ArticleMammalian genome : official journal of the International Mammalian Genome Society2006
Mapping of the murine type 1 diabetes locus Idd20 by genetic interaction.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- NOD alleles at Idd1 and Idd2 loci drive exocrine pancreatic inflammation.Immunogenetics · 2024Article
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines.Immunogenetics · 2021Article
- The Role of NOD Mice in Type 1 Diabetes Research: Lessons from the Past and Recommendations for the Future.Frontiers in endocrinology · 2018Article
- Increased autoimmune diabetes in pIgR-deficient NOD mice is due to a "Hitchhiking" interval that refines the genetic effect of Idd5.4.PloS one · 2015Article
- Congenic mice reveal genetic epistasis and overlapping disease loci for autoimmune diabetes and listeriosis.Immunogenetics · 2014Article
- 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
- Use of nonobese diabetic mice to understand human type 1 diabetes.Endocrinology and metabolism clinics of North America · 2010Review
- Induction of autoimmune cholangitis in non-obese diabetic (NOD).1101 mice following a chemical xenobiotic immunization.Clinical and experimental immunology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the nonobese diabetes mouse, the murine type 1 diabetes susceptibility locus Idd20 interacts genetically with the diabetes resistance locus Idd19. Both Idds are located on distal mouse Chromosome 6, and previous studies on NOD.C3H congenic strains have shown that C3H alleles at Idd20 can suppress the disease-promoting effects of C3H alleles at Idd19 in both spontaneous and cyclophosphamide-induced diabetes. In this article we present the construction of novel congenic strains which, while maintaining the C3H alleles at Idd19, have allowed the candidate interval of Idd20 to be reduced from 4 to 1.8 cM. The analysis of these strains shows that Idd20 controls the progression of insulitis. Idd20 also increases the suppressive but not the pathogenic activity of splenocytes in diabetes transfer experiments. Our results suggest that the two Chromosome 6 susceptibility loci, Idd6 and Idd20, interact with the resistance locus Idd19 by regulating the activity of suppressor cells in the peripheral immune system.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.