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.

Our preclinical efficacy testing services offer scientific expertise and an array of target-based and phenotype-based outcome measures, both in vivo and at endpoint, for flexible study designs and assay development in mouse models of Diabetes. See our full service platform.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

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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.Cg-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

De Groot AS; Skowron G; White JR; Boyle C; Richard G; Serreze D; Martin WD. 2019. Therapeutic administration of Tregitope-Human Albumin Fusion with Insulin Peptides to promote Antigen-Specific Adaptive Tolerance Induction. Sci Rep 9(1):16103PubMed: 31695065 MGI: J:281351
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
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
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
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
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

View All References

Genetics

Hc⁰

Allele Symbol: Hc⁰

Allele Name	deficient
Allele Type	Spontaneous
Allele Synonym(s)	C5-; C5-d; C5-def; C5-deficient; Hc^Hfib2; hc^o
Gene Symbol and Name	Hc, hemolytic complement
Gene Synonym(s)
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.

Cdh23^ahl

Allele Symbol: Cdh23^ahl

Allele Name	age related hearing loss 1
Allele Type	Spontaneous
Allele Synonym(s)	Cdh23^753A; mdfw
Gene Symbol and Name	Cdh23, cadherin 23 (otocadherin)
Gene Synonym(s)
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 coding nucleotide position 753 of Cdh23 (SNP rs257098870). This hypomorphic allele changes splice donor site G-GT to A-GT, causing frame skipping of exon 7. This 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: 129S1/SvImJ, C3H/HeSnJ, I/LnJ, YBR/Ei, MRL/MpJ.

H2^g7

Allele Symbol: H2^g7

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

mt-Tr^m1

Allele Symbol: mt-Tr^m1

Allele Name	mutation 1
Allele Type	Spontaneous
Allele Synonym(s)	10A
Gene Symbol and Name	mt-Tr, mitochondrially encoded tRNA arginine
Gene Synonym(s)
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.

Il2^m1

Allele Symbol: Il2^m1

Allele Name	mutation 1
Allele Type	Spontaneous
Allele Synonym(s)
Gene Symbol and Name	Il2, interleukin 2
Gene Synonym(s)
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 (Null/Knockout)
Allele Synonym(s)
Gene Symbol and Name	Gpr84, G protein-coupled receptor 84
Gene Synonym(s)
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.

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)	Del1Lt
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)
Gene Symbol and Name	Del(1)2Lt, deletion, Chr 1, Edward H Leiter 2
Gene Synonym(s)
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)
Gene Symbol and Name	Del(3)3Lt, deletion, Chr 3, Edward H Leiter 3
Gene Synonym(s)
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).

Cox7a2l^l

Allele Symbol: Cox7a2l^l

Allele Name	long
Allele Type	Not Applicable (Not Specified)
Allele Synonym(s)	SCAF1¹¹³
Gene Symbol and Name	Cox7a2l, cytochrome c oxidase subunit 7A2 like
Gene Synonym(s)
Strain of Origin	multiple strains
Chromosome	17
General Note	Querying the sequences of the Sanger Mouse Genomes Project reveals that the short allele with its 6 bp deletion exists in C57BL/6J, C57BL/10J, C57BL/6NJ, C58/J, BALB/cJ, C3H/HeH, 129S5/SvEvBrd, NZW/LacZ, and SEA/GnJ, but the long allele lacking the deletion exists in 129S1/SvImJ, A/J, AKR/J, BTBR T⁺ Itpr3^tf/J, BUB/BnJ, C3H/HeJ, C57BR/cdJ, C57L/J, CAST/EiJ, CBA/J, DBA/1J, DBA/2J, FVB/NJ, I/LnJ, KK/HiJ, LEWES/EiJ, LP/J, MOLF/EiJ, NOD/ShiLtJ, NZB/BlNJ, NZO/HlLtJ, PWK/PhJ, RF/J, SPRET/EiJ, ST/bJ, WSB/EiJ, ZALENDE/EiJ.
Molecular Note	This allele encodes the long isoform with 113 amino acids. It is found in 129S2/SvPasCrl, CBA/CaOlaHsd, Hsd:ICR, and NZB/OlaHsd.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Diabetes Onset – JAX® Mice Strain NOD/ShiLtJ (001976)
Body Weight Information - JAX^® Mice Strain NOD/ShiLtJ (001976)
Festing Inbred Strain Characteristics: NOD
JAX^® Physiological Data Summary [pdf]

References

De Groot AS; Skowron G; White JR; Boyle C; Richard G; Serreze D; Martin WD. 2019. Therapeutic administration of Tregitope-Human Albumin Fusion with Insulin Peptides to promote Antigen-Specific Adaptive Tolerance Induction. Sci Rep 9(1):16103PubMed: 31695065 MGI: J:281351
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
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
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
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
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

Additional References

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
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
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
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
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
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
Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction:1-34MGI: J:110093
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
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
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
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
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
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
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
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
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
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

Additional - Cdh23^ahl related

Additional - Cox7a2l^l 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.

A footpad injection of Complete Freund's Adjuvant (CFA) administered once at weaning will delay diabetes onset, thus extending the lifespan of breeders. A discussion on the use of Complete Freund's Adjuvant in NOD mice can be found in. Current Protocols in Immunology pages 15.9.1-15.9.23 (see PDF link under Immunological protocols).
- 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

Domestic
International

Live Mouse

Age

Genotype

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/Product	Description	Price
	Inbred, 1 pair minimum will be supplied

Related Products and Services

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Mouse ES Cells	NOD/ShiLtJ AC576/GrsJ mES cells	$2500.00
Mouse ES Cells	NOD/ShiLtJ AC576/GrsJ mES cells	$2500.00

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The Jackson Laboratory's Genotype Promise

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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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General Terms and Conditions

Questions about Terms of Use

Licensing Information

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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

Hc0

Allele Symbol: Hc0

Cdh23ahl

Allele Symbol: Cdh23ahl

H2g7

Allele Symbol: H2g7

mt-Trm1

Allele Symbol: mt-Trm1

Il2m1

Allele Symbol: Il2m1

Gpr84del

Allele Symbol: Gpr84del

Del(3)1Lt

Allele Symbol: Del(3)1Lt

Del(1)2Lt

Allele Symbol: Del(1)2Lt

Del(3)3Lt

Allele Symbol: Del(3)3Lt

Cox7a2ll

Allele Symbol: Cox7a2ll

Disease Terms

Research Areas By Phenotype

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 - Cox7a2ll 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

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Hc⁰

Allele Symbol: Hc⁰

Cdh23^ahl

Allele Symbol: Cdh23^ahl

H2^g7

Allele Symbol: H2^g7

mt-Tr^m1

Allele Symbol: mt-Tr^m1

Il2^m1

Allele Symbol: Il2^m1

Gpr84^del

Allele Symbol: Gpr84^del

Cox7a2l^l

Allele Symbol: Cox7a2l^l

Genotype: Hc⁰ related

Genotype: Cdh23^ahl related

Genotype: H2^g7 related

Additional - Cdh23^ahl related

Additional - Cox7a2l^l related

Additional - Gpr84^del related

Additional - H2^g7 related

Additional - Hc⁰ related

Additional - Il2^m1 related

Additional - mt-Tr^m1 related