SUMO4 M55V polymorphism affects susceptibility to type I diabetes in HLA DR3- and DR4-positive Swedish patients
SUMO4 M55V, located in IDDM5, has been a focus for debate because of its association to type I diabetes (TIDM) in Asians but not in Caucasians. The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated...
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| Veröffentlicht in: | Genes and immunity 2007-09, Vol.8 (6), p.518-521 |
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| description | SUMO4 M55V, located in IDDM5, has been a focus for debate because of its association to type I diabetes (TIDM) in Asians but not in Caucasians. The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR–RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. From the current study, we conclude that SUMO4 M55V is associated with TIDM in association with high-risk HLA-DR3 and DR4, but not by itself. |
| doi_str_mv | 10.1038/sj.gene.6364406 |
| format | Article |
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The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR–RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. From the current study, we conclude that SUMO4 M55V is associated with TIDM in association with high-risk HLA-DR3 and DR4, but not by itself.</description><identifier>ISSN: 1466-4879</identifier><identifier>ISSN: 1476-5470</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/sj.gene.6364406</identifier><identifier>PMID: 17554341</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adolescent ; Adult ; Alleles ; Antigens ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Case-Control Studies ; Child ; Child, Preschool ; Clinical Medicine ; Cohort Studies ; Diabetes ; Diabetes Mellitus ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Female ; Gene Expression ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Genetic susceptibility ; Genotype ; Haplotypes ; Health aspects ; Heterozygosity ; Histocompatibility antigen HLA ; HLA-DR3 Antigen - genetics ; HLA-DR3 Antigen - immunology ; HLA-DR3 Antigen/genetics/immunology ; HLA-DR4 Antigen - genetics ; HLA-DR4 Antigen - immunology ; HLA-DR4 Antigen/genetics/immunology ; Human Genetics ; Humans ; Immunology ; Infant ; Infant, Newborn ; Klinisk medicin ; Leukocytes ; Male ; MEDICAL AND HEALTH SCIENCES ; MEDICIN ; MEDICIN OCH HÄLSOVETENSKAP ; MEDICINE ; Newborn ; Physiological aspects ; Polymorphism ; Polymorphism, Single Nucleotide ; Preschool ; Proteins ; Risk factors ; short-communication ; Single Nucleotide ; Small Ubiquitin-Related Modifier Proteins - genetics ; Small Ubiquitin-Related Modifier Proteins - immunology ; Small Ubiquitin-Related Modifier Proteins/genetics/immunology ; Sweden ; Transcription factors ; Type 1 diabetes ; Type 1/genetics/immunology ; White people</subject><ispartof>Genes and immunity, 2007-09, Vol.8 (6), p.518-521</ispartof><rights>Springer Nature Limited 2007</rights><rights>COPYRIGHT 2007 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2007</rights><rights>Nature Publishing Group 2007.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c849t-2d7dcd16c28bdb2f694bda69592b92741ff7c843c4ab85faf19b4fe9e2e2e0423</citedby><cites>FETCH-LOGICAL-c849t-2d7dcd16c28bdb2f694bda69592b92741ff7c843c4ab85faf19b4fe9e2e2e0423</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.gene.6364406$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.gene.6364406$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17554341$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-108701$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-8961$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-14458$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/66317$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://lup.lub.lu.se/record/1140507$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:115877412$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Sedimbi, S K</creatorcontrib><creatorcontrib>Luo, X R</creatorcontrib><creatorcontrib>Sanjeevi, C B</creatorcontrib><creatorcontrib>Swedish Childhood Diabetes Study Group</creatorcontrib><creatorcontrib>Diabetes Incidence in Sweden Study Group</creatorcontrib><creatorcontrib>on behalf of the Swedish Childhood Diabetes and the Diabetes Incidence in Sweden Study Groups</creatorcontrib><title>SUMO4 M55V polymorphism affects susceptibility to type I diabetes in HLA DR3- and DR4-positive Swedish patients</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>SUMO4 M55V, located in IDDM5, has been a focus for debate because of its association to type I diabetes (TIDM) in Asians but not in Caucasians. The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR–RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. 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genetics</subject><subject>Small Ubiquitin-Related Modifier Proteins - immunology</subject><subject>Small Ubiquitin-Related Modifier Proteins/genetics/immunology</subject><subject>Sweden</subject><subject>Transcription factors</subject><subject>Type 1 diabetes</subject><subject>Type 1/genetics/immunology</subject><subject>White people</subject><issn>1466-4879</issn><issn>1476-5470</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNk11v0zAUhiMEYmNwzRXIAgkJQTo78edltQGr1GnSxnZrOYmdueSL2GH03-OsXasiCsiycnT8vK_tE58oeongBMGUH7vFpNSNntCUYgzpo-gQYUZjghl8PMaUxpgzcRA9c24BIaKIiqfRAWKE4BSjw6i9uj6_wOCckBvQtdWybvvu1roaKGN07h1wg8t1521mK-uXwLfALzsNZqCwKtNeO2AbcDafgtPLNAaqKUKA46511tsfGlzd6cK6W9Apb3Xj3fPoiVGV0y_W36Po-vOnrydn8fziy-xkOo9zjoWPk4IVeYFonvCsyBJDBc4KRQURSSYShpExLJBpjlXGiVEGiQwbLXQSBsRJehTFK193p7shk11va9UvZausXKe-hUhLQgUTLPBiL9_1bbEVPQgRIpyFk4x7zfdqq6ELMwtz1OgiFyLlSnIiuMTQCJmxXEmkVEEzxlluxqN83GtXBruQKu_dKE3RiH_Yi5_am6ls-1IOg0QYE_6fdD1ILij6axU3dGWDOeQMjvy7FR9K9n3QzsvahudTVarR7eAk5UmKmUj_CSLBSCoEDODb38BFO_RNeDoyoRixhGAqAvVmL4U4pxxitrUqVaWlbUzre5WP-8op4iQJjXJfzskfqDAKXdu8bbSxIb8jeL8jCIzXP32pBufk7Opylz1esXnfOtdrs6kognJsaOkWcmxouW7ooHi9vtmQ1brY8usODgBc_6Kw1JS63159v-erlaRRfuj1xvNh_Re5umBd</recordid><startdate>20070901</startdate><enddate>20070901</enddate><creator>Sedimbi, S K</creator><creator>Luo, X R</creator><creator>Sanjeevi, C B</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DG8</scope><scope>D93</scope><scope>DF2</scope><scope>F1U</scope><scope>D95</scope></search><sort><creationdate>20070901</creationdate><title>SUMO4 M55V polymorphism affects susceptibility to type I diabetes in HLA DR3- and DR4-positive Swedish patients</title><author>Sedimbi, S K ; Luo, X R ; Sanjeevi, C B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c849t-2d7dcd16c28bdb2f694bda69592b92741ff7c843c4ab85faf19b4fe9e2e2e0423</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Alleles</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Clinical Medicine</topic><topic>Cohort Studies</topic><topic>Diabetes</topic><topic>Diabetes Mellitus</topic><topic>Diabetes Mellitus, Type 1 - 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genetics</topic><topic>Small Ubiquitin-Related Modifier Proteins - immunology</topic><topic>Small Ubiquitin-Related Modifier Proteins/genetics/immunology</topic><topic>Sweden</topic><topic>Transcription factors</topic><topic>Type 1 diabetes</topic><topic>Type 1/genetics/immunology</topic><topic>White people</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sedimbi, S K</creatorcontrib><creatorcontrib>Luo, X R</creatorcontrib><creatorcontrib>Sanjeevi, C B</creatorcontrib><creatorcontrib>Swedish Childhood Diabetes Study Group</creatorcontrib><creatorcontrib>Diabetes Incidence in Sweden Study Group</creatorcontrib><creatorcontrib>on behalf of the Swedish Childhood Diabetes and the Diabetes Incidence in Sweden Study Groups</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - 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The current study aims to test the significance of M55V association to TIDM in a large cohort of Swedish Caucasians, and to test whether M55V is associated in those carrying human leukocyte antigen (HLA) class II molecules. A total of 673 TIDM patients and 535 age- and sex-matched healthy controls were included in the study. PCR–RFLP was performed to identify the genotype and allele variations. Our data suggest that SUMO4 M55V is not associated with susceptibility to TIDM by itself. When we stratified our patients and controls based on heterozygosity for HLA-DR3/DR4 and SUMO4 genotypes, we found that presence of SUMO4 GG increased further the relative risk conferred by HLA-DR3/DR4 to TIDM, whereas SUMO4 AA decreased the risk. From the current study, we conclude that SUMO4 M55V is associated with TIDM in association with high-risk HLA-DR3 and DR4, but not by itself.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>17554341</pmid><doi>10.1038/sj.gene.6364406</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Genes and immunity, 2007-09, Vol.8 (6), p.518-521 |
| issn | 1466-4879 1476-5470 1476-5470 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Adolescent Adult Alleles Antigens Apoptosis Biomedical and Life Sciences Biomedicine Cancer Research Case-Control Studies Child Child, Preschool Clinical Medicine Cohort Studies Diabetes Diabetes Mellitus Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Female Gene Expression Gene polymorphism Genes Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Genetic susceptibility Genotype Haplotypes Health aspects Heterozygosity Histocompatibility antigen HLA HLA-DR3 Antigen - genetics HLA-DR3 Antigen - immunology HLA-DR3 Antigen/genetics/immunology HLA-DR4 Antigen - genetics HLA-DR4 Antigen - immunology HLA-DR4 Antigen/genetics/immunology Human Genetics Humans Immunology Infant Infant, Newborn Klinisk medicin Leukocytes Male MEDICAL AND HEALTH SCIENCES MEDICIN MEDICIN OCH HÄLSOVETENSKAP MEDICINE Newborn Physiological aspects Polymorphism Polymorphism, Single Nucleotide Preschool Proteins Risk factors short-communication Single Nucleotide Small Ubiquitin-Related Modifier Proteins - genetics Small Ubiquitin-Related Modifier Proteins - immunology Small Ubiquitin-Related Modifier Proteins/genetics/immunology Sweden Transcription factors Type 1 diabetes Type 1/genetics/immunology White people |
| title | SUMO4 M55V polymorphism affects susceptibility to type I diabetes in HLA DR3- and DR4-positive Swedish patients |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T14%3A12%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=SUMO4%20M55V%20polymorphism%20affects%20susceptibility%20to%20type%20I%20diabetes%20in%20HLA%20DR3-%20and%20DR4-positive%20Swedish%20patients&rft.jtitle=Genes%20and%20immunity&rft.au=Sedimbi,%20S%20K&rft.aucorp=Swedish%20Childhood%20Diabetes%20Study%20Group&rft.date=2007-09-01&rft.volume=8&rft.issue=6&rft.spage=518&rft.epage=521&rft.pages=518-521&rft.issn=1466-4879&rft.eissn=1476-5470&rft_id=info:doi/10.1038/sj.gene.6364406&rft_dat=%3Cgale_swepu%3EA185248717%3C/gale_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=218868047&rft_id=info:pmid/17554341&rft_galeid=A185248717&rfr_iscdi=true |