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http://purl.uniprot.org/citations/15937668http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15937668http://www.w3.org/2000/01/rdf-schema#comment"

Aims/hypothesis

Although genetic susceptibility plays an important role in the pathogenesis of type 2 diabetes, most of the genes that influence susceptibility to type 2 diabetes have yet to be identified. Krüppel-like transcription factors are known to play important roles in development and cell differentiation, and have recently been implicated in the pathogenesis of type 2 diabetes. The present study aimed to examine the associations of single nucleotide polymorphisms (SNPs) in genes encoding members of the Krüppel-like-factor (KLF) family with type 2 diabetes in a large cohort of Japanese subjects.

Methods

We genotyped 33 SNP loci found in 12 KLF genes in subjects with type 2 diabetes and in subjects from the general population using the PCR-Invader assay. We also examined the effects of the overexpression of KLF7 on adipogenesis in 3T3-L1 cells.

Results

We identified a significant association between an SNP in KLF7 and type 2 diabetes (A vs C: p=0.004 after Bonferroni's correction, odds ratio=1.59, 95% CI 1.27-2.00). The expression of Klf7 decreased in response to the differentiation of 3T3-L1 adipocytes, and the overexpression of KLF7 resulted in significant inhibition of adipogenesis in 3T3-L1 cells.

Conclusions/interpretation

These results indicate that the gene encoding KLF7 is a novel candidate for conferring genetic susceptibility to type 2 diabetes."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.org/dc/terms/identifier"doi:10.1007/s00125-005-1797-0"xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kashiwagi A."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Iwamoto Y."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Nakamura Y."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Maeda S."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kawamura Y."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Matsuda M."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Tanaka Y."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Iida A."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Sekine A."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Fujioka T."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Tsunoda T."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kawai K."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kanazawa A."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kaku K."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kikkawa R."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Babazono T."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Kawamori R."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Imanishi M."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/author"Iiizumi T."xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/name"Diabetologia"xsd:string
http://purl.uniprot.org/citations/15937668http://purl.uniprot.org/core/pages"1315-1322"xsd:string