetics</topic><topic>Genetic Variation - genetics</topic><topic>Humans</topic><topic>Indexing in process</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Migraine</topic><topic>Migraine Disorders - genetics</topic><topic>Migraine Disorders - metabolism</topic><topic>Migraine Disorders - physiopathology</topic><topic>Neurology</topic><topic>Original</topic><topic>Pain Medicine</topic><topic>Pedigree</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Small-Conductance Calcium-Activated Potassium Channels - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cox, Hannah C.</creatorcontrib><creatorcontrib>Lea, Rod A.</creatorcontrib><creatorcontrib>Bellis, Claire</creatorcontrib><creatorcontrib>Carless, Melanie</creatorcontrib><creatorcontrib>Dyer, Tom</creatorcontrib><creatorcontrib>Blangero, John</creatorcontrib><creatorcontrib>Griffiths, Lyn R.</creatorcontrib><collection>Springer_OA刊</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of headache and pain</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cox, Hannah C.</au><au>Lea, Rod A.</au><au>Bellis, Claire</au><au>Carless, Melanie</au><au>Dyer, Tom</au><au>Blangero, John</au><au>Griffiths, Lyn R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate</atitle><jtitle>Journal of headache and pain</jtitle><stitle>J Headache Pain</stitle><addtitle>J Headache Pain</addtitle><date>2011-12-01</date><risdate>2011</risdate><volume>12</volume><issue>6</issue><spage>603</spage><epage>608</epage><pages>603-608</pages><issn>1129-2369</issn><eissn>1129-2377</eissn><coden>JHPOAT</coden><abstract>The calcium-activated potassium ion channel gene (KCNN3) is located in the vicinity of the familial hemiplegic migraine type 2 locus on chromosome 1q21.3. This gene is expressed in the central nervous system and plays a role in neural excitability. Previous association studies have provided some, although not conclusive, evidence for involvement of this gene in migraine susceptibility. To elucidate KCNN3 involvement in migraine, we performed gene-wide SNP genotyping in a high-risk genetic isolate from Norfolk Island, a population descended from a small number of eighteenth century Isle of Man ‘Bounty Mutineer’ and Tahitian founders. Phenotype information was available for 377 individuals who are related through the single, well-defined Norfolk pedigree (96 were affected: 64 MA, 32 MO). A total of 85 SNPs spanning the KCNN3 gene were genotyped in a sub-sample of 285 related individuals (76 affected), all core members of the extensive Norfolk Island ‘Bounty Mutineer’ genealogy. All genotyping was performed using the Illumina BeadArray platform. The analysis was performed using the statistical program SOLAR v4.0.6 assuming an additive model of allelic effect adjusted for the effects of age and sex. Haplotype analysis was undertaken using the program HAPLOVIEW v4.0. A total of four intronic SNPs in the KCNN3 gene displayed significant association (
P
< 0.05) with migraine. Two SNPs, rs73532286 and rs6426929, separated by approximately 0.1 kb, displayed complete LD (
r
2
= 1.00,
D
′ = 1.00,
D
′ 95% CI = 0.96–1.00). In all cases, the minor allele led to a decrease in migraine risk (beta coefficient = 0.286–0.315), suggesting that common gene variants confer an increased risk of migraine in the Norfolk pedigree. This effect may be explained by founder effect in this genetic isolate. This study provides evidence for association of variants in the KCNN3 ion channel gene with migraine susceptibility in the Norfolk genetic isolate with the rarer allelic variants conferring a possible protective role. This the first comprehensive analysis of this potential candidate gene in migraine and also the first study that has utilised the unique Norfolk Island large pedigree isolate to implicate a specific migraine gene. Studies of additional variants in KCNN3 in the Norfolk pedigree are now required (e.g. polyglutamine variants) and further analyses in other population data sets are required to clarify the association of the KCNN3 gene and migraine risk in the general outbred population.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>22030984</pmid><doi>10.1007/s10194-011-0392-7</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of headache and pain, 2011-12, Vol.12 (6), p.603-608 |
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| source | Publicly Available Content Database; Springer Nature - SpringerLink Journals - Fully Open Access ; PubMed Central |
| subjects | Adult Aged Female Genes Genetic Predisposition to Disease - genetics Genetic Variation - genetics Humans Indexing in process Internal Medicine Male Medicine Medicine & Public Health Middle Aged Migraine Migraine Disorders - genetics Migraine Disorders - metabolism Migraine Disorders - physiopathology Neurology Original Pain Medicine Pedigree Polymorphism, Single Nucleotide - genetics Small-Conductance Calcium-Activated Potassium Channels - genetics |
| title | Variants in the human potassium channel gene (KCNN3) are associated with migraine in a high risk genetic isolate |
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