ArticleGenetics2001
Statistical modeling of interlocus interactions in a complex disease: rejection of the multiplicative model of epistasis in type 1 diabetes.
Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 81 citations in OpenAlex.
- Article
- Targeting Neuroplasticity, Cardiovascular, and Cognitive-Associated Genomic Variants in Familial Alzheimer's Disease.Molecular neurobiology · 2019Article
- Neuroimaging genomics in psychiatry-a translational approach.Genome medicine · 2017Review
- Ptpn22 and Cd2 Variations Are Associated with Altered Protein Expression and Susceptibility to Type 1 Diabetes in Nonobese Diabetic Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Genome-wide interaction analysis reveals replicated epistatic effects on brain structure.Neurobiology of aging · 2015Article
- Genetic interactions among Idd3, Idd5.1, Idd5.2, and Idd5.3 protective loci in the nonobese diabetic mouse model of type 1 diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- An omnibus permutation test on ensembles of two-locus analyses can detect pure epistasis and genetic heterogeneity in genome-wide association studies.SpringerPlus · 2013Article
- Exhaustive search of the SNP-sNP interactome identifies epistatic effects on brain volume in two cohorts.Medical image computing and computer-assisted intervention : MICCAI ... International Conference on Medical Image Computing and Computer-Assisted Intervention · 2013Article
- A cooperative interaction between LPHN3 and 11q doubles the risk for ADHD.Molecular psychiatry · 2012Article
- Cellular mechanisms of restored β-cell tolerance mediated by protective alleles of Idd3 and Idd5.Diabetes · 2012Article
- Nonobese diabetic congenic strain analysis of autoimmune diabetes reveals genetic complexity of the Idd18 locus and identifies Vav3 as a candidate gene.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Epistasis and its implications for personal genetics.American journal of human genetics · 2009Review
- An ensemble learning approach jointly modeling main and interaction effects in genetic association studies.Genetic epidemiology · 2008Article
- Genome-wide microarray expression analysis of CD4+ T Cells from nonobese diabetic congenic mice identifies Cd55 (Daf1) and Acadl as candidate genes for type 1 diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- Retrospective analysis of main and interaction effects in genetic association studies of human complex traits.BMC genetics · 2007Article
- Allelic variation in GAD1 (GAD67) is associated with schizophrenia and influences cortical function and gene expression.Molecular psychiatry · 2007Article
- Both additivity and epistasis control the genetic variation for fruit quality traits in tomato.TAG. Theoretical and applied genetics. Theoretische und angewandte Genetik · 2007Article
- Integrative analysis for finding genes and networks involved in diabetes and other complex diseases.Genome biology · 2007Article
- Article
- Search for haplotype interactions that influence susceptibility to type 1 diabetes, through use of unphased genotype data.American journal of human genetics · 2003Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
In general, common diseases do not follow a Mendelian inheritance pattern. To identify disease mechanisms and etiology, their genetic dissection may be assisted by evaluation of linkage in mouse models of human disease. Statistical modeling of multiple-locus linkage data from the nonobese diabetic (NOD) mouse model of type 1 diabetes has previously provided evidence for epistasis between alleles of several Idd (insulin-dependent diabetes) loci. The construction of NOD congenic strains containing selected segments of the diabetes-resistant strain genome allows analysis of the joint effects of alleles of different loci in isolation, without the complication of other segregating Idd loci. In this article, we analyze data from congenic strains carrying two chromosome intervals (a double congenic strain) for two pairs of loci: Idd3 and Idd10 and Idd3 and Idd5. The joint action of both pairs is consistent with models of additivity on either the log odds of the penetrance, or the liability scale, rather than with the previously proposed multiplicative model of epistasis. For Idd3 and Idd5 we would also not reject a model of additivity on the penetrance scale, which might indicate a disease model mediated by more than one pathway leading to beta-cell destruction and development of diabetes. However, there has been confusion between different definitions of interaction or epistasis as used in the biological, statistical, epidemiological, and quantitative and human genetics fields. The degree to which statistical analyses can elucidate underlying biologic mechanisms may be limited and may require prior knowledge of the underlying etiology.
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