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. ssol@med.umich.edu.
3 Veterans Affairs Ann Arbor Health Care System, Ann Arbor, MI, 48105, USA. ssol@med.umich.edu.
# 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.

Name
Email *

	Sorry, but the email address you supplied was invalid.