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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CITATION STYLE
Gingerich, M. A., Sidarala, V., & Soleimanpour, S. A. (2020, February 1). Clarifying the function of genes at the chromosome 16p13 locus in type 1 diabetes: CLEC16A and DEXI. Genes and Immunity. Springer Nature. https://doi.org/10.1038/s41435-019-0087-7
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