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- Description
- Disease & phenotype
- Genes & alleles
- Genotyping
- Health & care
- References
- Pricing & purchasing
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Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Former Names c3 c17 (Changed: 15-DEC-04 ) Type Congenic; Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain C57BL/6 Donor Strain NOD/Uf H2 Haplotype b Generation NE7F?+14
Generation DefinitionsDonating Investigator Dr. Edward Leiter, The Jackson Laboratory Appearance
black
Related Genotype: a/aDescription
This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 by Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 43 cM segment (called c3 by Yui et al.) of Chr 3 extending from D3Mit132through Tshb(thyroid stimulating hormone, beta subunit) and including the insulin dependent diabetes susceptibility loci Idd3and Idd10.No information has been published for this doubly congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. B6.NOD-(D3Mit132-Tshb) singly congenic females also demonstrated a higher incidence of periinsulitis than controls, but the difference was not statistically significant. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one affected islet was observed in a single animal, even in cases where extensive perivascular/periductal infiltrates existed. While maleand female B6.NOD-(D17Mit21-D17Mit10) mice exhibited similar incidence of pancreatic infiltration, female B6.NOD-(D3Mit132-Tshb) mice developed periinsulitis at twice the frequency of males; female NOD mice are more susceptible than males to both insulitis and diabetes.Development
Genomic segments found in earlier linkage studies to include diabetogenic quantitative trait loci (QTLs) were transferred in the laboratory of E.K. Wakeland from NOD/Uf to C57BL/6 by six successive backcrosses (to N7). Sibs of each lineage were then intercrossed to generate mice homozygous for each segment. Microsatellite analysis was used to type mice for loci in the regions of interest. The B6.NOD-(D3Mit132-Tshb) (D17Mit21-D17Mit10) doubly congenic strain was created by crossing mice of the singly congenic strains B6.NOD-(D17Mit21-D17Mit10), bearing the NOD-derived Idd1QTL and the H2g7haplotype, and B6.NOD-(D3Mit132-Tshb), having the NOD QTLs Idd3and Idd10,then breeding to homozygosity for both congenic segments.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying H2g7 allele
View Strains carrying H2g7 (12 strains)
003059 B6.NOD-(D3Mit132-Tshb)/J
003059 B6.NOD-(D3Mit132-Tshb)/J
003059 B6.NOD-(D3Mit132-Tshb)/J
006500 129.NOD-(D17Mit175-H2)/J 010972 B10.NOD-(rs13459151-rs13483054)/1107MrkJ 004309 NOD.ALR-(D17Mit16-D17Mit10)/LtJ 004308 NOD.ALR-(D17Mit16-H2-D)/LtJ
003059 B6.NOD-(D3Mit132-Tshb)/J 003857 NOD.B6(PL)-(D3Mit267-D3Mit75)/Lt
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:H2g7 related
Idd10NOD/ShiLt relatedImmunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Idd3NOD relatedDiabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
NOD/ShiLtJ MHC Congenics
Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
NOD/ShiLtJ MHC Congenics
Immunology, Inflammation and Autoimmunity Research
Autoimmunity
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Genes & Alleles
Gene & Allele Information provided by MGI
| Gene Symbol and Name | D3Mit132, DNA segment, Chr 3, Massachusetts Institute of Technology 132 | ||
|---|---|---|---|
| Chromosome | 3 | ||
| Gene Symbol and Name | Tshb, thyroid stimulating hormone, beta subunit | ||
| Chromosome | 3 | ||
| Gene Common Name(s) | TSH-B; TSH-BETA; thyrotropin; | ||
| Gene Symbol and Name | D17Mit10, DNA segment, Chr 17, Massachusetts Institute of Technology 10 | ||
| Chromosome | 17 | ||
| Gene Symbol and Name | D17Mit21, DNA segment, Chr 17, Massachusetts Institute of Technology 21 | ||
| Chromosome | 17 | ||
| Allele Symbol | H2g7 | ||
| Allele Name | g7 variant | ||
| Allele Type | Not Applicable | ||
| Gene Symbol and Name | H2, histocompatibility-2, MHC | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | H-2; MHC-II; | ||
| Allele Symbol | Idd10NOD/ShiLt | ||
| Allele Name | NOD/ShiLt | ||
| Allele Type | QTL | ||
| Strain of Origin | NOD/ShiLt | ||
| Gene Symbol and Name | Idd10, insulin dependent diabetes susceptibility 10 | ||
| Chromosome | 3 | ||
| Gene Common Name(s) | Idd-10; | ||
| Molecular Note | This allele, in conjunction with NOD-derived alleles at Idd3 on a C57BL/6 background, confers defective cytokine response (IL-2, IL-4, IFN-gamma, CSF-2) when stimulated with antigens. | ||
| Allele Symbol | Idd1NOD/Uf | ||
| Allele Name | NOD/Uf | ||
| Allele Type | QTL | ||
| Strain of Origin | NOD/Uf | ||
| Gene Symbol and Name | Idd1, insulin dependent diabetes susceptibility 1 | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | Idd-1; | ||
| General Note |
NOD is homozygous for recessive alleles for susceptibility at all three loci, Idd1s, Idd2s, and Idd3s. The dominant alleles for non-susceptibility to IDD, Idd1r, etc., occur in the NON strain. Homozygosity for the recessive alleles at all three loci is necessary for the development of IDD.The Idd1 locus is linked to the major histocompatibility locus on Chr 17, but Idd2 is on Chr 9 (1) and Idd3 is on Chr 3 (J:8783, J:3351). This locus is also linked to peripheral CD4 lymphocytosis. | ||
| Molecular Note | This allele confers increased periinsulitis and increased CD4 lymphocytosis compared to C57BL/6. [MGI Ref ID J:33172] | ||
| Allele Symbol | Idd3NOD | ||
| Allele Name | NOD | ||
| Allele Type | QTL | ||
| Strain of Origin | NOD | ||
| Gene Symbol and Name | Idd3, insulin dependent diabetes susceptibility 3 | ||
| Chromosome | 3 | ||
| Gene Common Name(s) | Idd-3; | ||
| General Note |
Idd3 is also associated with insulitis. This allele (on a C57BL/6 background) also confers defective cytokine response (IL-2, IL-4, IFN-gamma, CSF-2) when stimulated with antigens (J:85823). Il2 is a proposed candidate gene for Idd3. The electrophoretic mobility pattern of IL-2 correlates with type 1 diabetes incidence. Resistant strain C57BL/6J displays a heterogeneous IL-2 mobility pattern with major protein species ranging from 17-19 kDa while susceptible strains 129 and NOD display a homogeneous IL-2 mobility pattern with one major protein species at approximately 21-22 kDa. | ||
| Molecular Note | This allele confers susceptibility to insulin dependent diabetes compared to C57BL/10. This allele confers decreased Ctla4 expression in activated T-cells compared to C57BL/6. [MGI Ref ID J:106844] [MGI Ref ID J:3351] | ||
References
References provided by MGI
Additional References
Lyons PA; Armitage N; Argentina F; Denny P; Hill NJ; Lord CJ; Wilusz MB; Peterson LB; Wicker LS; Todd JA. 2000. Congenic mapping of the type 1 diabetes locus, Idd3, to a 780-kb region of mouse chromosome 3: identification of a candidate segment of ancestral DNA by haplotype mapping. Genome Res 10(4):446-53. [PubMed: 10779485] [MGI Ref ID J:61763]
Podolin PL; Denny P; Armitage N; Lord CJ; Hill NJ; Levy ER; Peterson LB ; Todd JA ; Wicker LS ; Lyons PA. 1998. Localization of two insulin-dependent diabetes (Idd) genes to the Idd10 region on mouse chromosome 3. Mamm Genome 9(4):283-6. [PubMed: 9530623] [MGI Ref ID J:46659]
Yui MA; Muralidharan K; Moreno-Altamirano B; Perrin G; Chestnut K; Wakeland EK. 1996. Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: an approach for the genetic dissection of complex traits. Mamm Genome 7(5):331-4. [PubMed: 8661724] [MGI Ref ID J:33172]
H2g7 relatedIdd10NOD/ShiLt relatedAuger JL; Haasken S; Steinert EM; Binstadt BA. 2012. Incomplete TCR-beta allelic exclusion accelerates spontaneous autoimmune arthritis in K/BxN TCR transgenic mice. Eur J Immunol 42(9):2354-62. [PubMed: 22706882] [MGI Ref ID J:187944]
Belizaire R; Unanue ER. 2009. Targeting proteins to distinct subcellular compartments reveals unique requirements for MHC class I and II presentation. Proc Natl Acad Sci U S A 106(41):17463-8. [PubMed: 19805168] [MGI Ref ID J:153672]
Binstadt BA; Hebert JL; Ortiz-Lopez A; Bronson R; Benoist C; Mathis D. 2009. The same systemic autoimmune disease provokes arthritis and endocarditis via distinct mechanisms. Proc Natl Acad Sci U S A 106(39):16758-63. [PubMed: 19805369] [MGI Ref ID J:153217]
Carrasco-Marin E; Shimizu J; Kanagawa O; Unanue ER. 1996. The class II MHC I-Ag7 molecules from non-obese diabetic mice are poor peptide binders. J Immunol 156(2):450-8. [PubMed: 8543793] [MGI Ref ID J:30538]
Choisy-Rossi CM; Holl TM; Pierce MA; Chapman HD; Serreze DV. 2004. Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experience. J Immunol 173(6):3791-800. [PubMed: 15356126] [MGI Ref ID J:167508]
Driver JP; Chen YG; Zhang W; Asrat S; Serreze DV. 2011. Unmasking genes in a type 1 diabetes-resistant mouse strain that enhances pathogenic CD8 T-cell responses. Diabetes 60(4):1354-9. [PubMed: 21307079] [MGI Ref ID J:171763]
Driver JP; Scheuplein F; Chen YG; Grier AE; Wilson SB; Serreze DV. 2010. Invariant natural killer T-cell control of type 1 diabetes: a dendritic cell genetic decision of a silver bullet or Russian roulette. Diabetes 59(2):423-32. [PubMed: 19903740] [MGI Ref ID J:164162]
Ferreira C; Singh Y; Furmanski AL; Wong FS; Garden OA; Dyson J. 2009. Non-obese diabetic mice select a low-diversity repertoire of natural regulatory T cells. Proc Natl Acad Sci U S A 106(20):8320-5. [PubMed: 19359477] [MGI Ref ID J:148537]
Fossati G; Cooke A; Papafio RQ; Haskins K; Stockinger B. 1999. Triggering a second T cell receptor on diabetogenic T cells can prevent induction of diabetes. J Exp Med 190(4):577-83. [PubMed: 10449528] [MGI Ref ID J:108724]
Gray D; Abramson J; Benoist C; Mathis D. 2007. Proliferative arrest and rapid turnover of thymic epithelial cells expressing Aire. J Exp Med 204(11):2521-8. [PubMed: 17908938] [MGI Ref ID J:126040]
Jasinski JM; Yu L; Nakayama M; Li MM; Lipes MA; Eisenbarth GS; Liu E. 2006. Transgenic insulin (B:9-23) T-cell receptor mice develop autoimmune diabetes dependent upon RAG genotype, H-2g7 homozygosity, and insulin 2 gene knockout. Diabetes 55(7):1978-84. [PubMed: 16804066] [MGI Ref ID J:111874]
Klein J; Figueroa F; David CS. 1983. H-2 haplotypes, genes and antigens: second listing. II. The H-2 complex. Immunogenetics 17(6):553-96. [PubMed: 6407984] [MGI Ref ID J:7097]
Kouskoff V; Korganow AS; Duchatelle V; Degott C; Benoist C; Mathis D. 1996. Organ-specific disease provoked by systemic autoimmunity. Cell 87(5):811-22. [PubMed: 8945509] [MGI Ref ID J:36815]
Lee JS; Scandiuzzi L; Ray A; Wei J; Hofmeyer KA; Abadi YM; Loke P; Lin J; Yuan J; Serreze DV; Allison JP; Zang X. 2012. B7x in the periphery abrogates pancreas-specific damage mediated by self-reactive CD8 T cells. J Immunol 189(8):4165-74. [PubMed: 22972920] [MGI Ref ID J:190522]
Lee MS; Mueller R; Wicker LS; Peterson LB; Sarvetnick N. 1996. IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity. J Exp Med 183(6):2663-8. [PubMed: 8676087] [MGI Ref ID J:153576]
Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction. In: NOD Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, and Other Diseases. RG Landes, Austin. [MGI Ref ID J:110093]
Levisetti MG; Lewis DM; Suri A; Unanue ER. 2008. Weak proinsulin peptide-major histocompatibility complexes are targeted in autoimmune diabetes in mice. Diabetes 57(7):1852-60. [PubMed: 18398138] [MGI Ref ID J:138230]
Luhder F; Katz J; Benoist C; Mathis D. 1998. Major histocompatibility complex class II molecules can protect from diabetes by positively selecting T cells with additional specificities. J Exp Med 187(3):379-87. [PubMed: 9449718] [MGI Ref ID J:108722]
Ma YD; Park C; Zhao H; Oduro KA Jr; Tu X; Long F; Allen PM; Teitelbaum SL; Choi K. 2009. Defects in osteoblast function but no changes in long-term repopulating potential of hematopoietic stem cells in a mouse chronic inflammatory arthritis model. Blood 114(20):4402-10. [PubMed: 19759358] [MGI Ref ID J:154922]
Mahler M; Bristol IJ; Leiter EH; Workman AE; Birkenmeier EH; Elson CO; Sundberg JP. 1998. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 274(3 Pt 1):G544-51. [PubMed: 9530156] [MGI Ref ID J:46553]
Mangada J; Pearson T; Brehm MA; Wicker LS; Peterson LB; Shultz LD; Serreze DV; Rossini AA; Greiner DL. 2009. Idd loci synergize to prolong islet allograft survival induced by costimulation blockade in NOD mice. Diabetes 58(1):165-73. [PubMed: 18984741] [MGI Ref ID J:146982]
Martin-Orozco N; Chen Z; Poirot L; Hyatt E; Chen A; Kanagawa O; Sharpe A; Mathis D; Benoist C. 2003. Paradoxical dampening of anti-islet self-reactivity but promotion of diabetes by OX40 ligand. J Immunol 171(12):6954-60. [PubMed: 14662903] [MGI Ref ID J:86926]
Martinez RJ; Zhang N; Thomas SR; Nandiwada SL; Jenkins MK; Binstadt BA; Mueller DL. 2012. Arthritogenic self-reactive CD4+ T cells acquire an FR4hiCD73hi anergic state in the presence of Foxp3+ regulatory T cells. J Immunol 188(1):170-81. [PubMed: 22124124] [MGI Ref ID J:180819]
Pearson T; Markees TG; Serreze DV; Pierce MA; Marron MP; Wicker LS; Peterson LB; Shultz LD; Mordes JP; Rossini AA; Greiner DL. 2003. Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice. J Immunol 171(1):185-95. [PubMed: 12816997] [MGI Ref ID J:109845]
Podolin PL; Pressey A; DeLarato NH; Fischer PA; Peterson LB; Wicker LS. 1993. I-E+ nonobese diabetic mice develop insulitis and diabetes. J Exp Med 178(3):793-803. [PubMed: 8350054] [MGI Ref ID J:14178]
Serreze DV; Gallichan WS; Snider DP; Croitoru K; Rosenthal KL; Leiter EH; Christianson GJ; Dudley ME; Roopenian DC. 1996. MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD mice. Diabetes 45(7):902-8. [PubMed: 8666141] [MGI Ref ID J:33688]
Suwanai H; Wilcox MA; Mathis D; Benoist C. 2010. A defective Il15 allele underlies the deficiency in natural killer cell activity in nonobese diabetic mice. Proc Natl Acad Sci U S A 107(20):9305-10. [PubMed: 20439722] [MGI Ref ID J:160284]
Taylor JJ; Martinez RJ; Titcombe PJ; Barsness LO; Thomas SR; Zhang N; Katzman SD; Jenkins MK; Mueller DL. 2012. Deletion and anergy of polyclonal B cells specific for ubiquitous membrane-bound self-antigen. J Exp Med 209(11):2065-77. [PubMed: 23071255] [MGI Ref ID J:190897]
Turley SJ; Lee JW; Dutton-Swain N; Mathis D; Benoist C. 2005. Endocrine self and gut non-self intersect in the pancreatic lymph nodes. Proc Natl Acad Sci U S A 102(49):17729-33. [PubMed: 16317068] [MGI Ref ID J:104385]
Victoratos P; Kollias G. 2009. Induction of autoantibody-mediated spontaneous arthritis critically depends on follicular dendritic cells. Immunity 30(1):130-42. [PubMed: 19119026] [MGI Ref ID J:143728]
Wang JX; Bair AM; King SL; Shnayder R; Huang YF; Shieh CC; Soberman RJ; Fuhlbrigge RC; Nigrovic PA. 2012. Ly6G ligation blocks recruitment of neutrophils via a beta2-integrin-dependent mechanism. Blood 120(7):1489-98. [PubMed: 22661700] [MGI Ref ID J:189105]
Wei J; Loke P; Zang X; Allison JP. 2011. Tissue-specific expression of B7x protects from CD4 T cell-mediated autoimmunity. J Exp Med 208(8):1683-94. [PubMed: 21727190] [MGI Ref ID J:177612]
Wong FS; Du W; Thomas IJ; Wen L. 2005. The influence of the major histocompatibility complex on development of autoimmune diabetes in RIP-B7.1 mice. Diabetes 54(7):2032-40. [PubMed: 15983204] [MGI Ref ID J:109830]
Yoshida T; Jiang F; Honjo T; Okazaki T. 2008. PD-1 deficiency reveals various tissue-specific autoimmunity by H-2b and dose-dependent requirement of H-2g7 for diabetes in NOD mice. Proc Natl Acad Sci U S A 105(9):3533-8. [PubMed: 18299579] [MGI Ref ID J:132764]
Zhang C; Todorov I; Lin CL; Atkinson M; Kandeel F; Forman S; Zeng D. 2007. Elimination of insulitis and augmentation of islet beta cell regeneration via induction of chimerism in overtly diabetic NOD mice. Proc Natl Acad Sci U S A 104(7):2337-42. [PubMed: 17267595] [MGI Ref ID J:119749]
Idd1NOD/Uf relatedGhosh S; Palmer SM; Rodrigues NR; Cordell HJ; Hearne CM; Cornall RJ; Prins JB; McShane P; Lathrop GM; Peterson LB; Wicker LS; Todd JA. 1993. Polygenic control of autoimmune diabetes in nonobese diabetic mice. Nat Genet 4(4):404-9. [PubMed: 8401590] [MGI Ref ID J:13557]
Matsuki N; Stanic AK; Embers ME; Van Kaer L; Morel L; Joyce S. 2003. Genetic dissection of V alpha 14J alpha 18 natural T cell number and function in autoimmune-prone mice. J Immunol 170(11):5429-37. [PubMed: 12759418] [MGI Ref ID J:85823]
Mcaleer MA; Reifsnyder P; Palmer SM; Prochazka M; Love JM; Copeman JB; Powell EE; Rodrigues NR; Prins JB; Serreze DV; Delarato NH; Wicker LS; Peterson LB; Schork NJ; Todd JA; Leiter EH. 1995. Crosses of NOD mice with the related NON strain: A polygenic model for IDDM. Diabetes 44(10):1186-1195. [PubMed: 7556956] [MGI Ref ID J:28947]
Podolin PL; Denny P; Armitage N; Lord CJ; Hill NJ; Levy ER; Peterson LB ; Todd JA ; Wicker LS ; Lyons PA. 1998. Localization of two insulin-dependent diabetes (Idd) genes to the Idd10 region on mouse chromosome 3. Mamm Genome 9(4):283-6. [PubMed: 9530623] [MGI Ref ID J:46659]
Podolin PL; Denny P; Lord CJ; Hill NJ; Todd JA; Peterson LB; Wicker LS; Lyons PA. 1997. Congenic mapping of the insulin-dependent diabetes (Idd) gene, Idd10, localizes two gene mediating the Idd10 effect and eliminates the candidate Fcgr1. J Immunol 159(4):1835-1843. [PubMed: 9257847] [MGI Ref ID J:42103]
Idd3NOD relatedKoarada S; Wu Y; Yim YS; Wakeland EW; Ridgway WM. 2004. Nonobese diabetic CD4 lymphocytosis maps outside the MHC locus on chromosome 17. Immunogenetics 56(5):333-7. [PubMed: 15309345] [MGI Ref ID J:92304]
Prochazka M; Leiter EH; Serreze DV; Coleman DL. 1987. Three recessive loci required for insulin-dependent diabetes in nonobese diabetic mice [published erratum appears in Science 1988 Nov 11;242(4880):945] Science 237(4812):286-9. [PubMed: 2885918] [MGI Ref ID J:8783]
Todd JA; Aitman TJ; Cornall RJ; Ghosh S; Hall JR; Hearne CM; Knight AM; Love JM; McAleer MA; Prins JB; Rodrigues N; Lathrop M; Pressey A; DeLarato NH; Peterson LB; Wicker LS. 1991. Genetic analysis of autoimmune type 1 diabetes mellitus in mice [see comments] Nature 351(6327):542-7. [PubMed: 1675432] [MGI Ref ID J:3351]
Yui MA; Muralidharan K; Moreno-Altamirano B; Perrin G; Chestnut K; Wakeland EK. 1996. Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: an approach for the genetic dissection of complex traits. Mamm Genome 7(5):331-4. [PubMed: 8661724] [MGI Ref ID J:33172]
Brayer J; Lowry J; Cha S; Robinson CP; Yamachika S; Peck AB; Humphreys-Beher MG. 2000. Alleles from chromosomes 1 and 3 of NOD mice combine to influence Sjogren's syndrome-like autoimmune exocrinopathy. J Rheumatol 27(8):1896-904. [PubMed: 10955330] [MGI Ref ID J:71276]
Cornall RJ. 1993. Genetics of a multifactorial disease: autoimmune type 1 diabetes mellitus. Clin Sci (Colch) 84(3):257-62. [PubMed: 8384947] [MGI Ref ID J:17906]
Encinas JA; Wicker LS; Peterson LB; Mukasa A; Teuscher C; Sobel R; Weiner HL; Seidman CE; Seidman JG; Kuchroo VK. 1999. QTL influencing autoimmune diabetes and encephalomyelitis map to a 0.15-cM region containing Il2. Nat Genet 21(2):158-60. [PubMed: 9988264] [MGI Ref ID J:52572]
Lundholm M; Mayans S; Motta V; Lofgren-Burstrom A; Danska J; Holmberg D. 2010. Variation in the Cd3zeta (Cd247) gene correlates with altered T cell activation and is associated with autoimmune diabetes. J Immunol 184(10):5537-44. [PubMed: 20400699] [MGI Ref ID J:160996]
Lundholm M; Motta V; Lofgren-Burstrom A; Duarte N; Bergman ML; Mayans S; Holmberg D. 2006. Defective induction of CTLA-4 in the NOD mouse is controlled by the NOD allele of Idd3/IL-2 and a novel locus (Ctex) telomeric on chromosome 1. Diabetes 55(2):538-44. [PubMed: 16443792] [MGI Ref ID J:106844]
Matsuki N; Stanic AK; Embers ME; Van Kaer L; Morel L; Joyce S. 2003. Genetic dissection of V alpha 14J alpha 18 natural T cell number and function in autoimmune-prone mice. J Immunol 170(11):5429-37. [PubMed: 12759418] [MGI Ref ID J:85823]
Nguyen CQ; Kim H; Cornelius JG; Peck AB. 2007. Development of Sjogren's syndrome in nonobese diabetic-derived autoimmune-prone C57BL/6.NOD-Aec1Aec2 mice is dependent on complement component-3. J Immunol 179(4):2318-29. [PubMed: 17675493] [MGI Ref ID J:151221]
Nguyen CQ; Sharma A; She JX; McIndoe RA; Peck AB. 2009. Differential gene expressions in the lacrimal gland during development and onset of keratoconjunctivitis sicca in Sjogren's syndrome (SJS)-like disease of the C57BL/6.NOD-Aec1Aec2 mouse. Exp Eye Res 88(3):398-409. [PubMed: 19103199] [MGI Ref ID J:146559]
Nguyen CQ; Yin H; Lee BH; Chiorini JA; Peck AB. 2011. IL17: potential therapeutic target in Sjogren's syndrome using adenovirus-mediated gene transfer. Lab Invest 91(1):54-62. [PubMed: 20856230] [MGI Ref ID J:167186]
Podolin PL; Denny P; Lord CJ; Hill NJ; Todd JA; Peterson LB; Wicker LS; Lyons PA. 1997. Congenic mapping of the insulin-dependent diabetes (Idd) gene, Idd10, localizes two gene mediating the Idd10 effect and eliminates the candidate Fcgr1. J Immunol 159(4):1835-1843. [PubMed: 9257847] [MGI Ref ID J:42103]
Podolin PL; Wilusz MB; Cubbon RM; Pajvani U; Lord CJ; Todd JA; Peterson LB; Wicker LS; Lyons PA. 2000. Differential glycosylation of interleukin 2, the molecular basis for the NOD Idd3 type 1 diabetes gene? Cytokine 12(5):477-82. [PubMed: 10857762] [MGI Ref ID J:108210]
Todd JA; Aitman TJ; Cornall RJ; Ghosh S; Hall JR; Hearne CM; Knight AM; Love JM; McAleer MA; Prins JB; Rodrigues N; Lathrop M; Pressey A; DeLarato NH; Peterson LB; Wicker LS. 1991. Genetic analysis of autoimmune type 1 diabetes mellitus in mice [see comments] Nature 351(6327):542-7. [PubMed: 1675432] [MGI Ref ID J:3351]
Wilson EB; Livingstone AM. 2008. Cutting edge: CD4+ T cell-derived IL-2 is essential for help-dependent primary CD8+ T cell responses. J Immunol 181(11):7445-8. [PubMed: 19017930] [MGI Ref ID J:142211]
Yamanouchi J; Rainbow D; Serra P; Howlett S; Hunter K; Garner VE; Gonzalez-Munoz A; Clark J; Veijola R; Cubbon R; Chen SL; Rosa R; Cumiskey AM; Serreze DV; Gregory S; Rogers J; Lyons PA; Healy B; Smink LJ; Todd JA; Peterson LB; Wicker LS; Santamaria P. 2007. Interleukin-2 gene variation impairs regulatory T cell function and causes autoimmunity. Nat Genet 39(3):329-37. [PubMed: 17277778] [MGI Ref ID J:120349]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
Pricing and Purchasing
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $3000.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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Cryopreserved
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $3900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
Supply Notes
- Cryorecovery - Standard.
Progeny testing is not required.
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).
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Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
General Supply Notes
- This strain is included in the Type 1 Diabetes Repository collection.
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
Payment Terms and Conditions
Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.
See Terms of Use tab for General Terms and Conditions
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.Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
Contact information
General inquiries regarding Terms of UseContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice, Products & Services Conditions of Use
"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.No Warranty
MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.
In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.
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.
MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.
The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.
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.