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

  • Genes Immun. 2020 Feb;21(2):79-82. doi: 10.1038/s41435-019-0087-7.
Morgan A Gingerich  #  1 ,  Vaibhav Sidarala  #  1 ,  Scott A Soleimanpour  2  3
Affiliations
  • 1. Division of Metabolism, Endocrinology & Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48105, USA.
  • 2. Division of Metabolism, Endocrinology & Diabetes, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, 48105, USA. [email protected].
  • 3. Veterans Affairs Ann Arbor Health Care System, Ann Arbor, MI, 48105, USA. [email protected].
  • # Contributed equally.
PMID: 31570815 DOI: 10.1038/s41435-019-0087-7
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.