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
来源：
GENES AND IMMUNITY | 2020年 / 21卷 / 02期
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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