Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene

Cong Yi Wang, Robert Podolsky, Jin-Xiong She

Research output: Chapter in Book/Report/Conference proceedingConference contribution

36 Citations (Scopus)

Abstract

Genomewide linkage analyses since the early 1990s suggested over 20 genomic intervals that may contain susceptibility genes for type 1 diabetes. However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with genetic mapping and cloning of genes implicated in complex diseases. One of the difficulties is due to the presence of many weak and different susceptibility genes in different patients and populations, a phenomenon known as genetic heterogeneity. In 2004, we 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 susceptibility gene for type 1 diabetes mellitus (T1DM). In this article, we will summarize genetic association data suggesting that SUMO4 is consistently associated with T1DM in the Asian populations while the association is more heterogeneous in the Caucasian populations. We will also discuss the possible molecular pathways through which sumoylation may regulate T1DM and autoimmunity.

Original languageEnglish (US)
Title of host publicationImmunology of Diabetes IV
Subtitle of host publicationProgress in Our Understanding
PublisherBlackwell Publishing Inc.
Pages257-267
Number of pages11
ISBN (Print)1573316415, 9781573316415
DOIs
StatePublished - Jan 1 2006

Publication series

NameAnnals of the New York Academy of Sciences
Volume1079
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Fingerprint

Medical problems
Type 1 Diabetes Mellitus
Genes
Cloning
Organism Cloning
Modifier Genes
Sumoylation
Population
Genetic Heterogeneity
Chromosome Mapping
Ubiquitin
Autoimmunity
Chromosomes
Susceptibility
Gene
Diabetes
Diabetes Mellitus

Keywords

  • Antioxidant enzyme
  • Association
  • Autoimmunity
  • Genetic heterogeneity
  • IkBa
  • Linkage
  • NF-kB
  • Odds ratio (OR)
  • Oxidative stress
  • Pathogenesis
  • Risk assessment
  • Sumoylation
  • Susceptibility

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

Cite this

Wang, C. Y., Podolsky, R., & She, J-X. (2006). Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene. In Immunology of Diabetes IV: Progress in Our Understanding (pp. 257-267). (Annals of the New York Academy of Sciences; Vol. 1079). Blackwell Publishing Inc.. https://doi.org/10.1196/annals.1375.039

Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene. / Wang, Cong Yi; Podolsky, Robert; She, Jin-Xiong.

Immunology of Diabetes IV: Progress in Our Understanding. Blackwell Publishing Inc., 2006. p. 257-267 (Annals of the New York Academy of Sciences; Vol. 1079).

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Wang, CY, Podolsky, R & She, J-X 2006, Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene. in Immunology of Diabetes IV: Progress in Our Understanding. Annals of the New York Academy of Sciences, vol. 1079, Blackwell Publishing Inc., pp. 257-267. https://doi.org/10.1196/annals.1375.039
Wang CY, Podolsky R, She J-X. Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene. In Immunology of Diabetes IV: Progress in Our Understanding. Blackwell Publishing Inc. 2006. p. 257-267. (Annals of the New York Academy of Sciences). https://doi.org/10.1196/annals.1375.039
Wang, Cong Yi ; Podolsky, Robert ; She, Jin-Xiong. / Genetic and functional evidence supporting SUMO4 as a type 1 diabetes susceptibility gene. Immunology of Diabetes IV: Progress in Our Understanding. Blackwell Publishing Inc., 2006. pp. 257-267 (Annals of the New York Academy of Sciences).
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