ArticleDiabetes2009
NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in mice.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- Genomic prediction in a backcross population using relationship matrices.Archives animal breeding · 2025Article
- Robust regression based genome-wide multi-trait QTL analysis.Molecular genetics and genomics : MGG · 2021Article
- 'Fat's chances': Loci for phenotypic dispersion in plasma leptin in mouse models of diabetes mellitus.PloS one · 2019Article
- Molecular pathway alterations in CD4 T-cells of nonobese diabetic (NOD) mice in the preinsulitis phase of autoimmune diabetes.Results in immunology · 2014Article
- Recalculation of 23 mouse HDL QTL datasets improves accuracy and allows for better candidate gene analysis.Journal of lipid research · 2013Article
- Interleukin-15 plays an essential role in the pathogenesis of autoimmune diabetes in the NOD mouse.Diabetologia · 2012Article
- Paradigm shift or shifting paradigm for type 1 diabetes.Diabetes · 2012Article
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- Article
- Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.The review of diabetic studies : RDS · 2012Review
- Testing the role of P2X7 receptors in the development of type 1 diabetes in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- A recombination hotspot leads to sequence variability within a novel gene (AK005651) and contributes to type 1 diabetes susceptibility.Genome research · 2010Article
- An update on the use of NOD mice to study autoimmune (Type 1) diabetes.Expert review of clinical immunology · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
objectiveIntroduction of genes targeted in 129/Sv embryonic stem (ES) cells into NOD mice brings about linked genes that may modulate type 1 diabetes. Our objective was to identify 129S1/SvJ non-MHC regions contributing type 1 diabetes resistance or susceptibility in backcross to NOD/LtJ. RESEARCH DESIGN AND
methodsAfter congenic transfer of the NOD H2(g7) haplotype onto 129S1/Sv, 310 females were produced by NOD x (NOD x 129.H2(g7))F1 backcross (N2). A genome scan for quantitative trait locus (QTL) affecting clinical diabetes, age of diabetes onset, and insulitis severity was performed using subphenotype characteristics to improve power and resolution for detection of diabetes susceptibility loci.
resultsThirty-six of 310 (11.6%) N2 females developed type 1 diabetes between 14 and 40 weeks. Significant evidence of linkage for only a single previously reported Idd complex locus (Idd10/17/18, chromosome [Chr] 3) was indicated for clinical diabetes. The quantitative traits of insulitis either alone or combined with age at type 1 diabetes onset were significantly linked to known Idd regions on Chr 1 (Idd5 region), Chr 4 (Idd9 region), Chr 8 (Idd22), Chr 11 (Idd4.3), and proximal Chr 17 (Idd16 region). Significant 129S1/Sv resistance contributions were identified on Chr 1, 15 (two loci), and 19, with suggestive evidence for additional novel 129/Sv resistance QTL on Chr 5 and 17 and susceptibility on Chr 2.
conclusionsThe 129S1/SvJ genome harbors collections of both known and potentially novel non-MHC Idd loci. Investigators targeting 129/Sv genes mapping within chromosomal regions reported herein or elsewhere in the genome need to exclude potential contributions from linked Idd loci by generating a NOD.129 control strain expressing the nontargeted allele.
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