ArticleDiabetes2014
Fine mapping and functional studies of risk variants for type 1 diabetes at chromosome 16p13.13.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Is DEXI a Multiple Sclerosis Susceptibility Gene?International journal of molecular sciences · 2025Review
- The multi-omics signatures of telomere length in childhood.BMC genomics · 2025Article
- Review
- 3D genome organization and epigenetic regulation in autoimmune diseases.Frontiers in immunology · 2023Review
- Expression Profile and Bioinformatics Analysis of Circular RNAs in Patients with Vitiligo.Pharmacogenomics and personalized medicine · 2022Article
- Immune Regulation in Time and Space: The Role of Local- and Long-Range Genomic Interactions in Regulating Immune Responses.Frontiers in immunology · 2021Review
- Next steps in the identification of gene targets for type 1 diabetes.Diabetologia · 2020Review
- Clarifying the function of genes at the chromosome 16p13 locus in type 1 diabetes: CLEC16A and DEXI.Genes and immunity · 2020Article
- Replication study of susceptibility variants associated with allergic rhinitis and allergy in Han Chinese.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2020Article
- The type 1 diabetes candidate gene Dexi does not affect disease risk in the nonobese diabetic mouse model.Genes and immunity · 2020Article
- DEXI, a candidate gene for type 1 diabetes, modulates rat and human pancreatic beta cell inflammation via regulation of the type I IFN/STAT signalling pathway.Diabetologia · 2019Article
- Progress in understanding type 1 diabetes through its genetic overlap with other autoimmune diseases.Current diabetes reports · 2015Review
- Diabetes mellitus: The epidemic of the century.World journal of diabetes · 2015Review
- Multiple Sclerosis Risk Allele in CLEC16A Acts as an Expression Quantitative Trait Locus for CLEC16A and SOCS1 in CD4+ T Cells.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Single nucleotide polymorphisms (SNPs) located in the chromosomal region 16p13.13 have been previously associated with risk for several autoimmune diseases, including type 1 diabetes. To identify and localize specific risk variants for type 1 diabetes in this region and understand the mechanism of their action, we resequenced a 455-kb region in type 1 diabetic patients and unaffected control subjects, identifying 93 novel variants. A panel of 939 SNPs that included 46 of these novel variants was genotyped in 3,070 multiplex families with type 1 diabetes. Forty-eight SNPs, all located in CLEC16A, provided a statistically significant association (P < 5.32 × 10(-5)) with disease, with rs34306440 being most significantly associated (P = 5.74 × 10(-6)). The panel of SNPs used for fine mapping was also tested for association with transcript levels for each of the four genes in the region in B lymphoblastoid cell lines. Significant associations were observed only for transcript levels of DEXI, a gene with unknown function. We examined the relationship between the odds ratio for type 1 diabetes and the magnitude of the effect of DEXI transcript levels for each SNP in the region. Among SNPs significantly associated with type 1 diabetes, the common allele conferred an increased risk for disease and corresponded to lower DEXI expression. Our results suggest that the primary mechanism by which genetic variation at CLEC16A contributes to the risk for type 1 diabetes is through reduced expression of DEXI.
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