Source:http://linkedlifedata.com/resource/pubmed/id/14989711
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2004-3-1
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| pubmed:abstractText |
Type 1 diabetes is a multifactorial disease in which the genes of the major histocompatibility complex (MHC) play a key role. Recently, non-human leukocyte antigen (non-HLA) genes in the class III region of this complex have been presumed to be associated with type 1 diabetes by linkage analyses. We investigated the possibility of the inhibitor of kappaB-like (IKBL, also known as 'NFKBIL1') gene as one of these candidates. We carried out a case-control study of 124 patients with type 1 diabetes and 330 healthy control subjects. The haplotypes of the IKBL promoter, i.e., PA (-263A, -63T), PB (-263A, -63A), PC (-263G, -63T), were assigned by the single-nucleotide polymorphisms at positions -263 and -63 from the transcription start site. The frequency of the wild-type haplotype, PA, was elevated, while that of the variant-type haplotype, PC, was lower in patients than controls. In two-locus analyses with HLA-DRB1 alleles, the PA haplotype showed linkage disequilibrium with the DRB1*0405 allele and the PC haplotype with the DRB1*1502 allele. A notable observation was that the PC haplotype was significantly associated with protection in the DRB1*1502-negative population. Our study indicates the first evidence of a possible independent association between type 1 diabetes and polymorphisms in the promoter of the IKBL gene.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Mar
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| pubmed:issn |
0001-2815
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
63
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
223-30
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| pubmed:dateRevised |
2011-11-17
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| pubmed:meshHeading |
pubmed-meshheading:14989711-Adolescent,
pubmed-meshheading:14989711-Adult,
pubmed-meshheading:14989711-Alleles,
pubmed-meshheading:14989711-Case-Control Studies,
pubmed-meshheading:14989711-Child,
pubmed-meshheading:14989711-Child, Preschool,
pubmed-meshheading:14989711-Diabetes Mellitus, Type 1,
pubmed-meshheading:14989711-Female,
pubmed-meshheading:14989711-Gene Frequency,
pubmed-meshheading:14989711-Genetic Predisposition to Disease,
pubmed-meshheading:14989711-Genotype,
pubmed-meshheading:14989711-HLA-DR Antigens,
pubmed-meshheading:14989711-HLA-DRB1 Chains,
pubmed-meshheading:14989711-Haplotypes,
pubmed-meshheading:14989711-Histocompatibility Antigens Class II,
pubmed-meshheading:14989711-Humans,
pubmed-meshheading:14989711-Immunity, Innate,
pubmed-meshheading:14989711-Infant,
pubmed-meshheading:14989711-Japan,
pubmed-meshheading:14989711-Linkage Disequilibrium,
pubmed-meshheading:14989711-Male,
pubmed-meshheading:14989711-Middle Aged,
pubmed-meshheading:14989711-Polymorphism, Genetic,
pubmed-meshheading:14989711-Promoter Regions, Genetic
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| pubmed:year |
2004
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| pubmed:articleTitle |
IKBL promoter polymorphism is strongly associated with resistance to type 1 diabetes in Japanese.
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| pubmed:affiliation |
Department of Anatomy, Biology and Medicine (Internal Medicine I), Oita Medical University School of Medicine, Oita, Japan. khamaguc@med.oita-u.ac.jp
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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