rdf:type |
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lifeskim:mentions |
|
pubmed:issue |
6
|
pubmed:dateCreated |
2007-9-5
|
pubmed:abstractText |
In a large case-control study of Swedish incident type I diabetes patients and controls, 0-34 years of age, we tested the hypothesis that the GIMAP5 gene, a key genetic factor for lymphopenia in spontaneous BioBreeding rat diabetes, is associated with type I diabetes; with islet autoantibodies in incident type I diabetes patients or with age at clinical onset in incident type I diabetes patients. Initial scans of allelic association were followed by more detailed logistic regression modeling that adjusted for known type I diabetes risk factors and potential confounding variables. The single nucleotide polymorphism (SNP) rs6598, located in a polyadenylation signal of GIMAP5, was associated with the presence of significant levels of IA-2 autoantibodies in the type I diabetes patients. Patients with the minor allele A of rs6598 had an increased prevalence of IA-2 autoantibody levels compared to patients without the minor allele (OR=2.2; Bonferroni-corrected P=0.003), after adjusting for age at clinical onset (P=8.0 x 10(-13)) and the numbers of HLA-DQ A1*0501-B1*0201 haplotypes (P=2.4 x 10(-5)) and DQ A1*0301-B1*0302 haplotypes (P=0.002). GIMAP5 polymorphism was not associated with type I diabetes or with GAD65 or insulin autoantibodies, ICA, or age at clinical onset in patients. These data suggest that the GIMAP5 gene is associated with islet autoimmunity in type I diabetes and add to recent findings implicating the same SNP in another autoimmune disease.
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Sep
|
pubmed:issn |
1466-4879
|
pubmed:author |
pubmed-author:AiliMM,
pubmed-author:ArnqvistHansH,
pubmed-author:BååthL ELE,
pubmed-author:BOCKFF,
pubmed-author:BjörckElizabethE,
pubmed-author:BlaySS,
pubmed-author:CarlssonEE,
pubmed-author:DeutschKK,
pubmed-author:Diabetes Incidence in Sweden Study Group,
pubmed-author:EdenwallHH,
pubmed-author:ErikssonJanJ,
pubmed-author:ForsanderGG,
pubmed-author:GrahamJJ,
pubmed-author:GranströmB WBW,
pubmed-author:GustavssonII,
pubmed-author:HörnellHH,
pubmed-author:HellenbergLL,
pubmed-author:HellgrenHH,
pubmed-author:HolmbergEE,
pubmed-author:IvarssonSten-ASA,
pubmed-author:JanevAA,
pubmed-author:JohanssonCC,
pubmed-author:JonsellGG,
pubmed-author:KockumII,
pubmed-author:KockumKK,
pubmed-author:LernmarkAA,
pubmed-author:LindbladBB,
pubmed-author:LindhAA,
pubmed-author:LudvigssonJJ,
pubmed-author:McNeneyBB,
pubmed-author:MyrdalUU,
pubmed-author:NeiderudJJ,
pubmed-author:NyströmLennarthL,
pubmed-author:OhlsonLars OlofLO,
pubmed-author:OstmanJanJ,
pubmed-author:RousseauD LDL,
pubmed-author:SanjeeviC BCB,
pubmed-author:SchersténBengtB,
pubmed-author:SegnestamKK,
pubmed-author:SjöbladSS,
pubmed-author:SkogsbergLL,
pubmed-author:SnoyP JPJ,
pubmed-author:StåhleUU,
pubmed-author:StrömbergLL,
pubmed-author:Swedish Childhood Diabetes Study Group,
pubmed-author:ThalmeBB,
pubmed-author:TullusKK,
pubmed-author:TuvemoTT,
pubmed-author:WallensteenMM,
pubmed-author:WestphalOO
|
pubmed:issnType |
Print
|
pubmed:volume |
8
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
503-12
|
pubmed:dateRevised |
2010-9-24
|
pubmed:meshHeading |
pubmed-meshheading:17641683-Adolescent,
pubmed-meshheading:17641683-Adult,
pubmed-meshheading:17641683-Autoantibodies,
pubmed-meshheading:17641683-Case-Control Studies,
pubmed-meshheading:17641683-Child,
pubmed-meshheading:17641683-Child, Preschool,
pubmed-meshheading:17641683-Diabetes Mellitus, Type 1,
pubmed-meshheading:17641683-Female,
pubmed-meshheading:17641683-GTP-Binding Proteins,
pubmed-meshheading:17641683-Humans,
pubmed-meshheading:17641683-Infant,
pubmed-meshheading:17641683-Infant, Newborn,
pubmed-meshheading:17641683-Male,
pubmed-meshheading:17641683-Polymorphism, Single Nucleotide,
pubmed-meshheading:17641683-Sweden
|
pubmed:year |
2007
|
pubmed:articleTitle |
IA-2 autoantibodies in incident type I diabetes patients are associated with a polyadenylation signal polymorphism in GIMAP5.
|
pubmed:affiliation |
Department of Statistics and Actuarial Science, Simon Fraser University, Burnaby, British Columbia, Canada.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|