ArticleMammalian genome : official journal of the International Mammalian Genome Society2013
Fine mapping of type 1 diabetes regions Idd9.1 and Idd9.2 reveals genetic complexity.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Exploring the polygenic landscape of wool traits in Turkish Merinos through multi-locus GWAS approaches: middle Anatolian Merino.Scientific reports · 2025Article
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Selective ablation of thymic and peripheral Foxp3Frontiers in immunology · 2023Article
- Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines.Immunogenetics · 2021Article
- Integrative QTL analysis of gene expression and chromatin accessibility identifies multi-tissue patterns of genetic regulation.PLoS genetics · 2020Article
- Transcriptome Analyses in BV2 Microglial Cells Following Treatment With Amino-Terminal Fragments of Apolipoprotein E.Frontiers in aging neuroscience · 2020Article
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice.Immunogenetics · 2017Article
- Genome-wide transcriptional analyses of islet-specific CD4+ T cells identify Idd9 genes controlling diabetogenic T cell function.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Congenic mice reveal genetic epistasis and overlapping disease loci for autoimmune diabetes and listeriosis.Immunogenetics · 2014Article
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 2014Article
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9 authors.
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Abstract
Nonobese diabetic (NOD) mice congenic for C57BL/10 (B10)-derived genes in the Idd9 region of chromosome 4 are highly protected from type 1 diabetes (T1D). Idd9 has been divided into three protective subregions (Idd9.1, 9.2, and 9.3), each of which partially prevents disease. In this study we have fine-mapped the Idd9.1 and Idd9.2 regions, revealing further genetic complexity with at least two additional subregions contributing to protection from T1D. Using the NOD sequence from bacterial artificial chromosome clones of the Idd9.1 and Idd9.2 regions as well as whole-genome sequence data recently made available, sequence polymorphisms within the regions highlight a high degree of polymorphism between the NOD and B10 strains in the Idd9 regions. Among numerous candidate genes are several with immunological importance. The Idd9.1 region has been separated into Idd9.1 and Idd9.4, with Lck remaining a candidate gene within Idd9.1. One of the Idd9.2 regions contains the candidate genes Masp2 (encoding mannan-binding lectin serine peptidase 2) and Mtor (encoding mammalian target of rapamycin). From mRNA expression analyses, we have also identified several other differentially expressed candidate genes within the Idd9.1 and Idd9.2 regions. These findings highlight that multiple, relatively small genetic effects combine and interact to produce significant changes in immune tolerance and diabetes onset.
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