ArticleGenes and immunity2005
Conditioning the genome identifies additional diabetes resistance loci in Type I diabetes resistant NOR/Lt mice.
Article in Genes and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Minor genomic differences between related B6 and B10 mice affect severity of schistosome infection by governing the mode of dendritic cell activation.European journal of immunology · 2015Article
- Hidden in plain sight: spike-wave discharges in mouse inbred strains.Genes, brain, and behavior · 2014Article
- Molecular pathway alterations in CD4 T-cells of nonobese diabetic (NOD) mice in the preinsulitis phase of autoimmune diabetes.Results in immunology · 2014Article
- Subcongenic analyses reveal complex interactions between distal chromosome 4 genes controlling diabetogenic B cells and CD4 T cells in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Comparative genetics: synergizing human and NOD mouse studies for identifying genetic causation of type 1 diabetes.The review of diabetic studies : RDS · 2012Review
- 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
- Use of nonobese diabetic mice to understand human type 1 diabetes.Endocrinology and metabolism clinics of North America · 2010Review
- Genetic control of severe egg-induced immunopathology and IL-17 production in murine schistosomiasis.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- NOD x 129.H2(g7) backcross delineates 129S1/SvImJ-derived genomic regions modulating type 1 diabetes development in mice.Diabetes · 2009Article
- Idd9/11 genetic locus regulates diabetogenic activity of CD4 T-cells in nonobese diabetic (NOD) mice.Diabetes · 2008Article
- Diabetic modifier QTLs in F(2) intercrosses carrying homozygous transgene of TGF-beta.Mammalian genome : official journal of the International Mammalian Genome Society · 2008Article
- Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD mice.Immunogenetics · 2007Article
- Genes within the Idd5 and Idd9/11 diabetes susceptibility loci affect the pathogenic activity of B cells in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2006Article
- Genes mediating environment interactions in type 1 diabetes.The review of diabetic studies : RDS · 2005Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
While sharing the H2g7 MHC and many other important Type I diabetes susceptibility (Idd) genes with NOD mice, the NOR strain remains disease free due to resistance alleles within the approximately 12% portion of their genome that is of C57BLKS/J origin. Previous F2 segregation analyses indicated multiple genes within the 'Idd13' locus on Chromosome 2 provide the primary component of NOR diabetes resistance. However, it was clear other genes also contribute to NOR diabetes resistance, but were difficult to detect in the original segregation analyses because they were relatively weak compared to the strong Idd13 protection component. To identify these further genetic components of diabetes resistance, we performed a new F2 segregation analyses in which NOD mice were outcrossed to a 'genome-conditioned' NOR stock in which a large component of Idd13-mediated resistance was replaced with NOD alleles. These F2 segregation studies combined with subsequent congenic analyses confirmed the presence of additional NOR resistance genes on Chr. 1 and Chr. 4, and also potentially on Chr. 11. These findings emphasize the value for diabetes gene discovery of stratifying not only MHC loci conferring the highest relative risk but also as many as possible of the non-MHC loci presumed to contribute significantly.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.