ArticleG3 (Bethesda, Md.)2015
Genetic Analysis of Substrain Divergence in Non-Obese Diabetic (NOD) Mice.
Article in G3 (Bethesda, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- Multiple Mechanisms Contribute to Robust Type 1 Diabetes Protection in Nfkbid- Overexpressing NOD Mice.Diabetes · 2026Article
- Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Constructing the optimal experimental autoimmune thyroiditis mouse model using porcine thyroglobulin.Frontiers in immunology · 2025Article
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Murine MHC-Deficient Nonobese Diabetic Mice Carrying Human HLA-DQ8 Develop Severe Myocarditis and Myositis in Response to Anti-PD-1 Immune Checkpoint Inhibitor Cancer Therapy.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- HLA-DQ8 Supports Development of Insulitis Mediated by Insulin-Reactive Human TCR-Transgenic T Cells in Nonobese Diabetic Mice.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- De novo germline mutation in the dual specificity phosphatase 10 gene accelerates autoimmune diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Skeletal Response to Insulin in the Naturally Occurring Type 1 Diabetes Mellitus Mouse Model.JBMR plus · 2021Article
- T Cells from NOD-Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Lot-to-Lot Variation in Adeno-Associated Virus Serotype 9 (AAV9) Preparations.Human gene therapy methods · 2019Article
- C57BL/6 Substrain Differences in Pharmacological Effects after Acute and Repeated Nicotine Administration.Brain sciences · 2019Article
- Variations in hepatic lipid species of age-matched male mice fed a methionine-choline-deficient diet and housed in different animal facilities.Lipids in health and disease · 2019Article
- Immune Relevant and Immune Deficient Mice: Options and Opportunities in Translational Research.ILAR journal · 2018Review
- NOD and NOR mice exhibit comparable development of lacrimal gland secretory dysfunction but NOD mice have more severe autoimmune dacryoadenitis.Experimental eye research · 2018Article
- Type I and II Interferon Receptors Differentially Regulate Type 1 Diabetes Susceptibility in Male Versus Female NOD Mice.Diabetes · 2018Article
- A Protective Role for NKG2D-H60a Interaction via Homotypic T Cell Contact in Nonobese Diabetic Autoimmune Diabetes Pathogenesis.ImmunoHorizons · 2017Article
- High-Resolution Maps of Mouse Reference Populations.G3 (Bethesda, Md.) · 2017Article
- The Genetic Heterogeneity among Different Mouse Strains Impacts the Lung Injury Potential of Multiwalled Carbon Nanotubes.Small (Weinheim an der Bergstrasse, Germany) · 2017Article
- Whole genome sequence analysis of the TALLYHO/Jng mouse.BMC genomics · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The non-obese diabetic (NOD) mouse is a polygenic model for type 1 diabetes that is characterized by insulitis, a leukocytic infiltration of the pancreatic islets. During ~35 years since the original inbred strain was developed in Japan, NOD substrains have been established at different laboratories around the world. Although environmental differences among NOD colonies capable of impacting diabetes incidence have been recognized, differences arising from genetic divergence have not been analyzed previously. We use both mouse diversity array and whole-exome capture sequencing platforms to identify genetic differences distinguishing five NOD substrains. We describe 64 single-nucleotide polymorphisms, and two short indels that differ in coding regions of the five NOD substrains. A 100-kb deletion on Chromosome 3 distinguishes NOD/ShiLtJ and NOD/ShiLtDvs from three other substrains, whereas a 111-kb deletion in the Icam2 gene on Chromosome 11 is unique to the NOD/ShiLtDvs genome. The extent of genetic divergence for NOD substrains is compared with similar studies for C57BL6 and BALB/c substrains. As mutations are fixed to homozygosity by continued inbreeding, significant differences in substrain phenotypes are to be expected. These results emphasize the importance of using embryo freezing methods to minimize genetic drift within substrains and of applying appropriate genetic nomenclature to permit substrain recognition when one is used.
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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.