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Editorial
. 2020 Feb;21(2):79-82.
doi: 10.1038/s41435-019-0087-7. Epub 2019 Oct 1.

Clarifying the function of genes at the chromosome 16p13 locus in type 1 diabetes: CLEC16A and DEXI

Morgan A Gingerich #  1 , Vaibhav Sidarala #  1 , Scott A Soleimanpour  2   3
Affiliations
Editorial

Clarifying the function of genes at the chromosome 16p13 locus in type 1 diabetes: CLEC16A and DEXI

Morgan A Gingerich et al. Genes Immun. 2020 Feb.

Abstract

More than a decade after the discovery of a novel type 1 diabetes risk locus on chromosome 16p13, there remains complexity and controversy over the specific gene(s) that regulate diabetes pathogenesis. A new study by Nieves-Bonilla et al. shows that one of these genes, DEXI, is unlikely to contribute to type 1 diabetes pathogenesis and positions the endolysosomal E3 ubiquitin ligase CLEC16A as the primary culprit by which this gene locus influences diabetes risk.

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Conflict of interest statement

Conflict of interest The authors declare that they have no conflict of interest.

Figures

Fig. 1
Fig. 1
A deeper view of the chromosome 16p13.13 locus in type 1 diabetes. a Schematic of Homo sapiens chromosome region 16p13.13. Arrows indicate gene locations. b Location of CLEC16A, DEXI, and CIITA on Homo sapiens chromosome 16. c Schematic of CLEC16A exons (vertical bars), and introns (angled lines connecting exons). CLEC16A T1D risk associated SNPs are indicated in boxes. All SNPs are intronic. Underlined SNP indicates SNP that is associated with reduced CLEC16A expression in human islets [7]
See this image and copyright information in PMC

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References

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