Overview

Also Known As: Non-obese Diabetic, NOD

The NOD/ShiLtJ strain (commonly called NOD) is a polygenic model for autoimmune type 1 diabetes. Diabetes in NOD mice is characterized by hyperglycemia and insulitis, a leukocytic infiltration of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. A 2017 phenotyping study found that 90% of females and 52% of males became diabetic by 30 weeks; median female incidence was 18 weeks. Immune phenotypes in the NOD background consist of defects in antigen presentation, T lymphocyte repertoire, NK cell function, macrophage cytokine production, wound healing, and C5 complement. These defects make the NOD background a common choice for immunodeficient mouse strains. Diabetes onset data is available.

Genetic overview

Genetic Background	Generation
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Research Applications

Diabetes and Obesity Research
Immunology, Inflammation and Autoimmunity Research
Research Tools
Internal/Organ Research
Neurobiology Research
Sensorineural Research
Developmental Biology Research

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Details

Important Note

This strain is homozygous for Cdh23^ahl, the age related hearing loss 1 mutation, which on this background results in progressive hearing loss that is already severe by three months of age.

Detailed Description

Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some in vitro studies. The major component of diabetes susceptibility in NOD mice is the unique MHC haplotype (H2^g7 = K^d, Aa^d, Ab^g7, E^null, D^b). NOD mice also exhibit multiple aberrant immunophenotypes including defective antigen presenting cell immunoregulatory functions, defects in the regulation of theT lymphocyte repertoire, defective NK cell function, defective cytokine production from macrophages (Fan et al., 2004) and impaired wound healing. They also lack hemolytic complement, C5. NOD/ShiLtJ mice also are severely hearing-impaired. A variety of mutations causing immunodeficiencies, targeted mutations in cytokine genes, as well as transgenes affecting immune functions, have been backcrossed into the NOD/ShiLt inbred strain background.

Development

NOD inbred mice originated early on in the inbreeding of the Cataract Shionogi (CTS) strain. These mice were originally outbred Jcl:ICR mice. At F6, the progenitors of the future NOD/Shi mice were inbred on the basis of an elevated fasting blood glucose level in cataract-free mice. At F13, the NOD progenitors were separated from what is now the NON/Shi strain. High fasting blood glucose levels continued to be the basis for selection of the latter strain, while the NOD progenitors at F13 and later were selected on the basis of a normal fasting blood glucose level. In 1974, at F20, a female in the "normoglycemic" line spontaneously developed overt insulin-dependent diabetes mellitus with insulitis (IDDM). Selective breeding of the progeny of this diabetic female produced the nonobese diabetic (NOD) strain. Originally restricted to distribution in Japan, NOD substrains were distributed during the early 1980s to Australia and the United States. NOD and NON strains were imported from a colony in Kyoto, Japan by Dr. M. Hattori to the Joslin Diabetes Ceneter in Boston in 1984. Breeder pairs from this importation were sent from The Joslin Diabetes Center to Dr. E Leiter at The Jackson Laboratory, and are the source of the production strains NOD/ShiLtJ and NON/ShiLtJ.

Control Suggestions

Approximate Controls

001303 NOD.CB17-Prkdc^scid/J, (May be used as an approximate control for T and B cell dependent research)
002050 NOR/LtJ, (Recombinant congenic that carries a portion of the NOD/ShiLtJ genome)
002591 NOD.B10Sn-H2^b/J
003729 NOD.129S7(B6)-Rag1^tm1Mom/J, (May be used as an approximate control for T and B cell dependent research)
009122 ICR/HaJ, (Both the inbred ICR/HaJ (Stock #009122) and NOD/ShiLtJ are descended from ICR stock. Testing at The Jackson Laboratory confirms that ICR/HaJ carries the H2^g7 MHC haplotype. ICR/HaJ does not develop insulitis or diabetes and may be considered an approximate control for NOD/ShiLtJ.)

Additional Information

Considerations for Choosing Controls

Selected References

Leiter EH. 1993. The NOD mouse: A model for analyzing the interplay between heredity and environment in development of autoimmune disease ILAR News 35(1):4-14MGI: J:12784
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163PubMed: 28784771 MGI: J:244295
Makino S; Kunimoto K; Muraoka Y; Mizushima Y; Katagiri K; Tochino Y. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken Dobutsu 29(1):1-13PubMed: 6995140 MGI: J:25411
Simecek P; Churchill GA; Yang H; Rowe LB; Herberg L; Serreze DV; Leiter EH. 2015. Genetic Analysis of Substrain Divergence in Non-Obese Diabetic (NOD) Mice. G3 (Bethesda) 5(5):771-5PubMed: 25740934 MGI: J:257336
Serreze DV; Chapman HD; Varnum DS; Gerling I; Leiter EH; Shultz LD. 1997. Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent. J Immunol 158(8):3978-86PubMed: 9103469 MGI: J:39473

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Genetics

Il2^m1

Allele Symbol: Il2^m1

Allele Name	mutation 1
Allele Type	Spontaneous
Allele Synonym(s)	mutation 1; Il2^m1
Gene Symbol and Name	Il2, interleukin 2
Gene Synonym(s)	TCGF; IL-2; Il-2; lymphokine
Strain of Origin	multiple strains
Chromosome	3
Molecular Note	This hypoactive polymorphism, found in MRL/MpJ, SJL/J, and NOD/ShiLtJ inbred strains, includes a smaller polyglutamine tract predicted to shorten the first alpha helix, which forms part of the IL2 receptor binding site.

Gpr84^del

Allele Symbol: Gpr84^del

Allele Name	deletion
Allele Type	Spontaneous (Not Specified)
Allele Synonym(s)	deletion; Gpr84^del
Gene Symbol and Name	Gpr84, G protein-coupled receptor 84
Gene Synonym(s)	GPCR4; EX33
Strain of Origin	multiple strains
Chromosome	15
Molecular Note	This spontaneously arising frameshift deletion is located in exon 2 at position 103308576 bp (NCBI Build 37) and results in a premature stop codon. The mutation is predicted to result in a truncated protein lacking the transmembrane domains 4-7. The inbred strains BDP/J, DBA/1J, DBA/2J, I/LnJ, FVB/NJ, LG/J, MRL/MpJ, NODShi/LtJ, NOR/LtJ, P/J, PL/J, SKHIN/Sprd, SJL/J, SM/J are homozygous for the deletion. The allele is segregating in the outbred stocks ICR and CD-1.

Hc⁰

Allele Symbol: Hc⁰

Allele Name	deficient
Allele Type	Spontaneous
Allele Synonym(s)	deficient; Hc⁰
Gene Symbol and Name	Hc, hemolytic complement
Gene Synonym(s)	He; CPAMD4; ECLZB; C5b; He; C5; C5a; C5D; C5; Hfib2; hepatic fibrogenesis 2; Hfib2
Strain of Origin	multiple strains
Chromosome	2
General Note	This is an allele characteristic of various inbred mouse strains including the following: A/HeJ, A/J, AKR/J, DBA/2J, NZB/B1NJ, SWR/J, B10.D2/oSnJ Hc was identified as a candidate gene for Abhr2 in a microarray analysis of lung mRNA from A/J, C3H/HeJ, and (A/J x C3H/HeJ)F1 x A/J backcross animals. Hc genotype shows statistically significant correlation to allergen-induced bronchial hyperresponsive phenotype. The A/J allele contains a 2 bp deletion resulting in deficient Hc mRNA and protein production and is associated with susceptibility to allergen-induced bronchial hyperresponsiveness. (J:108211)
Molecular Note	A 2 base "TA" deletion at positions 62 and 63 of an 83 base pair exon near the 5' end of the gene is found in the following mouse strains: A/HeJ, A/J, AKR/J, DBA/2J, I/LnJ, KK/HlJ, MOLF/EiJ, NZB/B1NJ, RF/J, ST/bJ SWR/J, B10.D2/oSnJ. The consequence of this deletion is the creation of a stop codon starting four bases after the deletion. A truncated product of 216 amino acids is predicted as a result although contradictory reports exist that a larger pro-C5 protein may be synthesized. Nevertheless, macrophages from mouse strains carrying this allele do not secrete complement 5.

H2^g7

Allele Symbol: H2^g7

Allele Name	g7 variant
Allele Type	Not Applicable
Allele Synonym(s)	g7 variant; H2^g7
Gene Symbol and Name	H2, histocompatibility-2, MHC
Gene Synonym(s)	H-2; MHC-II; H-2
Strain of Origin	Not Applicable
Chromosome	17
General Note	The g7 variant has been observed in the following strains: DBR7, NON.NOD-H2^g7

Cdh23^ahl

Allele Symbol: Cdh23^ahl

Allele Name	age related hearing loss 1
Allele Type	Spontaneous
Allele Synonym(s)	age related hearing loss 1; Cdh23^ahl
Gene Symbol and Name	Cdh23, cadherin 23 (otocadherin)
Gene Synonym(s)	bob; bustling; bobby; nmf112; nmf252; nmf252; 4930542A03Rik; ahl; 4930542A03Rik; W; sals; mdfw; neuroscience mutagenesis facility, 181; neuroscience mutagenesis facility, 252; modifier of deaf waddler; age related hearing loss 1; v; USH1D; nmf181; RIKEN cDNA 4930542A03 gene; CDHR23; sals; waltzer; nmf112; nmf181; mdfw; neuroscience mutagenesis facility, 112; bus; ahl; bob; salsa; PITA5
Strain of Origin	multiple strains
Chromosome	10
Molecular Note	Genetic complementation tests have shown allelism between the mdfw (modifier of deaf waddler) locus and the ahl locus. Further analysis has shown this is caused by a G to A transition at nucleotide position 753 of Cdh23. This hypomorphic allele causes in frame skipping of exon 7, which is predicted to delete part of the 2nd and 3rd ectodomains, and cause reduced message stability. Twenty-seven strains classified with ahl and carrying the 753A allele include: CD-1, RBF/DnJ, PL/J, AKR/J, RF/J, BALB/cBy, A/WySnJ, P/J, SENCARA/PtJ, DBA/1J, ALS/LtJ, C58/J, C57BLKS/J, 129P1/ReJ, C57BR/cd, SKH2/J, BUB/Bn, MA/MyJ, LP/J, 129X1/SvJ, NOR/LtJ, A/J, C57BL/6, NOD/LtJ, DBA/2J, ALR/LtJ, C57L/J. Strains classified with ahl that DO NOT carry this mutation include: C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.

mt-Tr^m1

Allele Symbol: mt-Tr^m1

Allele Name	mutation 1
Allele Type	Spontaneous
Allele Synonym(s)	mutation 1; mt-Tr^m1
Gene Symbol and Name	mt-Tr, mitochondrially encoded tRNA arginine
Gene Synonym(s)	tRNA-Arg; tRNA; TrnR tRNA; MTTR
Strain of Origin	various
Chromosome	MT
General Note	This polymorphism is present in A/J, NZB/B1NJ, ALS/Lt and NOD/ShiLtJ. A variant with 9 adenines is found in NOD/ShiLtDvs, ALR/Lt and SKH2/J.
Molecular Note	The adenine repeat in the D stem is polymorphic with 10 adenines in this allele.

Del(3)1Lt

Allele Symbol: Del(3)1Lt

Allele Name	deletion, Chr 3, Edward H Leiter 1
Allele Type	Spontaneous (Null/Knockout)
Allele Synonym(s)	deletion, Chr 3, Edward H Leiter 1; Del(3)1Lt
Gene Symbol and Name	Del(3)1Lt, deletion, Chr 3, Edward H Leiter 1
Gene Synonym(s)
Strain of Origin	NOD/ShiLtJ
Chromosome	3
Molecular Note	This spontaneous 111,169 bp deletion spans from Chr 3: 24,170,854 bp to 24,282,022 bp (GRCm38/mm10), and includes several QTL and the gene N-acetylated alpha-linked acidic dipeptidase-like 2

Del(1)2Lt

Allele Symbol: Del(1)2Lt

Allele Name	deletion, Chr 1, Edward H Leiter 2
Allele Type	Spontaneous (Not Applicable)
Allele Synonym(s)	deletion, Chr 1, Edward H Leiter 2; Del(1)2Lt
Gene Symbol and Name	Del(1)2Lt, deletion, Chr 1, Edward H Leiter 2
Gene Synonym(s)	Del2Lt
Strain of Origin	NOD/ShiLtJ
Chromosome	1
Molecular Note	This spontaneous 25,703 bp deletion in Chromosome 1 spans from 39,088,990 bp to 39,114,692 bp (GRCm38).

Del(3)3Lt

Allele Symbol: Del(3)3Lt

Allele Name	deletion, Chr 3, Edward H Leiter 3
Allele Type	Spontaneous (Not Applicable)
Allele Synonym(s)	deletion, Chr 3, Edward H Leiter 3; Del(3)3Lt
Gene Symbol and Name	Del(3)3Lt, deletion, Chr 3, Edward H Leiter 3
Gene Synonym(s)	Del3Lt
Strain of Origin	NOD/ShiLtJ
Chromosome	3
Molecular Note	This spontaneous 4,289 bp deletion in Chromosome 3 spans from 33,746,227 bp to 33,750,515 bp (GRCm38).

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Diabetes and Obesity Research
- Hyperglycemia
- Type 1 Diabetes (IDDM)
- Hypoinsulinemia
- Impaired Wound Healing
- Islet Transplantation Studies
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - NK Cell Deficiency
Internal/Organ Research
- Wound Healing
  - delayed/impaired
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - Type 1 Diabetes
Neurobiology Research
- Hearing Defects
  - Age related hearing loss
Sensorineural Research
- Hearing Defects
  - Age related hearing loss
Developmental Biology Research
- Lymphoid Tissue Defects
  - hematopoietic defects

Genotype: Hc⁰ related

Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - specific complement deficiency
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - specific complement deficiency, C5 complement

Genotype: Cdh23^ahl related

Neurobiology Research
- Hearing Defects
  - Age related hearing loss
Sensorineural Research
- Hearing Defects
  - Age related hearing loss

Genotype: H2^g7 related

Immunology, Inflammation and Autoimmunity Research
- CD Antigens, Antigen Receptors, and Histocompatibility Markers

Mammalian Phenotype Terms by Genotype

Phenotype Information

References

Leiter EH. 1993. The NOD mouse: A model for analyzing the interplay between heredity and environment in development of autoimmune disease ILAR News 35(1):4-14MGI: J:12784
Timmermans S; Van Montagu M; Libert C. 2017. Complete overview of protein-inactivating sequence variations in 36 sequenced mouse inbred strains. Proc Natl Acad Sci U S A 114(34):9158-9163PubMed: 28784771 MGI: J:244295
Makino S; Kunimoto K; Muraoka Y; Mizushima Y; Katagiri K; Tochino Y. 1980. Breeding of a non-obese, diabetic strain of mice. Jikken Dobutsu 29(1):1-13PubMed: 6995140 MGI: J:25411
Simecek P; Churchill GA; Yang H; Rowe LB; Herberg L; Serreze DV; Leiter EH. 2015. Genetic Analysis of Substrain Divergence in Non-Obese Diabetic (NOD) Mice. G3 (Bethesda) 5(5):771-5PubMed: 25740934 MGI: J:257336
Serreze DV; Chapman HD; Varnum DS; Gerling I; Leiter EH; Shultz LD. 1997. Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent. J Immunol 158(8):3978-86PubMed: 9103469 MGI: J:39473

Additional References

Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction:1-34MGI: J:110093
Xie C; Sharma R; Wang H; Zhou XJ; Mohan C. 2004. Strain distribution pattern of susceptibility to immune-mediated nephritis. J Immunol 172(8):5047-55PubMed: 15067087 MGI: J:122988
Moy SS; Nadler JJ; Young NB; Nonneman RJ; Segall SK; Andrade GM; Crawley JN; Magnuson TR. 2008. Social approach and repetitive behavior in eleven inbred mouse strains. Behav Brain Res 191(1):118-29PubMed: 18440079 MGI: J:138681
Bowman MA; Leiter EH; Atkinson MA. 1994. Prevention of diabetes in the NOD mouse: implications for therapeutic intervention in human disease. Immunol Today 15(3):115-20PubMed: 8172643 MGI: J:17091
Keane TM; Goodstadt L; Danecek P; White MA; Wong K; Yalcin B; Heger A; Agam A; Slater G; Goodson M; Furlotte NA; Eskin E; Nellaker C; Whitley H; Cleak J; Janowitz D; Hernandez-Pliego P; Edwards A; Belgard TG; Oliver PL; McIntyre RE; Bhomra A; Nicod J; Gan X; Yuan W; van der Weyden L; Steward CA; Bala S; Stalker J; Mott R; Durbin R; Jackson IJ; Czechanski A; Guerra-Assuncao JA; Donahue LR; Reinholdt LG; Payseur BA; Ponting CP; Birney E; Flint J; Adams DJ. 2011. Mouse genomic variation and its effect on phenotypes and gene regulation. Nature 477(7364):289-94PubMed: 21921910 MGI: J:177037
Serreze DV; Leiter EH. 1994. Genetic and pathogenic basis of autoimmune diabetes in NOD mice. Curr Opin Immunol 6(6):900-6PubMed: 7710714 MGI: J:22216
Hui ST; Parks BW; Org E; Norheim F; Che N; Pan C; Castellani LW; Charugundla S; Dirks DL; Psychogios N; Neuhaus I; Gerszten RE; Kirchgessner T; Gargalovic PS; Lusis AJ. 2015. The genetic architecture of NAFLD among inbred strains of mice. Elife 4:e05607PubMed: 26067236 MGI: J:223755
Depis F; Kwon HK; Mathis D; Benoist C. 2016. Unstable FoxP3+ T regulatory cells in NZW mice. Proc Natl Acad Sci U S A 113(5):1345-50PubMed: 26768846 MGI: J:227903
Nutter CA; Jaworski EA; Verma SK; Deshmukh V; Wang Q; Botvinnik OB; Lozano MJ; Abass IJ; Ijaz T; Brasier AR; Garg NJ; Wehrens XH; Yeo GW; Kuyumcu-Martinez MN. 2016. Dysregulation of RBFOX2 Is an Early Event in Cardiac Pathogenesis of Diabetes. Cell Rep 15(10):2200-13PubMed: 27239029 MGI: J:238102
Odet F; Pan W; Bell TA; Goodson SG; Stevans AM; Yun Z; Aylor DL; Kao CY; McMillan L; de Villena FP; O'Brien DA. 2015. The Founder Strains of the Collaborative Cross Express a Complex Combination of Advantageous and Deleterious Traits for Male Reproduction. G3 (Bethesda) 5(12):2671-83PubMed: 26483008 MGI: J:244582
Mathews CE; Xue S; Posgai A; Lightfoot YL; Li X; Lin A; Wasserfall C; Haller MJ; Schatz D; Atkinson MA. 2015. Acute Versus Progressive Onset of Diabetes in NOD Mice: Potential Implications for Therapeutic Interventions in Type 1 Diabetes. Diabetes 64(11):3885-90PubMed: 26216853 MGI: J:249518
Serr I; Scherm MG; Zahm AM; Schug J; Flynn VK; Hippich M; Kalin S; Becker M; Achenbach P; Nikolaev A; Gerlach K; Liebsch N; Loretz B; Lehr CM; Kirchner B; Spornraft M; Haase B; Segars J; Kuper C; Palmisano R; Waisman A; Willis RA; Kim WU; Weigmann B; Kaestner KH; Ziegler AG; Daniel C. 2018. A miRNA181a/NFAT5 axis links impaired T cell tolerance induction with autoimmune type 1 diabetes. Sci Transl Med 10(422)PubMed: 29298866 MGI: J:254437
Dai H; Friday AJ; Abou-Daya KI; Williams AL; Mortin-Toth S; Nicotra ML; Rothstein DM; Shlomchik WD; Matozaki T; Isenberg JS; Oberbarnscheidt MH; Danska JS; Lakkis FG. 2017. Donor SIRPalpha polymorphism modulates the innate immune response to allogeneic grafts. Sci Immunol 2(12)PubMed: 28783664 MGI: J:261263
Lynch DM; Kay PH. 1995. Studies on the polymorphism of the fifth component of complement in laboratory mice. Exp Clin Immunogenet 12(4):253-60PubMed: 8919358 MGI: J:31912
Darby IA; Bisucci T; Hewitson TD; MacLellan DG. 1997. Apoptosis is increased in a model of diabetes-impaired wound healing in genetically diabetic mice. Int J Biochem Cell Biol 29(1):191-200PubMed: 9076954 MGI: J:40898
Serreze DV; Post CM; Chapman HD; Johnson EA; Lu B; Rothman PB. 2000. Interferon-gamma receptor signaling is dispensable in the development of autoimmune type 1 diabetes in NOD mice. Diabetes 49(12):2007-11PubMed: 11118001 MGI: J:65986
Nagy A; Nagashima H; Cha S; Oxford GE; Zelles T; Peck AB; Humphreys-Beher MG. 2001. Reduced oral wound healing in the NOD mouse model for type 1 autoimmune diabetes and its reversal by epidermal growth factor supplementation. Diabetes 50(9):2100-4PubMed: 11522677 MGI: J:71049
Trembleau S; Gregori S; Penna G; Gorny I; Adorini L. 2001. Il-12 administration reveals diabetogenic t cells in genetically resistant i-ealpha-transgenic nonobese diabetic mice: resistance to autoimmune diabetes is associated with binding of ealpha-derived peptides to the i-a(g7) molecule. J Immunol 167(7):4104-14PubMed: 11564833 MGI: J:71651
Chun T; Hermel E; Gaskins HR; Aldrich CJ. 2001. Cytotoxic T lymphocyte and cDNA sequence analyses of the MHC class Ib molecule Qa1 in nonobese diabetic mice. Immunogenetics 53(6):506-10PubMed: 11685462 MGI: J:72438
Quintana FJ; Cohen IR. 2001. Autoantibody Patterns in Diabetes-prone NOD Mice and in Standard C57BL/6 Mice. J Autoimmun 17(3):191-7PubMed: 11712856 MGI: J:72893
Pierce MA; Chapman HD; Post CM; Svetlanov A; Efrat S; Horwitz M; Serreze DV. 2003. Adenovirus early region 3 antiapoptotic 10.4K, 14.5K, and 14.7K genes decrease the incidence of autoimmune diabetes in NOD mice. Diabetes 52(5):1119-27PubMed: 12716741 MGI: J:83195
Petkov PM; Cassell MA; Sargent EE; Donnelly CJ; Robinson P; Crew V; Asquith S; Haar RV; Wiles MV. 2004. Development of a SNP genotyping panel for genetic monitoring of the laboratory mouse. Genomics 83(5):902-11PubMed: 15081119 MGI: J:89298
DiLorenzo TP; Lieberman SM; Takaki T; Honda S; Chapman HD; Santamaria P; Serreze DV; Nathenson SG. 2002. During the early prediabetic period in NOD mice, the pathogenic CD8(+) T-cell population comprises multiple antigenic specificities. Clin Immunol 105(3):332-41PubMed: 12498815 MGI: J:94192

Additional - Cdh23^ahl related

Additional - Gpr84^del related

Additional - H2^g7 related

Additional - Hc⁰ related

Additional - Il2^m1 related

Additional - mt-Tr^m1 related

Additional - Del(1)2Lt related

Additional - Del(3)1Lt related

Additional - Del(3)3Lt related

Technical Support

Contact Technical Support

Genotyping Protocols
- Genotyping resources and troubleshooting
Inbred mouse strains are maintained through sibling (sister x brother) matings; no genotyping required.
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is an exceptional breeder.
- Additional Breeding and Husbandry Support
Mating System
- Sibling x Sibling
Appearance
- albino
  Related Genotype: A/A Tyr^c/Tyr^c
Citation
When using the NOD mouse strain in a publication, please include JAX stock #001976 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX5 (Standard)

RB10 (Maximum)

Pricing & Availability

Readily Available

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Live Mouse

Age

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Price

weeks

Volume Pricing Details

QUANTITY	VOLUME PRICING

Volume Pricing Program
Quantities: Volume pricing is automatically applied when a minimum quantity per strain for a shipment is reached
Sexes: Sexes of the same strain may be combined to reach minimum quantity levels to receive the volume pricing
Shipment: All shipping destinations qualify

Cryorecovery - Pricing

Service	Genotype	Price
	Inbred

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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Credit for PRODUCTS or SERVICES

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of, PRODUCTS or SERVICES, JACKSON will, at its option, provide credit or replacement for the PRODUCT received or the SERVICES provided; JACKSON makes no other representations and this shall be the exclusive remedy of the purchaser. Please note specific policy for live mice.

Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS, or SERVICES, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS, or SERVICES from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

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Acceptance of delivery of MICE, PRODUCTS or SERVICES shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or SERVICES by JACKSON.

Also Known As: Non-obese Diabetic, NOD

Genetic overview

Research Applications

Base Price

Volume Pricing Available!

Important Note

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Il2m1

Allele Symbol: Il2m1

Gpr84del

Allele Symbol: Gpr84del

Hc0

Allele Symbol: Hc0

H2g7

Allele Symbol: H2g7

Cdh23ahl

Allele Symbol: Cdh23ahl

mt-Trm1

Allele Symbol: mt-Trm1

Del(3)1Lt

Allele Symbol: Del(3)1Lt

Del(1)2Lt

Allele Symbol: Del(1)2Lt

Del(3)3Lt

Allele Symbol: Del(3)3Lt

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Hc0 related

Genotype: Cdh23ahl related

Genotype: H2g7 related

Mammalian Phenotype Terms by Genotype

Phenotype Information

References

Additional References

Additional - Cdh23ahl related

Additional - Gpr84del related

Additional - H2g7 related

Additional - Hc0 related

Additional - Il2m1 related

Additional - mt-Trm1 related

Additional - Del(1)2Lt related

Additional - Del(3)1Lt related

Additional - Del(3)3Lt related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Volume Pricing Details

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Il2^m1

Allele Symbol: Il2^m1

Gpr84^del

Allele Symbol: Gpr84^del

Hc⁰

Allele Symbol: Hc⁰

H2^g7

Allele Symbol: H2^g7

Cdh23^ahl

Allele Symbol: Cdh23^ahl

mt-Tr^m1

Allele Symbol: mt-Tr^m1

Genotype: Hc⁰ related

Genotype: Cdh23^ahl related

Genotype: H2^g7 related

Additional - Cdh23^ahl related

Additional - Gpr84^del related

Additional - H2^g7 related

Additional - Hc⁰ related

Additional - Il2^m1 related

Additional - mt-Tr^m1 related