期刊
DIABETES-METABOLISM RESEARCH AND REVIEWS
卷 24, 期 2, 页码 93-102出版社
WILEY
DOI: 10.1002/dmrr.797
关键词
susceptibility; genetic heterogeneity; linkage; association; pathogenesis; autoimmunity; SUMO; sumoylation; NF kappa B; I kappa B alpha; cytokines; AP-1; JAK/STAT; PIAS; oxidative stress; apoptosis
资金
- NICHD NIH HHS [4R33 HD050196, HD37800] Funding Source: Medline
- NIDDK NIH HHS [DK074957, 4R33 DK069878-03] Funding Source: Medline
Susceptibility to type 1 diabetes (T1D) is determined by interactions of multiple genes with unknown environmental factors. Despite the characterization of over 20 susceptibility regions for T1D, identification of specific genes in these regions is still a formidable challenge. In 2004, we first reported the cloning of a novel, small ubiquitin-like modifier (SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a T1D susceptibility gene. Subsequent studies have consistently confirmed this association in multiple Asian populations despite controversial observations in Caucasians. In this review, we will update the genetic evidence supporting SUMO4 as a T1D susceptibility gene and discuss the possible explanations for the discrepant associations observed in Caucasians. We will then discuss the mechanisms through which SUMO4 contributes to the pathogenesis of T1D. Copyright (c) 2007 John Wiley & Sons, Ltd.
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