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

被引:10
|
作者
Gingerich, Morgan A. [1 ]
Sidarala, Vaibhav [1 ]
Soleimanpour, Scott A. [1 ,2 ]
机构
[1] Univ Michigan, Dept Internal Med, Med Sch, Div Metab Endocrinol & Diabet, Ann Arbor, MI 48105 USA
[2] Vet Affairs Ann Arbor Hlth Care Syst, Ann Arbor, MI 48105 USA
基金
美国国家卫生研究院;
关键词
GENOME-WIDE ASSOCIATION; BETA-CELL; EXPRESSION; COMPLEX;
D O I
10.1038/s41435-019-0087-7
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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.
引用
收藏
页码:79 / 82
页数:4
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