Search Criteria: Research Area is "Diabetes and Obesity Research: Type 1 Diabetes (IDDM) Analysis Strains"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl ..... For more information please see the full phenotype on the strain data sheet | ||
| 002423 | NON/ShiLtJ | Level 4 |
| Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, d ..... For more information please see the full phenotype on the strain data sheet | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/ShiLtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/ShiLtJ. | ||
| 000689 | SWR/J | Level 4 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l ..... For more information please see the full phenotype on the strain data sheet | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/ShiLtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the ..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 weeks of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males ..... For more information please see the full phenotype on the strain data sheet | ||
| 012943 | C57BL/6-Tg(Ins2-luc/EGFP/TK)300Kauf/J | Repository- Live |
| C57BL/6J mice carrying tri-fusion transgene Ins2-luc/EGFP/Tk, commonly called MIP-TF, line 300 express a luciferase/enhanced green florescent protein/thymidine kinase fusion protein (luc/EGFP/Tk) under the control of mouse insulin promoter (Ins2) and are viable, fertile and exhibit no gross physical or behavioral abnormalities. Transgene expression, determined by luciferase enzymatic activity and green florescence is exclusive to the pancreas, specifically the insulin producing cells. Transgene expression appears to have no effect on weight, islet morphology, fasting blood glucose, or response to glucose challenge when compared to wild-type controls. This trifusion reporter model should enable longitudinal noninvasive imaging of beta cells in the same animal by cooled charge coupled device (CCD) and micro positron emission tomography (microPET), and identification of beta cells at the cellular level by florescent microscopy. There is a correlation between CCD and microPET signals fr ..... For more information please see the full phenotype on the strain data sheet | ||
| 005564 | FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ | Repository- Live |
| Transgenic mice are viable, display small eyes with cataracts and are hyperglycemic within 24 hours of age. S1 Nuclease protection assays indicate expression of calmodulin in the pancreas of 40-60 day old transgenic mice. Immunofluorescence analysis of the pancreas indicates increased levels of camodulin in B-cells of the pancreas. Camodulin fluorescing cells were not detected in the pancreatic acinar cells or any other tissue. Digital image scanning indicates the concentration of camodulin in transgenic B-cells is 5-fold higher than in wild type controls. Pancreatic insulin is 28% of control levels by 15 days of age. Insulin mRNA levels were also reduced in the transgenic animals. Transgenic mice experience hypoalbuminemia, elevated blood pressure, impaired cardiomyocytes and late stage diabetic nephropathy. Although transgenic mice are hyperglycemic within 24 hours of age, they are able to survive over a year without insulin treatment. This stock is useful for studying systemic c ..... | ||
| 003729 | NOD.129S7(B6)-Rag1tm1Mom/J | Repository- Live |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdcscid/Prkdcscid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1tm1Mom/J mice have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice is severely involuted. The thymocytes are CD8-CD4- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that both B cell and T cell development have been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. Notable differences between this strain and the NOD.CB17-Prkdcscid/J strain (Stock No. 001303) include a longer life s ..... For more information please see the full phenotype on the strain data sheet | ||
| 010613 | NOD.ALR-(D8Mit205-D8Mit137)/MxJ | Repository- Live |
| This diabetes resistant NOD congenic strain, commonly called NOD.ALRc8 or NOD-Idd22ALR/Lt, contains a unique diabetes resistant ALR/Lt derived genomic segment on Chr. 8 extending from D8Mit205 (51.9Mb) through D8Mit137 (106Mb) and contains Idd22 (90.6Mb). NOD.ALRc8 mice treated with 45mg/kg of Alloxan are completely diabetes resistant seven days post injection, unlike male NOD/ShiLt controls that are diabetes susceptible at this dose. In contrast to ALR/Lt males, which are diabetes resistant at doses higher than 65mg/kg, the NOD.ALRc8 male mice are diabetes susceptible at doses of 50mg/kg. This strain may be useful to further study the role of oxidative stress in autoimmune diabetes and to identify diabetes resistant candidate genes in the Idd22 region. | ||
| 010971 | NOD.B-(D3Mit93-D3Mit124)(D4Mit114-D4Mit142)/1112MrkJ | Repository- Live |
| This NOD/MrkTac bicongenic strain carries a C57BL/6 derived genome on Chr. 3 that contains Idd3/17/10/18 and C57BL/10 derived genome on Chr. 4 containing Idd9.1, 9.2, 9.3. Unlike the parental strains, known to have low frequency diabetes, no diabetes and almost no insulitis has been detected by 12 months of age in this strain. However, at 9-11 months of age 50% of the females and 25% of the males develop autoimmune liver disease. Histological evaluation showed biliary cyst formation and obstruction which progresses with age and lymphocytic infiltrates adjacent to the cyst walls were observed. Further histological studies indicate that 44% of 8-week-old mice had early cyst formation and lymphocytic infiltrates and at 30 weeks of age 90% of the animals evaluated had cyst formation and lymphocytic infiltration, Koarada et al, 2004. The donating investigator has communicated that recent findings indicate the C57BL/6 genetic contamination on chromosome 1 is necessary for ..... For more information please see the full phenotype on the strain data sheet | ||
| 002591 | NOD.B10Sn-H2b/J | Repository- Live |
| This congenic strain serves as a diabetes-resistant control for comparison to the NOD/LtJ strain (Stock No. 001976). The diabetes resistant MHC H2b haplotype was transferred from C57BL/10J mice to the NOD/Lt strain. These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. They are useful in dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 012391 | NOD.B10Sn-Idd5.1C57BL/10SnJ/R46MrkTacJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.B10-Idd5R46, line 2193, carries a diabetes resistant C57BL/10SnJ (Stock No. 000666) chromosome 1 segment. The B10 introgressed segment is defined within D1Mit74 (57.6Mb) through AL671560 (SNP marker at approximately 62Mb) and includes the insulin dependent diabetes susceptibility (Idd)5.1; including candidate gene Ctla4.
Diabetes incidence is modest but significant among 7 month old female mice of this strain, which is reported at 62%, compared with more than 80% in NOD controls (Hunter, et al. 2007). This strain may be useful to understand the epistatic interactions of Idd5.1 alleles with other Idd loci. | ||
| 012396 | NOD.B10Sn-Idd5.2C57BL/10SnJ Idd5.3C57BL/10SnJ/7341MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd5R7341, contains two genomic segments containing Idd5.2 and Idd5.3, from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 1. The C57BL/10SnJ genomic segments include Idd5.2 that contains major candidate gene Nramp1 and Idd5.3 containing major candidate gene Ikcf2. Diabetes incidence similar to NOD is not protected in this NOD.B10-Idd5.2, Idd5.3 strain. This strain may be useful for understanding the variation in diabetic resistance conferred by Idd loci, in particular the epistatic interactions of Idd5.2, Idd5.3 alleles with other Idd alleles. | ||
| 012394 | NOD.B10Sn-Idd5.2C57BL/10SnJ/6146MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd5R6146, contains a 3.85Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 1 and is defined within markers D1Mit532 (73Mb) through D1Mit132 (77Mb). The C57BL/10SnJ genomic segment includes Idd5.2 and contains major candidate gene Nramp1. Diabetes incidence is significantly protected among 7-month old females. Diabetes incidence among 7-month old females is reported to be about 38%, compared with 80% in NOD controls or 62% in NOD.B10-Idd5.1 (Stock No. 012391) (Hunter, et al. 2007).
This strain may be useful for positional mapping the Idd5.2 region. In addition, this strain is useful for understanding the variation in diabetic resistance conferred by Idd loci, in particular the epistatic i ..... | ||
| 012395 | NOD.B10Sn-Idd5.3C57BL/10SnJ/7345MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd5.3R7345, contains a 3.55Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 1. The C57BL/10SnJ genomic segment includes Idd5.3 and contains major candidate gene Ikcf2 and Acadl. Diabetes incidence among 7-month old females is reported to be equivalent to published stock 6360 (Hunter, et al. 2007), which is significantly protected with about 69% of the females becoming diabetic, compared with 83% in NOD controls. This strain may be useful for positional mapping the Idd5.3 region. In addition, this strain is useful for understanding the variation in diabetic resistance conferred by Idd loci, in particular the epistatic interactions of Idd5.3 alleles with other Iddalleles | ||
| 013253 | NOD.B10Sn-Idd9.2C57BL/10SnJ/1566MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic stock, commonly referred to as NOD.B10-Idd9.2 line 1566, carries C57BL/10SnJ (Stock No. 000666) derived genome on chromosome 4 containing the Idd9.2 region. This strain is partially protected from diabetes. It has been reported that the Idd9.2 region contains a mechanism that strongly modulates CD8+tolerance. This strain may be useful for positional mapping of the Idd9.2 loci and studying candidate genes within the Idd9.2 region. | ||
| 013187 | NOD.B6-Idd10C57BL/6 Idd18.2C57BL/6J Idd18.3C57BL/6J/2412MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B6-Idd10/18R53, line 2412 is viable and fertile. . Mice of this strain contain a genomic segment from the diabetes resistant strain C57BL/6J (Stock No. 000664) introgressed into the NOD chromosome 3. The C57BL/6 genomic segment includes Idd10, Idd18.2 and Idd18.3; while the Idd3, Idd17 and Idd18.1 regions are of NOD origin. The Idd10 region contains major candidate gene Cd101 (100Mb); and the recently identified 966Kb (108.3Mb-109.3Mb) Idd18.3 region contains 22 genes and 1 pseudogene. Thymocytes of 3-week old male congenic mice express 1.46 fold more full length VAV3 mRNA than thymocytes of line 7754 (Stock No. 013186); which carries a C57BL/6J derived Idd18.1 (Vav3), Idd18.2 and Idd18.3. Diabetes incidence overlaps with line 7754 and is reported to ..... For more information please see the full phenotype on the strain data sheet | ||
| 013186 | NOD.B6-Idd10C57BL/6 Idd18C57BL/6/7754MrkTacJ | Repository- Live |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B6-Idd10/18, line 7754 is viable and fertile. Mice of this strain are derived from line 1101 and contain a genomic segment from the diabetes resistant strain C57BL/6J (Stock No. 000664) introgressed into the NOD chromosome 3. The C57BL/6 genomic segment includes Idd10, Idd18.1, Idd18.2 and Idd18.3; , while the Idd3 and Idd17 regions are of NOD origin. The Idd10 region contains major candidate gene Cd101 (100Mb); the Idd18.1 region contains major candidate gene Vav3 and the recently identified 966Kb Idd18.3 region contains 22 genes and 1 pseudogene. Thymocytes of 3-week old male congenic mice express 1.46 fold less full length VAV3 mRNA than thymocytes of line 2412 (Stock No. 013187); which carries a C57BL/6J derived Idd10, Idd18.2 and Idd18.3> ..... For more information please see the full phenotype on the strain data sheet | ||
| 014149 | NOD.B6-Ptprcb/6908MrkTacJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.Cd45.2, is viable and fertile. Mice of this strain contain a genomic segment from the diabetes resistant strain C57BL/6 introgressed into the NOD chromosome 1. The C57BL/6 genomic segment includes Ptprcb, commonly referred to as Cd45.2. Although reported to be significantly reduced compared to NOD, congenic female mice exhibit a high frequency of diabetes with about 60% of the females becoming diabetic by 200 days of age. As Ptprc is expressed on all adaptive and innate immune cells, this strain provides a unique cell surface marker that can be used to track lineage and phenotype of all hematopoietic donor derived or transferred cells making it useful in studies monitoring immune pathogenesis in the NOD model. | ||
| 013233 | NOD.B6-Tg(Itgax-cre,-EGFP)4097Ach/J | Repository- Live |
| Mice hemizygous for this Itgax-cre,-EGFP (Itgax, commonly referred to as CD11c) transgene are viable and fertile. The CD11c promoter directs bicistronic Cre and EGFP protein expression to dendritic cells (DCs). Expression of EGFP is expected to have equimolar expression with Cre recombinase. When bred with any mouse containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence. These CD11c-Cre-GFP transgenic mice may be useful for immunological studies, specifically in Type 1 Diabetes, utilizing Cre-lox technology or fluorescent protein expression in dendritic cells, . | ||
| 010606 | NOD.Cg-Ncf1m1J/MxJ | Repository- Live |
| On the C57BL/6 background, Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47phox protein in cells from these mice. Analysis for other NADPH oxidases involved in neutrophil superoxide production revealed that NCF2/p67phox was present at wild type levels and CYBB/gp91phox and CYBA/p22phox were expressed at higher than wild type levels. Other neutrophil products were assayed and found not to differ in bone marrow cells of C57BL/6J vs. mutant mice; (Huang et al. 2000). NOD.Ncf1 deficient mice lack functional NADPH oxidase enzymes and a ..... | ||
| 009377 | NOD.Cg-Rag1tm1Mom Tg(TcraBDC12-4.1)10Jos Tg(TcrbBDC12-4.1)82Gse/J | Repository- Live |
| This double transgenic, targeted mutation strain carries a rearranged Tcr beta gene and a Tcr alpha gene from the pathogenic anti-insulin CD4+ T-cell clone BDC12-4.1 and NOD.Rag1tm1Mom targeted mutation (Stock No. 003729). Triple mutant mice are viable and fertile. When the congenic NOD double transgenic is combined with a homozygous Rag1tm1Mom mutation, recombination of the endogenous TCR and immunoglobulin genes is prevented. As a result, mature T cells in these mice express only the BDC12-4.1 TCR. Further, approximately 50% of the TCR double transgenic, Rag1tm1Mom homozygote mice develop diabetes by 30 weeks of age. Histopathology indicates severe insulitis and/or destruction of all insulin-producing cells (Jasinski et al 2006). This BDC12-4.1 TCR double transgenic, Rag1 deficient strain is useful for further studying the pathogenesis of insulin autoimmuni ..... For more information please see the full phenotype on the strain data sheet | ||
| 008173 | NOD.Cg-Tg(Ins1-EGFP)1Hara/QtngJ | Repository- Live |
| Mice hemizygous for this "MIP-GFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Green Fluorescent Protein under the control of mouse insulin 1 promoter. Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adult. The human growth hormone sequence in the transgenic insert enhances expression of the EGFP but is not expressed. The donating investigator reports NOD transgenic female mice develop insulitis and autoimmune diabetes at a similar rate and kinetics as female wildtype controls, 62% and 58% respectively, while surprisingly, transgenic males develop insulitis and diabetes at a higher rate than male wildtype controls, 65% and 10% respectively. This transgenic MIP-GFP mouse strain is useful in studies of diabetes and pancreatic beta islet cell biology.
In ..... | ||
| 004460 | NOD.Cg-Tg(TcraBDC2.5,TcrbBDC2.5)1Doi/DoiJ | Repository- Live |
| These transgenic mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. When paired with a homozygous Rag1tm1Mom mutation (such as in Stock No. 003729), recombination of endogenous TCR and Ig is prevented so that mature T cells in these mice express only the BDC2.5 TCR. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks). When coupled with the homozygous Rag1tm1Mom mutation, mice develop diabetes extremely early (mean age of 25 days). (Katz et al 1993, Gonzalez et al 2001, Mombaerts et al 1992) | ||
| 010526 | NOD.Cg-Tg(TcraTcrbNY4.1)1Pesa/DvsJ | Repository- Live |
| NOD.Cg-Tg(TcraTcrbNY4.1Pesa/DvsJ, commonly called NY4.1-NOD, express rearranged Tcrα and Tcrβ transgenes derived from the pancreatic beta cell-cytotoxic CD4+ T cell clone NY4.1. CD4+CD8- thymocyte derived T cells are skewed toward V β11+ expression when compared to wild type controls. Transgenic females and males exhibit dramatically accelerated diabetes, the cumulative transgenic female diabetes incidence is similar to wildtype females; while transgenic males exhibit increased incidence compared to wildtype controls. Overall kinetics of disease are remarkably similar to their wild type cohorts. Insulitis scores of 3 week old transgenic mice are significantly lower, while insulitis scores of 6 week olds are significantly more severe than in wild types controls, Schmidt et al, 1997, J. Exp Med 186, 1059-1075. Transgenic animals bearing NY4.1 TCR alpha and beta transgenes offer a source of CTL ..... For more information please see the full phenotype on the strain data sheet | ||
| 008547 | NOD.FVB-Tg(ITGAM-DTR/EGFP)34Lan/JdkJ | Repository- Live |
| Transgenic mice have a diphtheria toxin (DT) inducible system that transiently depletes macrophages. The transgene insert contains a fusion product involving simian diphtheria toxin receptor and green fluorescent protein under the control of the human ITGAM (integrin alpha M) promoter (CD11b). RT-PCR analysis of bone marrow macrophages detects specific transgene expression. Cytological analysis of thioglycollate treated peritoneal cells shows the absence of macrophages. Intraperitoneal injection of DT ablates monocyte/macrophage cells in the peritoneal cavity. Unmanipulated CD11b/DTR NOD mice are viable, normal in size and develop spontaneous diabetes similar to NOD/ShiLtJ. Transgene expression of EGFP is not sufficient to be detected by FACS analysis. Twelve hours following DT administration all macrophages are ablated in the spleen and lymph nodes, including the pancreatic lymph node and pancreas for three to five days. Macrophage population is restored by day four following a ..... For more information please see the full phenotype on the strain data sheet | ||
| 004483 | NOD.NON-Thy1a/1LtJ | Repository- Live |
| 008694 | NOD/ShiLt-Tg(Foxp3-EGFP/cre)1cJbs/J | Repository- Live |
| Mice hemizygous for the Foxp3-EGFP/cre BAC transgene are viable and fertile. They express an enhanced green fluorescent protein and codon optimized "humanized" cre under the control of the mouse Foxp3 promoter. Transgene expression is specific to Cd4+Cd25 highCd127 low T cells from the lymph nodes, spleen and thymus. GFP expression is restricted to FoxP3+ cells. This mutant mouse strain may be useful for fluorescently labeling Foxp3+ T-cells to study regulatory T-cell function in autoimmunity specifically, type 1 diabetes. | ||
| 002574 | NOD.129P2(B6)-Il4tm1Cgn/Dvs | Research Strain |
| 002313 | NOD.Cg-Prkdcscid Emv30b/Dvs | Research Strain |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen ..... For more information please see the full phenotype on the strain data sheet | ||
| 006500 | 129.NOD-(D17Mit175-H2)/J | Cryopreserved - Ready for recovery |
| 129S1.NOD-H2g7 congenic mice are viable, fertile, normal in size, do not display any gross physical or behavioral abnormalities and are diabetes free. Because targeted mutations frequently are made using 129 ES cells, this strain may be useful for identifying Idds in 129 strains. | ||
| 010972 | B10.NOD-(rs13459152-rs13483054)/1107MrkJ | Cryopreserved - Ready for recovery |
| This C57BL/10SnJ congenic strain contains a 26.95 Mb segment of Chr 17 from NOD, extending from rs13459152 through rs13483054, that includes the major histocompatibility complex (MHC), H2, and the insulin dependent diabetes susceptibility locus, Idd1. The name given in the primary reference is B10.H2g7. Destructive insulitis and diabetes have not been observed. This B10.H2g7 strain may be useful for immunological studies requiring the NOD MHC on a Type 1 Diabetes resistant background and for mapping non-NOD MHC-linked phenotypes. | ||
| 006411 | B6.129-Gasttm1(INS)Ez/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this "G-InsKi" allele are viable and fertile. Human insulin expressed from this mutant allele retains full biological activity. Expression of human insulin is specific to gastrin-expressing cells (G cells of the antral stomach and some duodenum cells), and is released into portal circulation in response to the same meal-associated stimuli that control gastrin release. Heterozygous mice exhibit normal blood glucose levels, and toxic hypoglycemia is not observed. The donating investigators report that human insulin levels are sufficient to activate insulin signaling cascades in the liver but not in skeletal muscle. These mutant mice may be useful for diabetes and obesity research, specifically for studying the molecular and physiological mechanisms by which the hepatic action of transgenic insulin prolongs the survival of diabetic mice (e.g. Ins2Akita mutant mice). | ||
| 005715 | B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ | Cryopreserved - Ready for recovery |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Better than 70% of the B6.H2g7 transgenic mice become diabetic by 30 weeks of age compared the control B6.H2g7 which does not develop insulitis or diabetes. Spleens of diabetic B6.H2g7 transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ mice, yet failed to transfer disease to NOD.scid, B6.scid, CB17.scid, or irradiated B6/RIP-B7.1. B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ provides a tool for studying mechanisms of loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 003068 | B6.NOD-(Csf2-D11Mit42) (D17Mit21-D17Mit10)/J | Cryopreserved - Ready for recovery |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in the reference below) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 42 cM segment of Chr 11 (called c11 by Yui et al.)extending from Csf2(colony stimulating factor 2 (granulocyte-macrophage)) through D11Mit42and including the insulin dependent diabetes susceptibility locus Idd4.No information has been published for this double 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. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet ..... For more information please see the full phenotype on the strain data sheet | ||
| 003065 | B6.NOD-(Csf2-D11Mit42)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 42 cM segment of Chr 11 extending from Csf2(colony stimulating factor 2, granulocyte-macrophage) through D11Mit42that includes the insulin dependent diabetes susceptibility locus Idd4.The name given this segment in the primary reference is c11. Upon histological examination of the pancreas, the incidence and severity of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) in B6.NOD-(Csf2-D11Mit42) mice were found to be similar to those in C57BL/6 controls. | ||
| 003069 | B6.NOD-(D1Mit3-Bcl2) (D17Mit21-D17Mit10)/LtJ | Cryopreserved - Ready for recovery |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in the reference below) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 44 cM segment of Chr 1 (called c1c by Yui et al.)extending from D1Mit3through Bcl2(B-cell leukemia/lymphoma 2) and including Idd5(insulin dependent diabetes susceptibility 5). No information has been published for this double congenic. However, upon histologic examination of the pancreas, a significantly higher percentage of both B6.NOD-D1Mit3-Bcl2 (Idd5)and B6.NOD-D17Mit21-D17Mit10 (H2g7, Idd1)singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreas of these mice. The pancreatic infiltrates were not associated specifically with the islets. In ..... For more information please see the full phenotype on the strain data sheet | ||
| 003062 | B6.NOD-(D1Mit3-Bcl2)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 44 cM segment of Chr 1 extending from D1Mit3through Bcl2(B-cell leukemia/lymphoma 2) that includes Idd5(insulin dependent diabetes susceptibility 5). The name given this segment in the primary reference is c1c. Upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D1Mit3-Bcl2) 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. 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. Female B6.NOD-(D1Mit3-Bcl2) mice exhibited pancreatic infiltration at twice the frequency of males; female NOD mice are more susceptible than males to both insulitis and ..... For more information please see the full phenotype on the strain data sheet | ||
| 003867 | B6.NOD-(D1Mit5.1-D1Mit159)/LtJ | Cryopreserved - Ready for recovery |
| 003071 | B6.NOD-(D1Mit5.1-D1Mit15) (D17Mit21-D17Mit10)/J | Cryopreserved - Ready for recovery |
| 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 47 cM segment of Chr 1 (called c1t by Yui et al.) extending from D1Mit5through D1Mit15and including Idd5(insulin dependent diabetes susceptibility 5). No information has been published for this double congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of both B6.NOD-(D1Mit5-D1Mit15) and 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. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was ..... For more information please see the full phenotype on the strain data sheet | ||
| 003866 | B6.NOD-(D1Mit5.1-D1Mit15)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 47 cM segment of Chr 1 extending from D1Mit5 through D1Mit15 that includes Idd5 (insulin dependent diabetes susceptibility 5). The name given this segment in the primary reference is c1t. Upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-D1Mit5-D1Mit15 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. 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. Female B6.NOD-D1Mit5-D1Mit15 mice exhibited pancreatic infiltration at twice the frequency of males; female NOD mice are more susceptible than males to both insulitis and diabetes. | ||
| 003064 | B6.NOD-(D2Mit274-D2Mit343)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for an 32 cM segment of Chr 2 extending from D2Mit274through D2Mit343that includes the insulin dependent diabetes susceptibility locus Idd13(Myrick C, Leiter EH, Langley SH. 2000. Personal communication.) | ||
| 003067 | B6.NOD-(D3Mit132-Tshb) (D17Mit21-D17Mit10)/J | Cryopreserved - Ready for recovery |
| 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 per ..... For more information please see the full phenotype on the strain data sheet | ||
| 003059 | B6.NOD-(D3Mit132-Tshb)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 43 cM segment of chromosome 3 extending from D3Mit132through Tshb(thyroid stimulating hormone, beta subunit) that includes the diabetes susceptibility loci Idd3and Idd10 (which has been subsequently refined into three diabetes susceptibility loci: Idd10, Idd17, and Idd18). The name given this segment in the primary reference is c3. Upon histologic examination of the pancreas, B6.NOD-(D3Mit132-Tshb) female mice exhibited somewhat higher incidence of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) than did C57BL/6J controls, but the difference was not statistically significant. Female B6.NOD-(D3Mit132-Tshb) mice had twice the incidence of periinsulitis as males; female NOD mice are more susceptible than males to both insulitis and diabetes. | ||
| 003066 | B6.NOD-(D6Mit54-D6Mit14) (D17Mit21-D17Mit10)/J | Cryopreserved - Ready for recovery |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 24 cM segment (called c6 by Yui et al.)of Chr 6 extending from D6Mit54through D6Mit14and including the insulin dependent diabetes susceptibility locus Idd6.No information has been published for this double 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. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one a ..... For more information please see the full phenotype on the strain data sheet | ||
| 003063 | B6.NOD-(D6Mit54-D6Mit14)/J | Cryopreserved - Ready for recovery |
| This strain is congenic for a 24 cM segment of Chr 6 extending from D6Mit54through D6Mit14that includes the insulin dependent diabetes susceptibility locus Idd6.The name given this segment in the primary reference is c6. Upon histologic examination of the pancreas, the incidence and severity of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) of B6.NOD-(D6Mit54-D6Mit14) mice were found to be similar to those of C57BL/6 controls. | ||
| 005713 | C.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ | Cryopreserved - Ready for recovery |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Approximately 10% of the BALB transgenic mice become diabetic by 30 weeks of age compared the control BALBs which are diabetes resistant. Spleens of diabetic BALB transgenic mice used in adoptive transfer experiments do not transfer diabetes to NOD.scid/RIP-B7.1. C.Cg-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 002980 | C57BL/6-Tg(Cd152Ig)1Jbs/J | Cryopreserved - Ready for recovery |
| A soluble form of the CD152 antigen (CTLA4Ig)is expressed under the control of the K14 promoter that is primarily active in the skin, but also thymus and tongue. The animal produces blood circulating levels of CTLA4Ig that are easily detectable by ELISA or functional assays. | ||
| 002349 | CBcNO6/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003052 | CBcNO7A/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003053 | CBcNO7B/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003054 | CBcNO7C/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003055 | CBcNO7D/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 008063 | NOD-Chr 17NZM2328/McdfJ | Cryopreserved - Ready for recovery |
| This NOD consomic strain, commonly referred to as NOD.Zc17 carries Chromosome 17 alleles, D17Mit164 (38Mb) through D17Mit73 (79Mb) derived from NZM2328. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 0 in both females and males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain will be useful to identify candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 008062 | NOD-Chr 1NZM2328/McdfJ | Cryopreserved - Ready for recovery |
| This NOD consomic strain, commonly referred to as NOD.Zc1, carries Chromosome 1 alleles, D1Mit316 (10Mb) through D1Mit293 (194Mb) derived from NZM2328 that includes the Idd5 region. NOD.Zc1 is viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 10% in the females and 0% in males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain will be useful to identify candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 008064 | NOD-Chr 4NZM2328/McdfJ | Cryopreserved - Ready for recovery |
| This NOD consomic strain, commonly referred to as NOD.Zc4 carries Chromosome 4 alleles, D4Mit18 (13Mb) through D4Mit59 (154Mb) derived from NZM2328. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 7% in females and 0 for males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain is useful for identifying candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases such as Type 1 diabetes and Lupus. | ||
| 005739 | NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. RT/PCR indicates transgene expression in the spleen and thymus. Blood glucose levels of transgenic and non-transgenic littermates are identical. 90-98 % of the transgenic islets of females and males are insulitis free. Transgenic mice do not develop spontaneous diabetes and are resistant to cyclophosphamide-induced diabetes. Sialitis is not statistically different between transgenic and littermate controls (French MB, Diabetes 1997 46:34-9). Transgenic bone marrow transplanted into 4-week-old irradiated NOD female’s almost entirely prevented diabetes compared to control NOD to irradiated NOD transplants, which have an overall diabetes incidence similar to untreated controls. Thymoma incidence was similar in both irradiated groups.(Steptoe RJ, J Clin Invest 2003 111:1357-63) This model may be helpful for looking at antigen speci ..... For more information please see the full phenotype on the strain data sheet | ||
| 005020 | NOD-Tg(Igh-6/Igh-V281)3Jwt/JwtJ | Cryopreserved - Ready for recovery |
| The double transgenic produced by crossing this stock with Stock No. 005018 serves as a control to the double transgenic which results from crossing Stock No. 005018 with Stock No. 005019. | ||
| 005522 | NOD-Tg(Ins2*Y16A)1Ell/GseJ | Cryopreserved - Ready for recovery |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)1Ell mutation. Approximately 75% of line B female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. Donating investigator reports male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. In contrast, transgenic female mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). Donating investigator reports line B transgenics have lower expression levels than line F and that male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. NOD-Tg(Ins2*Y16A)1Ell/GseJ is usefu ..... | ||
| 005523 | NOD-Tg(Ins2*Y16A)3Ell/GseJ | Cryopreserved - Ready for recovery |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). NOD-Tg(Ins2*Y16A)3Ell/GseJ is useful to study insulin-reactive autoimmunity. | ||
| 005356 | NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ | Cryopreserved - Ready for recovery |
| NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ is homozygous for linkage markers delineating Idd1-5, 7-10 and 13-15 loci of NOD origin and do not become diabetic. Histology indicates normal islet tissue structure with no cellular infiltration. Islets are intact and produce insulin. FACs analysis of peripheral blood cells of mice homozygote for B2mtm1Unc and C2tatm1Ccum confirmed the absence of MHC I or MHC II cell surface expression, reduced peripheral T-cell populations, deficiency of CD4+ and CD8+ T-cells and there is no difference in B-cell numbers when compared with wild-type controls. Additionally, B2mtm1Unc,C2tatm1Ccum double homozygous animals exhibit lower IgG titers and higher IgM titers than wild-type controls. Diabetic NOD females receiving purified islets from NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ transplanted under the kidney capsule remain normal ..... For more information please see the full phenotype on the strain data sheet | ||
| 005144 | NOD.129(B6)-Ctla4tm1All/DoiJ | Cryopreserved - Ready for recovery |
| Heterozygous Ctla4tm1All mice are viable, fertile, and normal in size and exhibit diabetes incidence comparable to NOD. Ctla4tm1All homozygous mice on various backgrounds, including C57BL/6, BALB/c, 129 and NOD, die at 3-4 weeks of age due to massive polyclonal expansion of T-cells and massive lymphocyte infiltration into non-lymphoid organs, such as heart, liver, lung and pancreas. Treatment with murine Ctla4Ig or depletion of CD4+ T-cells blocks this lymphoproliferative disease. Splenic and lymph node T-cells display an activated phenotype characterized as CD69+, CD25+, CD44hi, Mel14lo, CD45RBlo and Sca1hi and have down regulated the TCR. Lymph node and spleen cells cultured from Ctla4tm1All homozygous mice spontaneously proliferate while wild-type controls do not. Cells from whole lymph nodes or purified T-cells are unresponsive to anti CD28mAb stimu ..... | ||
| 009618 | NOD.129(B6)-Il12btm1Lky/JbsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for this bicistronic "yet40" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The IRES-EYFP is inserted downstream of the endogenous stop codon, allowing for normal expression of the endogenous gene and simultaneous EYFP reporter expression. ELISA assays confirm that p40 protein is expressed at similar levels in homozygous mutant and wildtype mice. The EYFP reporter marks dendritic cell (DC) and macrophage lineage cells that produce p40 following stimulation with toll-like receptor (TLR) ligands both in vivo and in vitro. NOD congenic female mice carrying this bicistronic "yet40" allele experience slightly accelerated diabetes. These mice may be useful for labeling activated IL12/23 p40 expressing cells in studies of immunology and immunity, TLR signal cascades, cancer immunity, vaccine development and diabetes. | ||
| 004673 | NOD.129(B6)-Rag1tm1Mom Cd80tm1Shr/JbsJ | Cryopreserved - Ready for recovery |
| The NOD.129(B6)Rag1tm1MomCd80tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1tm1Mom and Cd80tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1tm1MomCd80tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation. | ||
| 005352 | NOD.129-(D19Mit10-D19Mit54)/GseJ | Cryopreserved - Ready for recovery |
| This NOD/ShiLt congenic strain, commonly called NOD.Ins1 control, is carrying Chromosome 19 alleles derived from strain 129S1/SvImJ at the Ins1 loci. Diabetes onset and incidence among NOD.129-(D19Mit10-D19Mit54)/GseJ congenic mice is similar to NOD, Nakayama M, Nature 2005 435:220-3. This strain is useful as a control for the exploration of Ins1 in the context of the NOD congenic Ins1 targeted mutation (Stock No. 005035). | ||
| 005353 | NOD.129-(D7Mit105-D7Mit223)/GseJ | Cryopreserved - Ready for recovery |
| This NOD/ShiLt congenic strain, commonly called NOD.Ins2 control, is carrying Chromosome 7 alleles derived from strain 129S1/SvImJ at the Ins2 loci. Diabetes onset and incidence among NOD.129-(D7Mit105 -D7Mit223)/GseJ congenic mice is similar to NOD. (Nakayama M, Nature 2005 435:220-3) This strain is useful as a control for the exploration of Ins2 in the context of the NOD congenic Ins2 targeted mutation (Stock No. 005036). | ||
| 006611 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| NOD mice carrying only the HLA-A/H2-D/B2M transgene, commonly referred to as NOD.HHD, (Stock No. 006604) develop significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice.
This mutant stock is also homozygous for the B2mtm1Unc mutation which normally prevents the development of of CD8+ T cells. The presence of the transgene in the B2m-deficient background, however, restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2M component encoded into the transgene, the transgenic construct is unable to rescue murine MHC class 1 molecules in the NOD.B2m deficient (Stock No. 002309) mice. Thus, these double mutant mice only express human HLA-A2.1. Fifty-five percent of these NOD transgenic B2m-deficient mice develop diabetes b ..... For more information please see the full phenotype on the strain data sheet | ||
| 010565 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A24/H2-D/B2M)3Dvs/J | Cryopreserved - Ready for recovery |
| NOD mice carrying only the HLA-A24/H2-D/B2M transgene and homozygous for the B2mtm1Unc mutation, commonly referred to as NOD.B2mnull. A24/HHD, are viable, normal in size, do not display any gross physical or behavioral abnormalities and are reported to be poor breeders. The presence of the transgene in the B2m deficient background restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2m component incorporated into the transgene, the transgenic construct is unable to rescue expression of murine MHC class I molecules in the NOD. B2m deficient (Stock No. 003914) mice. FACS analysis confirms the NOD. B2m null. A24/HHD mice express human HLA-24, but no murine MHC class I molecules. NOD.B2m null, A24/HHD mice develop insulitis, but progression to overt diabetes is reported to be rare.
This model provides humanized HLA-24 restricted T cells that will be useful tools ..... For more information please see the full phenotype on the strain data sheet | ||
| 002309 | NOD.129P2(B6)-B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cell deficiency, NK1+ T cells deficiency and decreased levels of serum Ig. Some forms of lupus autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). The B2mtm1Un mutation backcrossed to the NOD/Lt strain serves as a MHC class I-negative, CD8+ deficient diabetes resistant stock ..... For more information please see the full phenotype on the strain data sheet | ||
| 002573 | NOD.129P2(B6)-Il2tm1Hor/DvsJ | Cryopreserved - Ready for recovery |
| Heterozygotes and homozygotes have accelerated diabetes onset, compared with NOD controls, with homozygotes dying by 5 to 7 weeks of age and heterozygotes having an average lifespan of approximately 100 days. Treatment with complete Freund?s adjuvant can delay disease onset and extend lifespan to permit homozygotes to reproduce. | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001) | ||
| 004444 | NOD.129P2(C)-Tcratm1Mjo/DoiJ | Cryopreserved - Ready for recovery |
| NOD mice homozygous for the Tcratm1Mjo targeted mutation lack alpha beta T cells, and therefore, are completely protected from diabetes development. Because of the complete elimination of alpha beta T cells, these mice are useful in adoptive transfer experiments (as in Hoglund et al. 1999). | ||
| 014163 | NOD.129S2(B6)-Alox15tm1Fun/NadlJ | Cryopreserved - Ready for recovery |
| Homozygous Alox15tm1Fun (12/15-LO-deficient) mutant mice are viable and fertile. Macrophages of 12/15-LO-deficient mice exhibit an absence of 12/15-LO by Rt-PCR and immunoblotting; and protein is undetectable. Diabetes incidence of mutant mice is significantly reduced compared to NOD and is reported at 2% of females and 0% of males by 7 months of age. When challenged with Glucose Tolerance Test, non-diabetic, 8-month-old, 12/15-LO-deficient females cleared glucose more efficiently than age matched, non-diabetic NOD females. Histological evaluation of the pancreas from 30 week old females shows significantly reduced insulitis and beta cell damage, compared to age-matched NOD females. This model is useful to further study the role of Alox15 in macrophage regulation and autoimmune diabetes. | ||
| 004448 | NOD.129S2(B6)-Ciitatm1Ccum/FlvJ | Cryopreserved - Ready for recovery |
| In humans, a non-functional C2ta (or Ciita) gene causes bare lymphocyte syndrome (BLS), which is characterized by the lack of HLA class II gene expression and a reduced number of mature CD4+ T cells in the periphery. On the C57BL/6 congenic background (see Stock No. 003239) disruption of C2ta results in a lack of MHC Class II expression by splenic B cells, dendridic cells, and both resting and interferon gamma stimulated macrophages. However, thymic epithelium retains MHC class II expression. Homozygotes also exhibit a significant decrease in the levels of invariant chain and H-2M gene transcripts. Non-conventional MHC Class II molecules such as H-2O alpha and H-2O beta, are not affected by the disruption of C2ta. Despite the continued expression of MHC Class II molecules on cells of the thymic epithilium, few CD4 positive cells exist in the periphery of homozygotes. (Chang et al 1996) Because of ..... | ||
| 004672 | NOD.129S2(Cg)-Stat6tm1Gru/JbsJ | Cryopreserved - Ready for recovery |
| NOD mice homozygous for the Stat6tm1Gru mutation exhibit an increased diabetes incidence compared to NOD controls and show a striking defect in the generation of Th2 cells. Lymphocytes are unable to respond to IL4 as measured in a variety of in vitro and in vivo assays. This strain can be used to look at the role of Il4 in diabetes development. | ||
| 008252 | NOD.129S4(B6)-Art2atm1Fkn Art2btm1Fkn/LtJ | Cryopreserved - Ready for recovery |
| Art2a, Art2b, commonly referred to as ART2, deficient mice are viable and fertile and do not show any overt phenotype. RT-PCR and FACS analysis confirm the absence of ART2 expression on the cell surface of thymic and lymph node purified T cells. No detectable histological abnormalities were observed in the thymus, spleens, lymph nodes, Peyer's patches, thyroid, brain, lung, kidney, intestine, liver, pancreas and thyroid. The disrupted introgression of ART2 onto the NOD background resulted in no significant difference in diabetes onset or incidence when compared to NOD. When the Cd38 targeted mutation is introduced to the NOD.ART2 deficient stock, the NOD.CD38, ART2 deficient males and females are completely resistant to diabetes. This is a surprising result as the NOD.CD38 deficient stock experiences accelerated diabetes onset and incidence in both males and females. Cd4+ and CD8+ T cells from ART2 deficient NOD mice are complet ..... For more information please see the full phenotype on the strain data sheet | ||
| 002575 | NOD.129S7(B6)-Ifngtm1Ts/DvsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. This Ifng -deficient mutant develops type 1 diabetes at the same rate as the NOD/ShiLt parental strain. | ||
| 007931 | NOD.A-Idd3A/J/MrkJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.A/J-Idd3, is carrying Chr 3 alleles, SNPS rs168642 (18.178Mb) through rs13477164, (66.638Mb) derived from strain A/J including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain is reported to be similar to NOD/MrkTac, with approximately 65% of the females becoming diabetic by 200 days of age. The congenic NOD.A/J-Idd3 females are predisposed to autoimmune ovarian dysgenesis. Thymocytes and splenocytes, either non-activated or activated of this T1D susceptible stock produce less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). Il2 molecules derived from the A/J strain are identical to NOD. This congenic strain, one of a set of 5 strains (007930, For more information please see the full phenotype on the strain data sheet | ||
| 005073 | NOD.ABH-(D18Mit19-D18Mit4)/TrmJ | Cryopreserved - Ready for recovery |
| NOD.ABH-(D18Mit19-D18Mit4)/TrmJ, commonly referred to as NOD. Chr18ABH, has a significantly decreased diabetes rate (34%by 30 weeks of age) when compared to wild-type or NOD controls (approximately 80-85% by 30 weeks of age). This strain is useful for dissecting the role of non-MHC susceptibility genes in autoimmune diabetes. | ||
| 004309 | NOD.ALR-(D17Mit16-D17Mit10)/LtJ | Cryopreserved - Ready for recovery |
| This allelic congenic strain commonly called D.R1, carries a defined segment of Chr. 17 that includes the ALR H2gx complex and insulin dependent diabetes susceptibility locus 16, Idd16aALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with about 60% of the females and less than 20% of the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Histological exam of the pancreas of 40-week old pre-diabetic animals showed widespread intra-islet insulitis. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes. | ||
| 004308 | NOD.ALR-(D17Mit16-H2-D)/LtJ | Cryopreserved - Ready for recovery |
| This allelic congenic strain commonly called D.R2, carries a defined segment of Chr 17 that includes the ALR H2gx complex and insulin dependent diabetes susceptibility locus 16, Idd16aALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with 50% of the females and almost 15% the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Similar to Stock No. 004309 pancreatic histological examination of pre-diabetic 8-week old males show lower mean insulitis scores than controls. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes. | ||
| 012393 | NOD.B-Idd5C57Bl/10SnJIdd3C57BL/6/6109MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac bicongenic strain carries C57BL/6 derived genome on Chr. 3 that contains Idd3 and C57BL/10SnJ derived genome on Chr. 1 containing Idd5.1, Idd5.2 and Idd5.3. No diabetes was observed in NOD.B-Idd3/5 congenic female mice by 7 months of age (Hunter et al. 2007) and are almost completely protected from insulitis and the occurrence insulin autoantibodies. . This strain is useful for understanding the variation in diabetic resistance conferred by Idd loci, in particular the epistatic interactions of Idd3 alleles with alleles at Idd5 and for conducting mapping experiments to further define the Idd5 and Idd3 regions | ||
| 004343 | NOD.B10-Idd9C57BL/10SnJ/R905MrkDvsJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd9, line R905 contains a 31Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 4 and is defined within markers D4Mit258 (119Mb) and D4Mit42 (150Mb). The C57BL/10SnJ genomic segment includes Idd9.1, Idd9.2 and Idd59.3. Line 905 replaces and exhibits the same phenotype as line R28, which had a slight larger congenic interval. Congenic females and males are significantly protected from diabetes (less than 10% diabetic by 220 days of age), yet histological evaluation of 3 and 7 to9-month old females and males showed mild to extensive insulitis and were indistinguishable from the pancreas of NOD controls. When compared with NOD controls, insulin autoantibodies (IAA) are essentially the same at 13-15 weeks of age.
This strain may be useful for positional mappi ..... | ||
| 016147 | NOD.B10Sn-(D4Dil31-D4Dil43)/9142MrkTacJ | Cryopreserved - Ready for recovery |
|
This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd9.4, line 9142 contains a 2Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 4 and is defined within markers D4Dil31 (87Mb) and D4Dil43 (88.5Mb). The C57BL/10SnJ genomic segment includes an interferon gene cluster thought to be involved with autoimmunity. The donating investigator indicates that homozygous congenic females exhibit significantly diminished diabetes development compared to NOD/MrkTac controls. This strain may be useful for positional mapping of the Idd9.4 loci and studying interferon candidate genes affecting autoimmunity. | ||
| 008893 | NOD.B10Sn-Idd5C57BL/10SnJ/1092MrkJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.B10-Idd5, line R2 (also known as line 1092), carries two C57BL/10SnJ (Stock No. 000666) Chromosome 1 segments. The first proximal segment is defined within D1Mit5 (63.8Mb) and D1Mit101 (147.31Mb) that includes the insulin dependent diabetes susceptibility (Idd) 5.2, 5.3 and part of the Idd5.4 loci (Idd5b, Idd5c, and Idd5d, respectively). The second distal segment is defined within D1Mit346 (152.63Mb) and D1Mit267 (157.94Mb) and contains the remainder of the Idd5.4 (Idd5d) region. This strain differs from its sister strain, NOD.B6-Idd5C57BL/10SnJ/974MrkJ (Stock No. 008894), in that both Cd28 and Ctla4 are NOD in origin. Diabetes incidence among 200-day old female mice of this strain has been reported at 70%, c ..... For more information please see the full phenotype on the strain data sheet | ||
| 004344 | NOD.B10Sn-Idd5C57BL/10SnJ/444MrkDvsJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd5R444, line 1094 contains a 19.4Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 1 and is defined within markers D1Mit124 (57.7Mb) and D1Mit124 (77.1Mb). The C57BL/10SnJ genomic segment includes Idd5.1, Idd5.3 and Idd5.2. The major candidate genes for Idd5.1 and Idd5.2 are Ctla4 and Nramp1, respectively. The Idd5.3 is defined to a 3.55Mb region. Within this region there are 11 annotated genes; including possible candidate genes IKAROS family zinc finger 2 (Ikzf2) and acyl-Coenzyme A dehydrogenase, long-chain (Acadl). Diabetes incidence among 7-month old, significantly protected, females is reported to be 13%, compared with more than 80% in NOD controls or 62% in NOD.B10-Idd5.1 (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 008894 | NOD.B10Sn-Idd5C57BL/10SnJ/974MrkJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.B10-Idd5, line 974, carries two C57BL/10SnJ (Stock No. 000666) Chromosome 1 segments. The first proximal segment is defined within D1Mit249 (60.89Mb) and D1Mit101 (147.31Mb) and includes the insulin dependent diabetes susceptibility (Idd)5.1, 5.2, 5.3 and part of the Idd5.4 loci (Idd5a, Idd5b, Idd5c, and Idd5d, respectively). The second distal segment is defined within D1Mit346 (152.63Mb) and D1Mit267 (157.94Mb) and contains the remainder of the Idd5.4 (Idd5d) region. This strain contains a rare recombination event captured at the proximal end of the congenic segment where it recombines between the genes encoding Cd28 (NOD allele) and Ctla4 (B10 allele). Diabetes incidence among 200 day old female mice of this strain is reported at 17%, compared with more than 80% in NOD controls ( ..... For more information please see the full phenotype on the strain data sheet | ||
| 012392 | NOD.B10Sn-Idd5C57Bl/10SnJ/R193MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac congenic strain, commonly referred to as NOD.B10-Idd5R193, line 2574 contains a 16.2Mb genomic segment from the diabetes resistant strain C57BL/10SnJ (Stock No. 000666) introgressed into chromosome 1 and is defined within markers D1Mit124 (57.7Mb) and D1Mit180 (73.9Mb). The C57BL/10SnJ genomic segment includes Idd5.1 and recently identified Idd5.3. The major candidate gene for Idd5.1 is Ctla4. The Idd5.3 is defined to a 3.55Mb region. Within this region there are 11 annotated genes; including possible candidate genes IKAROS family zinc finger 2 (Ikzf2) and acyl-Coenzyme A dehydrogenase, long-chain (Acadl) Diabetes incidence is significantly protected among 7-month old females. Diabetes incidence among 7-month old females is reported to be 47%, compared with more than 80% in NOD controls or 62% in NOD.B10-Idd5.1 (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 012309 | NOD.B10Sn-Idd9.1C57BL/10SnJ/1565MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac congenic stock, commonly referred to as NOD.B10-Idd9R1565 or NOD.B10-Idd9.1), carries C57BL/10SnJ (Stock No. 000666) derived genome on Chromosome 4 containing Idd9.1 region. This congenic interval wholly contains the 8Mb region defining Idd11 described by Brodnicki et al, 2000. The Idd9.1 region contains 329 genes, including candidate gene Lck.
This strain exhibits significantly diminished diabetes development when compared to NOD controls; with approximately 36% of the females becoming diabetic by 200 days of age. NOD-Idd9.1 mice are significantly more protected from diabetes development than NOD.B10-Idd9.3 (Stock No. 012311). NOD.B10-Idd9.1 exhibit enhanced development and function of CD4+CD25+ regulatory T cells than NOD controls. Data suggests that the Idd9.1 ..... | ||
| 012311 | NOD.B10Sn-Idd9.3C57BL/10SnJ/1106MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac congenic stock, commonly referred to as NOD.B10-Idd9R35 or NOD.Idd9.3) carries C57BL/10SnJ (Stock No. 000666) derived genome on Chromosome 4 containing the Idd9.3 region. The Idd9.3 region contains 15 genes, including candidate gene Tnfrsf9 (commonly referred to as 4-1BB or Cd137). While this strain exhibits significantly diminished diabetes development compared to NOD/MrkTac controls, it is significantly less protected from diabetes development compared to NOD.B10-Idd9.1R1565 (Stock No. 0012309). Tnfrsf9 is biologically more active in this congenic strain than in the control NOD/MrkTac. There is a variation in the Tnfrsf9 coding region between NOD and C57BL/10, including a leucine to proline alteration in the cytoplasmic domain. This strain may be useful for positional mapping of the Idd9.3 loci and studying candidate genes within the Idd9.3 region. | ||
| 007934 | NOD.B6(PL)-Idd3C57BL/6/MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.B6-Idd3, commonly referred to as NOD.B6-Idd3R450, is carrying Chromosome 3 alleles, rs3022959 through rs3140619, derived from strain C57BL/6 including the insulin dependent diabetes susceptibility 3 loci (Idd3). This NOD.B6 congenic strain is diabetes resistant, with approximately 10% of the females becoming diabetic by 250 days of age. Activated and non-activated thymocytes and splenocytes of this T1D protected stock produce more Il2 mRNA than T1D susceptible strains (Stock No's. 007930, 007931, and 007932). This congenic strain, one of a set of 5 strains (Stock No's. 007930, 007931, 007932> ..... For more information please see the full phenotype on the strain data sheet | ||
| 006809 | NOD.B6-(D11Nds1-D11Mit41)/J | Cryopreserved - Ready for recovery |
| Chromosome 11 congenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The reported conclusion of diabetes resistance in this Chr 11 congenic has been re-evaluated now that the B6 contaminating genome on Chr 1 has been eliminated. Diabetes incidence studies preformed at The Jackson Laboratory show an accelerated onset and incidence of diabetes in females when compared with NOD/ShiLtJ controls and the original stock 005311, while the diabetes onset and incidence in males is accelerated compared to the original Stock 005311 and is slightly reduced compared to NOD/ShiLtJ controls. 006809 incidence study and fine mapping data.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterize ..... For more information please see the full phenotype on the strain data sheet | ||
| 005311 | NOD.B6-(D1Mit18-D1Mit445)(D11Nds1-D11Mit41)/DelJ | Cryopreserved - Ready for recovery |
| The donating investigator reports diabetes onset of female NOD.B6-(D1Mit18-D1Mit445) (D11Nds1-D11Mit41)/DelJ (commonly called NOD.B6-Idd4A, Chromosome 11, 43.8-49cM) is delayed, with 15% of the females and 5% of the males becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4A mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 10% of NOD.B6-Idd4A islets are infiltrated compared to 80% in NOD controls. Until 25-30 weeks of age, NOD.B6-Idd4A mice only develop periductal infiltrates with mild non-destructive insulitis. Additionally, immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4A females alone are able to induce diabetes in NOD.Prkdcscid female ..... For more information please see the full phenotype on the strain data sheet | ||
| 005313 | NOD.B6-(D1Mit180-D1Mit143)(D11Mit38-D11Mit41)/DelJ | Cryopreserved - Ready for recovery |
| The donating investigator reports diabetes onset of female NOD.B6-(D11Mit38-D11Mit41)/DelJ (commonly called NOD.B6-Idd4C, Chromosome 11, 49cM) is delayed, with 20% of the females becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4C mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 45% of NOD.B6-Idd4C islets are infiltrated compared to 80% in NOD controls. Immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4C females alone are able to induce diabetes in NOD.Prkdcscid female recipients. Diabetes onset is delayed in recipients of NOD.B6-Idd4C T-cells only, with about 40% becoming diabetic by 70 days post transfer compared to 80% diabetic in recipients r ..... For more information please see the full phenotype on the strain data sheet | ||
| 005312 | NOD.B6-(D1Mit18-D1Jmp12)(D11Mit325-D11Mit41)/DelJ | Cryopreserved - Ready for recovery |
| The donating investigator reports diabetes onset of female NOD.B6-(D11Mit38-D11Mit325)/DelJ (commonly called NOD.B6-Idd4B, Chromosome 11, 49cM) is delayed, with 40% of the females becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4B mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 45% of NOD.B6-Idd4B islets are infiltrated compared to 80% in NOD controls. Immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4B females alone are able to induce diabetes in NOD.Prkdcscid female recipients. Diabetes onset is delayed in recipients of NOD.B6-Idd4B T-cells only, with about 50% becoming diabetic by 70 days post transfer compared to 80% diabetic in recipien ..... For more information please see the full phenotype on the strain data sheet | ||
| 007573 | NOD.B6-(D6Mit254-D6Mit289)/CarJ | Cryopreserved - Ready for recovery |
| Klrb1ca (Nk1.1) homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Nk1.1 expression in the strain has been confirmed by FACS analysis of peripheral blood cells. The C57BL/6-derived congenic interval on Chromosome 6 which contains the Nk1.1 locus is shorter in these mice than that carried in the original strain (Stock No. 004482). Diabetes incidence in this strain is higher than that reported in strain 004482 (65% in females and 15% in males by 27 weeks for this strain versus 30% in the females and 0% males by 30 weeks of age for Stock No. 004482). Histological examination of the pancreas from 27-week old, non-diabetic mice reveals extensive insulitis that is not significantly different from that seen in similarly ..... For more information please see the full phenotype on the strain data sheet | ||
| 004482 | NOD.B6-(D6Mit254-D6Mit339)/CarJ | Cryopreserved - Ready for recovery |
| Klrb1ca homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Diabetes incidence as reported by donating investigator and confirmed in the T1DR, prior to shortening the congenic interval, is significantly decreased (30% females and 0% males at 30 weeks of age) as compared to standard NOD (NK1.2) controls (85% females and 60% males at 30 weeks of age) . FACS analysis of NKT cells derived from thymus or spleen of NOD animals homozygous for this genomic segment revealed the presence of NK1.1+/TCR alpha beta +, V beta8+ and CD44+, but at lower levels than in C57BL/6 controls. NK cells of NOD.B6-(D6Mit254-D6Mit14) exhibit an equivalent number of NK1.1/DX5 double positive cells when compared to C57BL/6. Histological examination of 10-12 week old animals indicates no significant difference in insulitis severity between NOD.B6-(D6Mit254-D6Mit14) and NOD control islets (Carnaud et al, 2001). Confir ..... For more information please see the full phenotype on the strain data sheet | ||
| 003585 | NOD.B6-(Gpi1-D7Mit346)/LtJ | Cryopreserved - Ready for recovery |
| NOD.B6-(Gpi1-D7Mit346)/LtJ mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Congenic NOD Gpib mice become diabetic at a similar rate and onset as NOD/Lt (Chen et al, 2005). Gpi1b in these mice can be used as a marker for transplant studies. | ||
| 013185 | NOD.B6-Idd3C57BL/6J Idd10C57BL/6J Idd18C57BL/6J/1538MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD/MrkTac bi-congenic strain, commonly referred to as NOD.B6-Idd3/10/18R323, line 1538 is viable and fertile. Mice of this strain contain 2 C57BL/6J genomic segments from the diabetes resistant strain C57BL/6J (Stock No. 000664) introgressed into the NOD chromosome 3. The C57BL/6 genomic segments include Idd3, Idd10, Idd18.1, Idd18.2 and Idd18.3, while the Idd17 region is of NOD origin. The Idd3 region contains major candidate gene Il2 (37Mb); the Idd10 region contains major candidate gene Cd101 (100Mb); the Idd18.1 region contains major candidate gene Vav3 (109Mb) and the recently identified 966Kb Idd18.3 region contains 22 genes and 1 pseudogene. Congenic female mice are completely protected from diabetes at 7-months of age. This strain is useful for understanding the variation in diabetic resistance conferred by Idd loci, in partic ..... For more information please see the full phenotype on the strain data sheet | ||
| 003505 | NOD.B6-Prf1tm1Sdz/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Prf1tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4- CD8+ T cells in the spleen. CD4- CD8- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.) | ||
| 005512 | NOD.B6-Tg(HLA-A2.1)1Enge/DvsJ | Cryopreserved - Ready for recovery |
| Homozygous mice carrying the (HLA-A2.1)1Enge transgene ubiquitously express significant quantities of the human MHC class I HLA-A2.1 molecules. These HLA-A2.1 molecules mediate beta cell auto-reactive CD8 T cell responses that when added to those elicited by endogenous murine MHC class I variants results in a significantly accelerated rate of diabetes onset in either the hemizygote or homozygote transgenic mouse when compared to NOD/Lt controls (Marron et al., 2002). This model is useful for studying the role of MHC class I molecules in Type 1 Diabetes. | ||
| 006345 | NOD.B6-Tg(IghelMD4)4Ccg/DvsJ | Cryopreserved - Ready for recovery |
| NOD.B6-Tg(IghelMD4)4Ccg/DvsJ (commonly referred to as NOD.IgHEL) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The transgene encodes IgM and IgD molecules specific for the pancreatic beta cell-irrelevant Hen Egg Lysozyme (HEL) protein. NOD transgenic mice have a 2-fold increase in the total numbers of splenic B-lymphocytes when compared to NOD wildtype mice, a value that is comparable to that seen in B6 mice. The total number of CD4+ and CD8+ T-lymphocytes did not differ significantly between NOD transgenic and NOD wildtype mice. Ninety-nine percent of splenic B-lymphocytes express the transgenic IgMa; however 8% of the B-lymphocytes from transgenic mice escaped allelic exclusion, and express endogenous IgMb molecules. Diabetes onset in NOD.IgHEL females is significantly delayed, although the final incidence at 30 weeks of age did not differ significan ..... For more information please see the full phenotype on the strain data sheet | ||
| 006610 | NOD.B6-Tg(ML5sHEL)5Ccg/DvsJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size, agouti in color and express a soluable form of hen egg lysozyme. They become diabetic at a rate similar to NOD controls. This strain can be used to study B-cell selection and tolerance as it relates to Type 1 Diabetes. | ||
| 005616 | NOD.C-(Ptprc-D1Mit262)/WehiJ | Cryopreserved - Ready for recovery |
| This NOD/LtJWehi congenic strain is carrying Chr 1alleles derived from BALB/cWehi including Ptprcb. Diabetes onset and incidence is similar between NOD.C-(Ptprc-D1Mit262)/WehiJ congenic mice (6/8 by 300 days of age) and NOD/LtJWehi (17/24 by 300 days of age). NOD.C-(Ptprc-D1Mit262)/WehiJ bone marrow transplanted into irradiated NOD/LtJWehi recipients yielded incomplete replacement of donor leukocytes at 16 weeks post transfer versus nearly complete replacement of donor leucocytes in C57BL/6Wehi and B6.SJL/Wehi irradiated mice (Steptoe, et al., 2004, Journal of AutoImmunity, Vol 22, p131-138). This strain provides a unique cell surface marker that can be used to track lineage and phenotype of all hematopoietic donor derived or transferred cells making it useful in studies monitoring diabetes progression. | ||
| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Cryopreserved - Ready for recovery |
| NOD congenic mice homozygous for the Faslgld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 007932 | NOD.CAST-Idd3CAST/EiJ/MrkJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.CAST-Idd3, is carrying Chr 3 alleles, SNPs rs3022948 (7.43Mb) through rs13477164, (66.638Mb) derived from strain CAST/EiJ including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain is reported to be similar to NOD/MrkTac. Thymocytes and splenocytes of this T1D susceptible stock produce 2 fold less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). This congenic strain, one of a set of 5 strains (Stock No's. 007930, 007931, 007933, 007934), has been useful to positionally clone Idd3 and to st ..... For more information please see the full phenotype on the strain data sheet | ||
| 004306 | NOD.CBALs-Hc1/LtJ | Cryopreserved - Ready for recovery |
| This NOD/Lt congenic strain is carrying Chr 2 alleles derived from CBA/Ls including Hc1. Diabetes onset and incidence is the same as NOD/Lt. | ||
| 004304 | NOD.CBALs-Tyr+/LtJ | Cryopreserved - Ready for recovery |
| This Chr 7 congenic strain in which the tyrosinase allele Tyr+ of the CBA/JLsLt strain is fixed on the NOD/Lt background, therefore making the strain agouti in color. This strain should be a good donor for blastocysts in which to microinject targeted NOD ES cells, and may alleviate unwanted genome integration experienced with use of the C57BL/6 blastocysts. The congenic segment on Chromosome 7 slightly supresses spontaneous T1D development which is an asset when these females are used as blastocyst recipients. | ||
| 007933 | NOD.CZI-Idd3CZECHI/EiJ/MrkTacJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.CZECH-Idd3, is carrying Chr 3 alleles, rs13477023 (20.01Mb) through rs13477134 (58.91Mb), derived from strain CZECH/EiJ including the insulin dependent diabetes susceptibility 3 loci (Idd3). Il2 exon 1 sequence and glycosylation pattern is similar to NOD/MrkTac. Surprisingly, the diabetes frequency of this strain of mice is identical to that of NOD.B6-Idd3 mice. Activated and non-activated thymocytes and splenocytes of this T1D protected stock produce 2 fold more Il2 mRNA than T1D susceptible strains (Stock No's. 007930, 007931, and 007932). However, the NOD.CZECH-Idd3 congenic produces more Il2 mRNA than the NOD.B6-Idd3 congenic. This congenic strain, one of a set of 5 strains (Stock No's For more information please see the full phenotype on the strain data sheet | ||
| 005345 | NOD.Cg-Cd38tm1Lnd Prkdcscid/LtJ | Cryopreserved - Ready for recovery |
| CD38 is an ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase. This ubiquitously expressed ectoenzyme is the major NAD hydrolase in mice. NOD/Lt mice homozygous for the Cd38tm1Lnd targeted allele develop accelerated Type 1 diabetes associated with an ART2 (T cell ADP-ribosyltransferase)-dependent and NAD-mediated loss of regulatory CD4+CD25+ Foxp3+ and CD4+iNKT cells (Chen, J. et al 2006; Chen, Y.G et al 2006). Combining the Prkdcscid mutation with the Cd38tm1Lnd targeted allele completely prevents diabetes development. For investigators wishing to study the role of CD38 in beta cell biology, the presence of the Prkdcscid allele provides insultis-free islets for analysis. Congenic, doubly homozygous NOD.Cd38tm1Lnd Prkdcscid mutant mice exhibit no significant difference in glucose tolerance when compared to NOD or NOD. Prkdcscid, thus not suppor ..... For more information please see the full phenotype on the strain data sheet | ||
| 006775 | NOD.Cg-Foxp3sf/DoiJ | Cryopreserved - Ready for recovery |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development. | ||
| 006021 | NOD.Cg-H2-Ab1tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ | Cryopreserved - Ready for recovery |
| The NOD transgenic HLA DQ8, H2-Ab1deficient mouse is diabetes resistant but develops cardiomyopathy resulting in early death from heart failure in both males and females. Histological exam indicates hearts are 3-4x larger than wildtype. Pathology results from an autoimmune response against normal cardiomyocytes in the atrial and ventricular walls, as well as against myocytes present in the outermost muscle layer surrounding the pulmonary veins. Disease progression can be blocked by cyclosporin A treatment and is accelerated with Complete Freund's Adjuvant (Elliott et al, 2003, PNAS) . This model is useful for studying autoimmune myocarditis, idiopathic dilated cardiomyopathy and heart failure and to understand the role of MHC class II in autoimmunity.. | ||
| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain contains a targeted H2-Ab1 mutation also carries two transgenes: one expressing human CD4 under the regulation of the mouse Cd4 enhancer and a second expressing human HLA-DQ6. The latter transgene confers dominant protection to development of Type 1 diabetes in humans. These double transgenic, H2-Ab1-deficient mice are viable, fertile, normal in size, and free of both autoimmune diabetes and cardiomyopathy, a phenotype found in an NOD stock expressing an HLA-DQ8 transgene (Elliot JF et al. Proc Natl Acad Sci U S A 2003; 100:13447-52). By 55 weeks of age, 100% of the H2-Ab1-deficient, DQ6 transgenic mice develop thyroiditis and thyroid autoantibodies. Of these, 25% develop thyroid gland enlargement and goiter, and a subset of these animals develops thyroid failure with elevated serum TSH levels.
This model is useful for studying autoimmune thyroid disease and to understand the role of MHC class II in au ..... | ||
| 004447 | NOD.Cg-H2h4/DilTacUmmJ | Cryopreserved - Ready for recovery |
| NOD.Cg-H2h4/DilTacUmm mice are completely protected from diabetes; however, a low incidence of perivascular and periductal insulitis is detected (20-30%). Protection from diabetes is complete even upon treatment with cyclophosphamide. These mice do, however, develop spontaneous thyroiditis and produce IgG autoantibodies when treated with 0.05% NaI in water (100% incidence in both sexes 6-8 week post treatment or by 4 months of age). Without treatment, thyroiditis is delayed and incomplete (60-70% incidence in 7-10 month old mice). This strain is an excellent model for autoimmune thyroiditis. | ||
| 006608 | NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ | Cryopreserved - Ready for recovery |
| NOD.Cg-Ighmtm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Ighm-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Ighm-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Ighm-deficient mice express Ig molecules specific for hen egg lyzozyme (HEL). There is no significant difference in the total number of B and T lymphocytes between NOD.IgHEL Ighm-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Ighm-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Ighm-deficient mice shows that most mice have low levels of insulitis compared to NOD/ShiLt control mice, although an occasional animal had extensive insulitis. In additio ..... For more information please see the full phenotype on the strain data sheet | ||
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 004291 | NOD.Cg-Il10tm1Cgn Il4tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10 and Il4 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 005078 | NOD.Cg-Il1r1tm1Roml/HetJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Il1r1tm1Roml targeted mutation develop normally, exhibit a reduced inflammatory response and no response to interleukin-1 alpha or beta. Homozygous mice have a reduced acute phase and delayed type hypersensitivity response and are highly susceptible to Listeria monocytogenes infection. Equilibrium binding experiments using radiolabeled anti-mouse IL1R1 antibody, 35F5, show no detectable expression of IL1R1 protein in primary murine embryonic fibroblasts (Labow et al, 1997). NOD females homozygous for the Il1r1tm1Roml mutation experience a slight, yet significant delay in diabetes development, with an overall incidence of 75% compared to 100% in wild types. There is no statistical difference between mutant and wild type NOD mice in diabetes development following cyclophosphamide treatment or in the rate at which they mediate autoimmune rejection of syngeneic fetal pancreatic grafts. Adoptive transfer of NOD.Cg-Tg(TcraBDC ..... For more information please see the full phenotype on the strain data sheet | ||
| 006698 | NOD.Cg-Il4tm1Lky/JbsJ | Cryopreserved - Ready for recovery |
| A "knock-in" replaces the endogenous gene with an Il4/IRES/EGFP bicistronic construct, which places both IL4 and EGFP expression under the control of the endogenous Il4 gene regulatory elements. IL4 activity in these mutant mice remains intact. Cells activated to express IL4 also express EGFP allowing reliable in vivo tracking of both innate and adaptive immune cells and enabling their isolation without further stimulation. Because the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice also can be used to report competence for IL4 production upon stimulation. This knock-in allele has been backcrossed to NOD for 15 generations. Diabetes incidence in mutant mice is reported to be about 60%, which is not statistically different from wild-type cohorts or NOD inbred mice. | ||
| 004346 | NOD.Cg-Prkdcscid Tg(Ins2-CD80)3B7Flv/DvsJ | Cryopreserved - Ready for recovery |
| These mice are characterized by pancreatic beta cells that express a rat insulin promoter (Rip) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. They are an excellent source of MHC class I positive, CD80 transgene-expressing islet cells, a potent antigenic reagent for propagating diabetogenic CD8+ T lymphocytes derived from NOD mice in vitro. The presence of the Prkdcscid allele eliminates the possibility that isolated islet cells will introduce contaminating T lymphocytes onto cultures. | ||
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies. | ||
| 006605 | NOD.Cg-Prkdcscid Emv30b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets. | ||
| 006609 | NOD.Cg-Prkdcscid Tg(HLA-A2.1)1Enge/DvsJ | Cryopreserved - Ready for recovery |
| Although transgenic NOD mice develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) mice, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells) and therefore does not become diabetic. This strain is useful for adoptive transfer experiments and as a source of insulitis free pancreatic islets. | ||
| 007840 | NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ | Cryopreserved - Ready for recovery |
| Tg(Ins2-CD86)12B7 mice homozygous for the Prkdcscid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdcscid homozygous mice lack functional T cells and B cells, and do not become diabetic.
In the absence of the Prkdcscid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d ..... | ||
| 004347 | NOD.Cg-Rag1tm1Mom Tg(TcraAI4)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| The rearranged Tcra transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcrbAI4)1DvsRag1tm1Mom/DvsJ (004348), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile. | ||
| 006024 | NOD.Cg-Rag1tm1Mom H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Cryopreserved - Ready for recovery |
| Rag1 and H2-Ab1 deficient NOD mice carrying transgenes encoding humanized CD4 and HLA-DQ6 lack T and B cells and are free of autoimmune diabetes and cardiomyopathy, and do not develop thyroiditis. This model is useful in adoptive transfer experiments and in studying MHC class II-based resistance and susceptibility in autoimmunity. | ||
| 006022 | NOD.Cg-Rag1tm1Mom H2-Ab1tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ | Cryopreserved - Ready for recovery |
| Rag1 and H2-Ab1 deficient NOD mice carrying transgenes coding for human CD2-CD4 and HLA-DQ8 lack T and B cells, and are diabetes free. Also, unlike the H2-Ab1 deficient, transgenic CD4, HLA-DQ8 mice (see Stock No. 006021), this strain does not develop cardiomyopathy. This model is useful in adoptive transfer experiments and to understand the role of MHC class II in autoimmunity. | ||
| 005853 | NOD.Cg-Tg(HLA-A2/H2-K)1Scr/ShrmJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. FACs analysis indicates expression of HLA-A201 on peripheral blood lymphocytes. The level of expression of this chimeric MHC I molecule in transgenic mice is similar to the observed expression in human PBL's. Diabetes incidence of mice carrying this transgene (88%) is similar to NOD (79%) at 25 weeks of age. Splenocytes from transgenic mice immunized with GAD65 peptides together with MHC class II helper peptide were re-stimulated with peptide pulsed irradiated syngeneic APC?s in-vitro 10 days post immunization Transgenic mice immunized with three different GAD65 peptides (position: 144-149, sequence: LLQEYNWEL; position: 114-122, sequence: VMNILLQYV; and position 573-581, sequence: FLIEEIERL) gave vigorous CTL responses when tested by standard chromium release assays. FACs analysis indicates presence of CFSE expression on CD8+ T-cells in transgenic mice given CFSE-labeled ..... For more information please see the full phenotype on the strain data sheet | ||
| 005019 | NOD.Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ | Cryopreserved - Ready for recovery |
| 005018 | NOD.Cg-Tg(Igk-C/Igk-V125)1Jwt/JwtJ | Cryopreserved - Ready for recovery |
| 005524 | NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Cryopreserved - Ready for recovery |
| Transgenic mice reportedly express the mutant Ins2*Y16A protein in the pancreatic islets and thymus. The donating investigator reports approximately 75% of female transgenic mice (founder line B) become diabetic in the presence of native insulin genes by 35 weeks of age. In contrast, NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and neither diabetes nor insulitis develops by 26 weeks of age. Sialitis does occur, however. Line B transgenics have lower expression levels than line F (see Stock No. 005525), and 50% of the line B male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes, with little to no insulitis, before 10 weeks of age. This strain is useful to study insulin-reactive autoimmunity. | ||
| 005525 | NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Cryopreserved - Ready for recovery |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). This stock is useful to study insulin-reactive autoimmunity. | ||
| 006254 | NOD.Cg-Tg(Ins2-Ccl21b)2Cys/JbsJ | Cryopreserved - Ready for recovery |
| Ins2-Ccl21-leu (commonly referred to as SLC) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Immunohistochemistry of pancreatic sections with antibodies to CCL21 demonstrate detectable chemokine protein within the pancreatic beta cells. In transgenic mice on the B6.D2 background, SLC pancreatic expression leads to highly organized infiltrates in the pancreatic islets. These infiltrates contain B cells, CD4+ and CD8+ T cells and dendritic cells (DCs) with the DCs and and T cells localized close to the CCL21b expressing islet cells. According to the donating investigator, SLC expression in the pancrease of transgenic mice on the NOD congenic background prevents diabetes development (unpublished communication). This strain is useful for the study of T cells, B cells and chemokines in the development of diabetes. | ||
| 006154 | NOD.Cg-Tg(Ins2-Cxcl13)1Cys/JbsJ | Cryopreserved - Ready for recovery |
| Ins2-Cxcl13 (commonly referred to as BLC) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. On the B6.D2 background pancreatic islet structure is disrupted, strongly resembling severe insulitis. However, these mice have normal blood glucose levels, no decrease in B-cells and do not become overtly diabetic. Immunohistochemistry indicates Cxcl13 expression is significantly higher in the pancreatic islets than the follicular stromal cells of the lymph nodes while no expression was observed in the liver or kidney. Histopathology indicates 50% of the pancreatic islets are infiltrated with small nucleated cells. Immunohistochemistry and FACS analysis reveals that 90% of the infiltrating cells are B220+ naďve B lymphcytes. In addition, CD4+ and CD8+ cells were present. Transgenic expression leads to the development of lymph node like structures that contain B and T cell zones, high endoth ..... For more information please see the full phenotype on the strain data sheet | ||
| 003869 | NOD.Cg-Tg(Ins2-E3)1Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 004602 | NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ | Cryopreserved - Ready for recovery |
| Tg(Ins2-rtTA)2Doi encodes the reverse tetracycline regulatable transactivator (rtTA) regulated by the rat insulin promoter (Ins2, commonly designated RIP), and is expressed in the pancreatic beta cells. Mice hemizygous for this transgenic insert are viable, fertile, normal in size, display normal NOD diabetes onset, but do not display any other gross physical or behavioral abnormalities. When transgenic are mated to a second transgenic strain carrying a target gene regulated by the tetO responsive elements, expression of the target gene is turned on by the tetracycline analog, doxycycline (dox). Dox can be administered orally in the food or water. This strain provides a Tet-On tool that permits the inducible expression of genes in the pancreatic beta cells during various stages of diabetes development (As reported by donating investigator, data unpublished). | ||
| 009422 | NOD.Cg-Tg(Itgax-Venus)1Mnz/QtngJ | Cryopreserved - Ready for recovery |
| This transgenic strain expresses yellow fluorescent protein (YFP) under the transcriptional control of the mouse integrin alpha X (Cd11c) promoter which is exclusively expressed in dendritic cells of the immune system. The Donating investigator indicates diabetes incidence of this stock has not been determined. | ||
| 005732 | NOD.Cg-Tg(Lck-cre)548Jxm/AchJ | Cryopreserved - Ready for recovery |
| This strain expresses Cre recombinase in thymocytes and is active in T-cells during development. | ||
| 005076 | NOD.Cg-Tg(tetO-EGFP/FADD)1Doi/DoiJ | Cryopreserved - Ready for recovery |
| Mice hemizygous for this transgenic insert are viable, fertile, normal in size. Diabetes incidence and onset is similar to that observed in NOD inbred mice, but otherwise, the mice do not display any gross physical or behavioral abnormalities. These transgenic mutant mice may be mated to strains carrying either rtTA (reverse tetracycline trans-activator protein) or tTA (the tetracycline trans-activator) transgenes regulated by tissue specific promoters. In the bi-transgenic offspring of such crosses, tissue-specific expression of the EGFP/FADD fusion protein can be either induced (in rtTA transgenic mice) or suppressed (in tTA transgenice mice) by administration of the tetracycline analog, doxycycline (dox). Dox may be administered in the animals water supply.
Double transgenic mice generated by intercrossing Tg(tetO-EGFP/FADD)1Doi transgenic mice with NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ (Stock No. 004602) transgenic mice express th ..... | ||
| 005115 | NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset, especially in males, and have coat color pigmentation. Immunohistochemical staining with metallothionein specific antibodies confirms pancreatic islet cell specific expression of the INS-MT2A transgene. There is a 40-fold increase in metallothionein activity in transgenic islets when compared to wild-type controls. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase in ROS florescence in wild-type islets, but a very small increase in transgenic islets. Transgenic beta cells are diabetes resistant to diabetes when treated with streptozotocin. Transgenic beta cells generate less ROS fluorescence when treated with hydrogen peroxid ..... For more information please see the full phenotype on the strain data sheet | ||
| 005113 | NOD.FVB-Tg(INS-SOD2)3Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Immunohistochemical staining with mitochondrial superoxide dismutase specific antibody confirms INS-SOD2 transgene expression localized to the mitochondria of pancreatic islet cell. There is a significant increase in SOD2 activity in transgenic islets when compared to wild-type controls. There is no statistical difference in insulin and DNA content, insulin staining and islet morphology or diabetes development following cyclophosphamide treatment between mutant and wild type NOD mice. Transgenic mice are resistant to diabetes when treated with streptozotocin. Islet beta cells from transgenics generate less ROS when treated with peroxynitrite or superoxide. Untreated mutants do not display accelerated spontaneous diabetes. This model provides a tool for looking at the role of oxidative stress in diabetes. | ||
| 007769 | NOD.FVB-Tg(Igh-6-Cd80)1Gjf/JbsJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. High levels of the transgene are expressed on B cells, but not on T cells. At 30 weeks of age transgenic mice are diabetes resistant and insulitis was significantly reduced when compared with wildtype NOD controls. When compared to wildtype NOD controls, the circulating B cells in congenic NOD transgenic mice is 2-3 fold lower in 2 week old mice and 10 fold lower in 5-6 week old mice and persists throughout life. Significantly reduced percentage of B cells were found in the spleen and bone marrow. Analysis of bone marrow shows the more mature B cell subsets (B220+, IgM+) are affected. Elisa tests indicate reduced circulating levels of all Ig types, Ighm (formerly Igh-6), Igh-3 (IgG2b), and Ighg1 (IgG1) in the serum of transgenic mice. MHC class II expression of splenic B cells was significantly increased by more than 2 fold, indicati ..... For more information please see the full phenotype on the strain data sheet | ||
| 005114 | NOD.FVB-Tg(Ins1-Cat,Tyr)25Pne/PneJ | Cryopreserved - Ready for recovery |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset in males, and have coat color pigmentation. Northern blot analysis and immunohistochemistry confirm pancreatic islet specific expression of the Ins1-Cat transgene. There is a 50-fold increase in catalase activity in transgenic islets when compared to wild-type controls, which approximates catalase activity normally found in the liver. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase of ROS florescence in control islets, but much smaller increase in transgenic islets. Transgenic mice are resistant to diabetes when treated with streptozotocin or alloxan. Transgenic beta cells generate less ROS fluorescence when treated with ..... | ||
| 008549 | NOD.FVB-Tg(Itgax-DTR/EGFP)57Lan/JdkJ | Cryopreserved - Ready for recovery |
| Unmanipulated NOD congenic Itgax-DTR/EGFP (Cd11c-DTR) transgenic mice are viable, normal in size and develop spontaneous diabetes similar to NOD/ShiLtJ. All splenic CD8+ and CD8- DC express EGFP and are diphtheria toxin (DT) sensitive. Upon DT administration, mice harboring this transgene are transiently depleted of dendritic cell (DC) populations. Immunohistochemical and flow cytometric analysis reveals EGFP expression and DT-inducible depletion of CD11chigh DC in spleen, lymph node, lung, liver and lamina propria tissues, as well as the defined macrophage subpopulations of the alveolar, lamina propria, metallophillic and marginal zone. Rapid reduction of CD11c+ DC populations induced by intraperitoneal injection of DT persists for approximately 2 days, after which the cell population gradually recovers. While transient DC depletion was not associated with sign of illness or long-term defects, repeated DT inductio ..... For more information please see the full phenotype on the strain data sheet | ||
| 006303 | NOD.FVB-Tg(TcraBDC12-4.1)10Jos/GseJ | Cryopreserved - Ready for recovery |
| This transgenic strain carries a rearranged Tcr alpha gene from the pathogenic anti-insulin CD4+ T-cell clone BDC12-4.1. Transgenic mice are viable and fertile. When hemizygotes are crossed with Stock No. 006304 NOD.FVB-Tg(TcrbBDC12-4.1)82Gse/GseJ, expression of the BDC12-4.1 T-cell receptor is confirmed by FACS analysis of PBMCs from the double transgenic mice. Double transgenic mice develop insulitis, but spontaneous diabetes does not develop, even in older animals (60 weeks of age), nor can insulin autoantibodies be detected in any age group. Splenocytes from double transgenic mice stimulated with B9-23 peptide produce IFN-gamma, whereas no response is observed in controls. When the congenic NOD double transgenic is combined with a homozygous Rag1tm1Mom mutation (such as in Stock No. 003729), recombination of the endogenous TCR and immunoglobul ..... For more information please see the full phenotype on the strain data sheet | ||
| 006304 | NOD.FVB-Tg(TcrbBDC12-4.1)82Gse/GseJ | Cryopreserved - Ready for recovery |
| This transgenic strain carries a rearranged Tcr beta gene from the pathogenic anti-insulin CD4+ T-cell clone BDC12-4.1. Transgenic mice are viable and fertile. When hemizygotes are crossed with Stock No. 006303 - NOD.FVB-Tg(TcraBDC12-4.1)10Jos/GseJ, expression of the BDC12-4.1 T-cell receptor is confirmed by FACS analysis of PBMCs from the double transgenic mice. Double transgenic mice develop insulitis but spontaneous diabetes does not develop, even in older animals (60 weeks of age), nor can insulin autoantibodies be detected in any age group. Splenocytes from double transgenic mice stimulated with B9-23 peptide produce IFN-gamma, whereas no response is observd in controls. When the congenic NOD double transgenic is combined with a homozygous Rag1tm1Mom mutation (such as in Stock No. 003729), recombination of the endogenous TCR and immunoglobuli ..... For more information please see the full phenotype on the strain data sheet | ||
| 008056 | NOD.L-(Csf2-D11Mit339)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11e or DR3e carries Chromosome 11 alleles, D11Mit164 (56Mb) through D11Mit339 (63Mb) derived from C57L/J including a small part of Idd4 that includes candidate gene Csf2. Diabetes incidence in this strain is reported to be about 53% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al 2007). There appear to be multiple diabetes resistant regions (Idd4) on Chromosome 11, therefore, this strain is useful to identify candidate genes associated with diabetes resistance and to positionally clone the Idd4 resistant loci. | ||
| 008055 | NOD.L-(D11Mit314-Csf2)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11b or DR3b, carries a small C57L/J derived congenic interval on Chromosome 11, D11Mit314 (51Mb) through Csf2 (54Mb) that encodes a cluster of cytokine genes including candidate gene Csf2 (Idd4.3) and excludes all of the telomeric regions downstream of Csf2. Stat5a, Stat5b, Stat3, are of NOD origin. Csf2 production by macrophages is significantly lower that of NOD macrophages. Stat5 phosphorylation levels of NOD.Lc11b macrophages is significantly lower than NOD macrophages(Litherland et al, 2005). Diabetes incidence in females is reported to be about 30% compared to 70% in NOD control mice (Davoodi-Semiromi et al, 2007). This strain is useful to further study the role of Csf2 and to identify other Idd4 candidate genes and their role in autoimmune diabetes. | ||
| 008060 | NOD.L-(D11Mit314-D11Mit339)(D11Mit132-D11Mit42)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11j or DR3j carries Chromosome 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit132 (86Mb) through D11Mit42 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a, Stat5b and Stat3. Diabetes incidence in this strain is reported to be about 12% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al. 2007). This strain is useful to further study the role of Csf2, Stat5a, Stat5b and Stat3 in autoimmune diabetes; to identify additional candidate diabetes resistant genes and to positionally clone the Idd4 diabetes resistant loci. | ||
| 008059 | NOD.L-(D11Mit314-D11Mit339)(D11Mit325-D11Mit42)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11i or DR3i, carries two C57L/J derived congenic intervals on Chromosome 11, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit325 ((86Mb) through D11Mit42 (112Mb) that encodes C57L/J derived Csf2 and Stat5a, Stat5b, Stat3. The donating investigator reports diabetes incidence in females to be 4% compared to 70% in NOD control mice (Davoodi-Semiromi et al. 2007). This strain is useful to further study the roles of Csf2 and Stat5a, Stat5b, Stat3 in autoimmune diabetes. | ||
| 008058 | NOD.L-(D11Mit314-D11Mit339)(D11Mit364-D11Mit168)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11g or DR3g carries Chromosome 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit364 (72Mb) through D11Mit168 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a/Stat5b/Stat3 as well as Idd4.1, Idd4.2. Diabetes incidence in this strain is reported to be about 21% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al, 2007). This strain is useful to further study the role of Csf2 and Stat5a/Stat5b/Stat3 alleles in autoimmune disorders; to identify candidate diabetes resistant genes in the Idd4.1 and Idd4.2 regions and to positionally clone the Idd4 diabetes resistant loci. | ||
| 008054 | NOD.L-(D11Mit314-D11Mit339)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11a or DR3a, carries a C57L/J derived congenic interval on Chromosome 11, D11Mit51 (51Mb) through D11Mit339 (63Mb) that includes the Idd4.3 region, containing candidate gene Csf2, and the Idd4.5 region. Stat5a, Stat5b, Stat3. Candidate genes in the Idd4.4 region along with Idd4.1, 4.2 regions are of NOD origin. Diabetes incidence in females is reported to be about 39% compared to 70% in NOD control mice. (Davoodi-Semiromi et al, 2007). This strain is useful to further study the role of Csf2 and to identify other Idd4 candidate genes and their role in autoimmune diabetes. | ||
| 008057 | NOD.L-(D11Mit314-D11Mit33)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11f or DR3f, carries a small C57L/J derived congenic interval on Chromosome 11, D11Mit314 (51Mb) through D11Mit33 (81Mb) that encodes C57L/J derived Csf2 and part of Idd4 down to the overlap of Idd4.1 and Idd4.2. Stat5a, Stat5b, Stat3, candidate genes in the Idd4.4 region along with Idd4.1, 4.2 and Idd4.5 regions are of NOD origin. Csf2 production by macrophages is significantly lower than in macrophages of NOD mice. Stat5 phosphorylation levels from macrophages of NOD.Lc11f mice were significantly higher than the levels seen in C57L/J mice (Litherland et al, 2005). Diabetes incidence in females is reported to be about 44% compared to 70% in NOD control mice. (Davoodi-Semiromi et al, 2007).
This strain is useful to further study the role of Csf2 and to identify other Idd4 candidate genes and their role in autoimm ..... | ||
| 008061 | NOD.L-(D7Mit253-D7Mit242)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc7 or DR4, carries Chr. 7 alleles, D7Mit253 (115Mb) through D7Mit242 (138Mb), derived from C57L/J and is distal to either Idd7 or Idd27. Diabetes incidence in this diabetes resistant strain is reported to be 10% in females and 0% in males compared to 70% in female and 40% in male NOD/Bdc controls. Both males and females develop widespread islet associated infiltrates and invasive insulitis, although the beta cell mass and insulin content are well maintained. NOD.Lc7 neonates injected with T-cells from old NOD mice were resistant to diabetes, however 100% of the female and 38% of the male NOD recipients receiving T cells from non diabetic, 5+ month old NOD.Lc7 mice developed diabetes starting at 12 weeks of age. This strain is useful for identifying candidate genes within this new and unique Idd region and to eventually positionally clone the newly identified resistance loci. | ||
| 008053 | NOD.L-(D11Mit314-D11Mit42)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Lc11 or DR3, carries Chromosome 11 alleles, D11Mit314 (51Mb) through D11Mit42 (112Mb), derived from C57L/J including Idd4 and a candidate gene Csf2. Diabetes incidence in this diabetes resistant strain is reported to be 9% in the females and 0% in males compared to 70% in female and 40% in male NOD/Bdc control mice. NOD.Lc11 mice develop mild periductular infiltrates early in life and by 44 weeks of age histological analysis indicates healthy islet beta cells and normal amounts of stored insulin. Neonates injected with T cells from 8-week-old prediabetic NOD females and from old NOD mice were resistant to diabetes by 25 weeks of age. Splenic and lymph node derived T cells from NOD.Lc11 mice fail to cause diabetes or beta cell damage in NOD.scid neonatal mice, however 6 weeks post transfer the recipients develop severe invasive insulitis. Adult NOD.scid females that received T cells from NOD.Lc11 mice ..... For more information please see the full phenotype on the strain data sheet | ||
| 004519 | NOD.MRL(C3)-Faslpr/DoiJ | Cryopreserved - Ready for recovery |
| NOD mice homozygous for the Tnfrsf6 lpr mutation are deficient in Fas antigen expressed on cell surfaces, and the disruption of the Fas-mediated apoptotic pathway results in severe lymphoma in NOD by 4 months of age. This lymphoma is characterized by an expansion of unusual CD4 -, CD8 -, CD3 low , B220 + lymphocytes. Forty week-old NOD mice homozygous for the Tnfrsf6 lpr mutation are completely protected from spontaneous diabetes and insulitis (as compared to 68% diabetes incidence in the control NOD), even after adoptive transfer of lymphocytes from diabetic NOD mice (0% diabetes incidence 12 weeks post transfer, as compared to NOD controls with 85% incidence 12 weeks post transfer). Recent evidence indicates that Fas-deficient NOD mice are resistant to the adoptive transfer because the abnormal subset of CD4 -, CD8 -, CD3 low , B220 + lymphocytes ..... For more information please see the full phenotype on the strain data sheet | ||
| 001626 | NOD.NON-H2nb1/LtJ | Cryopreserved - Ready for recovery |
| This congenic strain carries the diabetes-resistant MHC from the NON/LtJ strain (Stock No. 002423) and is used as a comparison to the NOD/LtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 002721 | NOD.NON-Thy1a/J | Cryopreserved - Ready for recovery |
| The NOD.NON-Thy1a/J have been very useful in adoptive transfer of diabetes in the NOD/LtJ mouse model. Donor T cells can be easily distinguished from recipient T cells by both flow cytometric and histological analysis. | ||
| 005511 | NOD.NOR-(D1Mit380-D1Mit8)/DvsJ | Cryopreserved - Ready for recovery |
| This NOD/Lt congenic strain is carrying chr 1 alleles derived from strain NOR/Lt including the insulin dependent diabetes susceptibility 5 loci. Diabetes onset and incidence among NOD.NOR-D1Mit380-D1Mit8 congenic mice is significantly later and reduced. Similar to the Irvakine et al, 2005 publication it has been reported that this NOD.NOR- Idd5 congenic stock is resistant to Cyclophosphamide induced insulitis in both males and females. This strain is useful for dissecting the role of non-MHC susceptibility genes in autoimmune diabetes. | ||
| 002346 | NOD.NOR-(D2Mit490-Ada)/LtJ | Cryopreserved - Ready for recovery |
| This NOD/Lt congenic strain is carrying alleles derived from strain NOR/Lt at the interleukin 1b (Il1bNOR) and the insulin dependent diabetes susceptibility 13 (Idd13r) loci. Incidence of diabetes among NOD.NOR-D2Mit490-Ada (Idd13r, Il1bNOR) females was 16% and 26% at 30 weeks and 52 weeks of age, respectively, compared with 100% diabetes incidence by 30 weeks in NOD/Lt females; no diabetes was observed in congenic males. Histologic examination of the pancreases of year-old non-diabetic congenic mice revealed extensive perivascular/periductal leukocytic infiltration; infiltrates associated with islets "were primarily peri-insular, with granulated beta cell mass largely preserved in >80% of the islets. This histopathology is similar to that observed in year-old NOR/Lt mice of both sexes. "Thus, Idd13rdoes not mediate IDDM resistance in NOR mice by preventing lymphocyte infiltration of the pancre ..... For more information please see the full phenotype on the strain data sheet | ||
| 005510 | NOD.NOR-(D4Mit31-D4Mit310)/DvsJ | Cryopreserved - Ready for recovery |
| This NOD/Lt congenic strain is carrying chr 4 alleles derived from strain NOR/Lt at the insulin dependent diabetes susceptibility 9 and 11 loci. Diabetes onset and incidence among NOD.NOR-D4Mit31-D4Mit310 congenic mice is significantly later and reduced. Similar to the Irvakine et al, 2005 publication it has been reported that this NOD.NOR- Idd9/11 congenic stock is resistant to Cyclophosphamide induced insulitis in both males and females. This strain is useful for dissecting the role of non-MHC susceptibility genes in autoimmune diabetes. | ||
| 003051 | NOD.NOR-(Il1a-Pcna)/LtJ | Cryopreserved - Ready for recovery |
| At 30 weeks of age, incidence of diabetes among both male and female NOD.NOR-Il1a-Pcna (Idd13r, Il1aNOR)mice was significantly lower (for females, 62% vs.100%) than in NOD/Lt mice, but in females was significantly higher (62% vs.16%) than in NOD.NOR-D2Mit490-D2Mit144 (Idd13r, Il1aNOR),which carries a larger NOR/Lt-derived segment of Chr 2. By 46 weeks, IDDM incidence in females and males of the former strain had reached 75% and 12%, respectively, of that in control NOD/Lt mice. Thus, NOD.NOR-Il1a-Pcna (Idd13r, Il1aNOR)retains the NOR allele(s) for "at least one, but not the complete set" of genes comprising the complex Idd13IDDM susceptibility/resistance locus. | ||
| 003050 | NOD.NOR-(Zfp106-Il1a)/LtJ | Cryopreserved - Ready for recovery |
| At 30 weeks of age, incidence of diabetes among both male and female NOD.NOR-Zfp106-Il1a (Idd13r, Il1aNOR)mice was significantly lower than in NOD/Lt mice, but in females was significantly higher than in NOD.NOR-D2Mit490-D2Mit144 (Idd13r, Il1aNOR),which carries a larger NOR/Lt-derived segment of Chr 2. At 30 weeks, 56% of female NOD.NOR-Zfp106-Il1a (Idd13r, Il1aNOR)mice had developed IDDM, compared to 100% of female NOD/Lt mice. By one year, IDDM incidence in females and males of the former strain had reached 62% and 25%, respectively, of that in control NOD/Lt mice. Thus, NOD.NOR-Zfp106-Il1a (Idd13r, Il1aNOR)retains the NOR allele(s) for "at least one, but not the complete set" of genes comprising the complex Idd13IDDM susceptibility/resistance locus. | ||
| 014164 | NOD.NOR-Idd4NOR/LtJ/JsdDvsJ | Cryopreserved - Ready for recovery |
| Mice, from this NOD/Jsd congenic strain, carry chromosome 11 alleles derived from strain NOR/LtJ at the insulin dependent diabetes susceptibility 4 (Idd4) loci. The Idd4 region contains candidate genes Psmb6, Pld2, Alox15, Alox12e and Cxcl16. Diabetes onset and incidence, among NOD-Idd4NOR/LtJ congenic mice, is significantly later and reduced, with less than 30% of the females becoming diabetic by 30 weeks of age. Cyclophosphamide treated NOD-Idd4NOR/LtJ females, but not males, are resistant to diabetes. This strain may be useful for studying sexual dimorphism of type 1 diabetes; identifying candidate genes associated with diabetes resistance and positionally cloning the Idd4 resistant loci. | ||
| 008065 | NOD.NZM2328-(D4Mit76-D4Mit59)/McdfJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.Zc4c carries Chromosome 4 alleles, D4Mit76 (120Mb) through D4Mit59 (154Mb) derived from NZM2328. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 7% in females and 0 for males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain is useful for identifying candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 002032 | NOD.SW-H2q/J | Cryopreserved - Ready for recovery |
| This congenic strain carries the diabetes-resistant MHC from the from SWR/J (Stock No. 000689) and is used as a comparison to the NOD/ShiLtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 007930 | NOD.SWR-Idd3SWR/J/MrkJ | Cryopreserved - Ready for recovery |
| This NOD congenic strain, commonly referred to as NOD.SWR-Idd3, is carrying Chr 3 alleles, SNPs rs13476974 (11.10Mb) through rs13477217 (78.79Mb), derived from strain SWR/J including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain reported reported to be similar to NOD/MrkTac. Thymocytes and splenocytes of this T1D susceptible stock produce 2 fold less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). This stock has been useful to positionally clone Idd3 and to study the biological effects of variation of genes within the Idd3 region, specifically the Il2 gene and continue to be valued for studying long-range chromosome remodeling. | ||
| 005870 | NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J | Cryopreserved - Ready for recovery |
| This transgene expresses human glutamic acid decarboxylase 2 cDNA under the control of the rat insulin 2 promoter. FISH analysis and pseudo-giemsa metaphase spead analysis establish the insertion site of this transgene on proximal Chr 15 near the centromere. Expression of the transgene in the islets has been confirmed by RT-PCR and Western blot analysis. Southern blot analysis confirm 4-5 copies of the transgene are present. Homozygotes are developmentally lethal. Transgene positive animals are significantly protected from diabetes onset (females- 14%, Males- 15% at 50 weeks) compared to NOD/ShiLt controls (Females- 100%, Males-50% by 50 weeks). Insulitis in 9 week old females is not significantly different between transgenics and controls. This model provides a tool for studying at the role of autoantigens, specifically GAD2, in diabetes. | ||
| 005082 | NOD/ShiLt-Tg(ACTB-Ica1/EGFP)18Mdos/MdosJ | Cryopreserved - Ready for recovery |
| ACTB-Ica1/EGFP (commonly referred to as Ica69/EGFP) Line 18 transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Tissue fluorescence is strongest in the heart, intermediate in the exocrine pancreas and kidney and weak in the liver. Tissue fluorescence is observed in isolated transgenic islets. No fluorescence was observed in the brain, thymocytes or spleen cells. NOD transgenic females exhibit reduced diabetes incidence (45%) by 40 weeks of age and more rapid insulitis onset (50%, severe infiltration) at 12 weeks of age compared with NOD controls (80% diabetic by 40 wk and 20% insulitis-positive at 12 weeks). Intra-islet lymphocytes expressing interferon gamma were 50 times more frequent in sections from transgenic Line 18 than in wild-type controls, while IL4 stained cells were barely detectable in either. NOD-Tg(ACTB-Ica1/EGFP)18Mdos/MdosJ can be used as a tool to study the constant over expression of Ica1 in NOD m ..... | ||
| 005328 | NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that hemizygous transgenic mice are viable, fertile and normal in size. FACS analysis of splenic lymphocytes shows transgenic expression in 36% of CD4+ and 6% of CD8+ T cells and minimal expression (background levels) in B cells and macrophages. When compared to wild-type NOD/ShiLt mice, the diabetes incidence is lower (50%) and diabetes onset is delayed. Adoptive transfer experiments with splenocytes and bone marrow from hemizygous CD4-DsRed transgenic mice does not confer diabetes protection on NOD inbred mice, suggesting that the agent of protection is not dependent on hematopoietic cells. No homozygous transgenic mice have been identified in litters produced from hemizygote intercrosses, suggesting that homozygotes are not viable. This strain is useful for tracking resting and activated T cells in vivo and in vitro. | ||
| 005334 | NOD/ShiLt-Tg(Cd4-EGFP)1Lt/J | Cryopreserved - Ready for recovery |
| Homozygous transgenic mice are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. The donating investigator reports uniform transgenic expression, about 81% of inactivated or resting CD8+ T cells and CD4+ T cells, with minimal expression in B cells (2.3%) and macrophages (1.5%). Over a three day period following activation in vitro with anti-CD3, gating on live populations of CD4+ and CD8+ subsets show continued GFP expression in both. However, there is a greater diminution of GFP fluorescence in the activated CD8+ T population by day three in vitro. Diabetes onset is similar to wild-type NOD/ShiLt mice. These CD4-GFP transgenic mice may be useful for fluorescent monitoring of T cells both in vivo and in vitro. | ||
| 012310 | NOD/ShiLt-Tg(GFAP-Cd274)5Mdos/J | Cryopreserved - Ready for recovery |
| NOD/ShiLt-Tg(GFAP-Cd274)5Mdos/J mice, commonly referred to as GFAP-tg, express Cd274 (B7-H1), under the control of glial fibrillary acidic protein promoter (GFAP). Hemizygous and homozygous mice are viable and fertile. Rt-PCR indicates B7-H1 transgenic expression appears in neuronal tissues, including the brain and sciatic nerve, pancreas, colon, salivary gland and purified or cultured peri-islet Schwann cells (pSC). Protein expression does not correlate with transcription profiles as protein expression was only found to be elevated in the pSC and brains of transgenic mice when compared to wildtype mice. At 4-weeks of age, transgenic and non-transgenic mice exhibit no difference in glucose and insulin sensitivity tests. By 8-weeks of age, there was enhanced loss of pSC in transgenic females; which followed elevated GFAP autoreactivity. Insulitis is enhanced and more invasive in the transgenic female when compared to wildtype controls (Males not reported). By ..... For more information please see the full phenotype on the strain data sheet | ||
| 006778 | NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ | Cryopreserved - Ready for recovery |
| Gfap-Cd80 (GFAP-B7-1) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator reports that transgenic mice are protected from diabetes development. | ||
| 002035 | NOD/ShiLt-Tg(H2-Ead)12Lt/J | Cryopreserved - Ready for recovery |
| A requirement for developing insulin-dependent diabetes mellitus (IDDM) in mice is the absence of functional H2-Ea and H2-Ab1 genes. NOD/Lt mice (H2g7 = Kd, Ag7, Enull, Db) fulfill this requirement and develop IDDM. Two homozygous transgenic lines (NOD/ShiLt-Tg(H2-Ead)5Lt/J (Stock No. 002034) commonly referred to as line 5; and NOD/ShiLt-Tg(H2-Ead)12Lt/J (Stock No. 002035), referred to as line 12) were created to further examine the quantitative thresholds of MHC class II expression and the mechanisms involved in preventing IDDM development in NOD mice. These strains harbor a construct containing a complete H2-Ead gene from BALB/cByJ mice. Only a single copy of the Ead transgene integrated into the genome of line 12 where as four copies are present in line 5. Diabetes incidence in line 12 is greatly reduced (25% of females, 0% of males) where H2-Ea expression on antig ..... For more information please see the full phenotype on the strain data sheet | ||
| 002034 | NOD/ShiLt-Tg(H2-Ead)5Lt/J | Cryopreserved - Ready for recovery |
| A requirement for developing insulin-dependent diabetes mellitus (IDDM) in mice is the absence of functional H2-Ea and H2-Ab1 genes. NOD/Lt mice (H2g7 = Kd, Ag7, Enull, Db) fulfill this requirement and develop IDDM. Two homozygous transgenic lines (NOD/ShiLt-Tg(H2-Ead)5Lt/J (Stock No. 002034) commonly referred to as line 5; and NOD/ShiLt-Tg(H2-Ead)12Lt/J (Stock No. 002035), referred to as line 12) were created to further examine the quantitative thresholds of MHC class II expression and the mechanisms involved in preventing IDDM development in NOD mice. These strains harbor a construct containing a complete H2-Ead gene from BALB/cByJ mice. Only a single copy of the Ead transgene integrated into the genome of line 12 where as four copies are present in line 5. Diabetes incidence in line 12 is greatly reduced (25% of females, 0% of males) where H2-Ea expression on antig ..... For more information please see the full phenotype on the strain data sheet | ||
| 006777 | NOD/ShiLt-Tg(Ins2-Cd274)2Mdos/MdosJ | Cryopreserved - Ready for recovery |
| Ins2-Cd274 (Rip-B7H1) transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator indicates transgenic mice over express Cd274 in pancreatic beta cells and reports accelerated diabetes in Ins2-Cd274 transgenic mice compared to wildtype cohorts. This strain is useful to study the role of Cd274 in autoimmunity and peripheral tolerance. | ||
| 005733 | NOD/ShiLt-Tg(Ins2-Fas*I246N)1Ach/AchJ | Cryopreserved - Ready for recovery |
| Diabetes onset is significantly delayed in Rip-Fascg transgenic mice (45% diabetic by 30 weeks of age) compared to wildtype cohorts (90% diabetic by 30 weeks of age). Adoptive transfer studies using splenocytes from diabetic NOD/Lt mice into Rip-Fascg transgenic mice indicate the transgenic mice become diabetic later than wildtype controls. This transgenic strain is useful in studies looking at the effects of Fas on pancreatic islets. | ||
| 003074 | NOD/ShiLt-Tg(Ins2-GAD2)1Lt/LtJ | Cryopreserved - Ready for recovery |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter 7, Ins2, regulated transgene encoding a human B-cell autoantigen, GAD2. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. This NOD/Lt transgenic demonstrates a Y Chr. integration-site as only male progeny are transgenic. Expression of the transgene in the islets has been confirmed by RT-PCR and Western blot analysis. Southern analysis confirms 17 copies of the transgene are present, compared to the A-line that has 4-5 copies (Stock No. 5870). Elevated levels of GAD2 expression in transgenic B-cells do not influence non-fasting plasma levels of insulin and glucagon. At 50 weeks of age 55% of the transgenic males were diabetic, this is not significantly different from NOD/Lt male cohorts. Insulitis in 9 week old females is not significantly different between transgenics and controls. This model provides a tool f ..... | ||
| 004986 | NOD/ShiLt-Tg(Ins2-cre)3Lt/LtJ | Cryopreserved - Ready for recovery |
| This transgenic strain uses the rat insulin 2 promoter to drive expression of Cre recombinase in pancreatic beta cells. Hemizygous mice develop a diabetes that is characteristic of the NOD/ShiLt inbred strain. The investigator reports that insulin expression appears to be moderately suppressed. | ||
| 003855 | NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ | Cryopreserved - Ready for recovery |
| This strain expresses Cre recombinase under the control of the rat insulin II promoter. Hemizygous mice carrying this transgene are phenotypically normal and overexpresss cre specifically in pancreatic beta cells. Homozygous transgenic mice experience delayed onset diabetes compared to wildtype controls. This transgenic strain is used in combination with mice carrying floxed targeted mutations to create various pancreatic beta cell-specific gene knockouts using the Cre/loxP system. | ||
| 004987 | NOD/ShiLt-Tg(Ins2-cre)6Lt/LtJ | Cryopreserved - Ready for recovery |
| 006604 | NOD/ShiLtDvs-Tg(HLA-A/H2-D/B2M)1Dvs/J | Cryopreserved - Ready for recovery |
| This transgenic NOD mouse model, commonly referred to as NOD.HHD, develops significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice.
When transgenic mice are bred to NOD-B2m-deficient mice (e.g. Stock No. 002309), which completely lack CD8+ T cells, CD8+ T cells are restored in the double mutant mice, but at significantly lower levels than in NOD inbred mice. FACS analysis indicates that the transgenic NOD-B2m-deficient mice express only the HLA-A2.1/H2-Db chimeric class I molecule. In contrast to NOD.B2mtm1Unc females, which are diabetes free, 55% of the transgenic NOD B2m-deficient females develop diabetes by 30 weeks of age. Insulitis scores determined by histological examination are similar between the NOD double mutant mice and NOD/ShiLtDvs inbred mice, and cultured pancreatic islets from transgenic NOD B2m-deficient mice an ..... | ||
| 004226 | NOD/ShiLtDvs-Tg(Ins2-E3*309)5Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 004227 | NOD/ShiLtDvs-Tg(Ins2-E3*704)2Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 004968 | NOD/ShiLtDvs-Tg(Ins2-E3*734)3Dvs/DvsJ | Cryopreserved - Ready for recovery |
| Carriers of this transgene express the transcripts of the adenoviral E3 19K, 11.6K, 14.5K, 14.7K, and 10.4K glycoproteins in the islets but the adenovirus death protein is not expressed due to point mutations in the first two methionines of the 11.6K open reading frame. Female carriers of this transgene have slower kinetics and rates of development of diabetes through 30 weeks of age relative to NOD/Lt controls. These carriers do not display a significantly different diabetes rate than un-mutated adenovirus E3 carriers. | ||
| 004990 | NOD/ShiLtDvs-Tg(Ins2-E3*734)4Dvs/DvsJ | Cryopreserved - Ready for recovery |
| 005282 | NOD/ShiLtJ-Tg(Ins1-EGFP/GH1)14Hara/HaraJ | Cryopreserved - Ready for recovery |
| Donating investigator reports transgenic mice develop normally and behave similarly to controls with respect to glucose tolerence and and pancreatic insulin content. Histology confirms transgenic mice have normal islet architecture with coexpression of insulin and GFP. The enhanced GFP reporter allows the beta cells to be easily identified and purified for further studies. Studies completed at The Jackson Laboratory indicate there is strong non-mosaic expression of green fluorescent protein in NOD/LtJ-Tg(Ins1-EGFP/GH1)14Hara/HaraJ islets. 100% of homozygous Ins1-EGFP transgenic males and females, identified by qPCR, become diabetic by 9 weeks of age. Pancreatic histopathology of homozygous mice shows beta cell loss without insulitis. | ||
| 005309 | NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ | Cryopreserved - Ready for recovery |
| Transgenic mice carrying the Ighmtm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells. The number of B-cells is reduced and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is significantly more severe, especially in males. No diabetes was observed in NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ mice by 50 weeks of age. This model serves as a control for the membrane bound, non-secreted, NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ (Stock No. 005306). | ||
| 005306 | NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ | Cryopreserved - Ready for recovery |
| Transgenic mice carrying the Ighmtm1Cgn allele are viable, fertile, and normal in size and restores the B220+ B-cells to normal. The number of B-cells is normal and the ratio of CD4 to CD8 is normal. Although only a fraction of the transgenic mice have an increased amount of insulitis, it is more severe, especially in males. Diabetes incidence is partially restored in NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/Fsw with approximately, 11% females and 0% males becoming diabetic by 50 weeks of age compared to approximately 2% Ighmtm1Cgn female controls and 0% Ighmtm1Cgn male controls by 50 weeks of age or 90% female NOD controls and 70% male NOD controls by 30 weeks of age. T- cell depleted spleen cells from Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk mice stimulated with lipopolysaccharide (LPS) respond normally. NODCaj.Cg-Ighmtm1Cgn Tg(Igh-VB1-8/Igh-6m )2Mjsk/Fsw like NOD.129S2(B6)-<> ..... For more information please see the full phenotype on the strain data sheet | ||
| 005714 | NOR.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ | Cryopreserved - Ready for recovery |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Approximately 50% of the NOR (backcross 5) transgenic mice become diabetic by 30 weeks of age compared the control NOR which is diabetes resistant. Spleens of diabetic NOR transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic NOR.Cg-Tg(Ins2-CD80)3B7Flv/FswJ mice, yet failed to transfer disease to NOD.scid, B6.scid, or CB17.scid. NOR.-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 002347 | NOR.NOD-(Il1-Ada)/LtJ | Cryopreserved - Ready for recovery |
| This NOR/Lt congenic strain is carrying alleles derived from strain NOD/Lt for interleukin 1a (Il1aNOD), adenosine deaminase (Ada) and insulin dependent diabetes susceptibility 13 (Idd13NOD) loci. Neither males nor females from this congenic strain when aged to 40 weeks showed diabetes development. This strain is useful for dissecting the role of non-MHC susceptibility genes in autoimmune diabetes. | ||
| 002348 | NOcCB1/LtJ | Cryopreserved - Ready for recovery |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 016603 | NOD.B6-Gt(ROSA)26Sortm1(HBEGF)Awai/DvsJ | Under Development for Cryo |
| Mice homozygous for this iDTR mutation are viable and fertile. These mice have the simian Diphtheria Toxin Receptor (DTR; from simian Hbegf) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of DTR is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTR expression. Cells expressing DTR are rendered susceptible to ablation following Diphtheria toxin administration. For instance, the role of a particular cell population in T1D development can be determined by injecting Diphtheria toxin to deplete the specific cells in a timely fashion. For example, when bred to a strain expressing Cre recombinase in dendritic cells (see Stock No. 013233 for example), this mutant mouse strain may be useful for studies involving the immunology of diabetes. When crossed t ..... | ||
| 001627 | NON.NOD-H2g7/LtJ | Under Development for Cryo |
| This histocompatibility congenic strain carries the diabetogenic MHC from NOD/ShiLtJ mice and is used as a comparison strain for NOD/ShiLtJ (Stock No. 001976) and NON/ShiLtJ (Stock No. 002423). These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 013116 | NOD.B6-Tg(Ins2-luc/EGFP/TK)300Kauf/J | Under Development - Now Accepting Orders |
| Mice carrying tri-fusion transgene Ins2-luc/EGFP/Tk, commonly called MIP-TF, line 300 express a luciferase/enhanced green florescent protein/thymidine kinase fusion protein (luc/EGFP/Tk) under the control of mouse insulin promoter (Ins2) and are viable, fertile and exhibit no gross physical or behavioral abnormalities. On the C57BL/6 background, transgene expression, determined by luciferase enzymatic activity and green florescence is exclusive to the pancreas, specifically the insulin producing cells. Transgene expression appears to have no effect on weight, islet morphology, fasting blood glucose, or response to glucose challenge when compared to wild-type controls. This trifusion reporter model should enable longitudinal noninvasive imaging of beta cells in the same animal by cooled charge coupled device (CCD) and micro positron emission tomography (microPET), and identification of beta cells at the cellular level by florescent microscopy. There is a correlation between CCD and mic ..... For more information please see the full phenotype on the strain data sheet | ||
(198 stocks) Back to Top
How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.
New Strains Awaiting TransferThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
- Receive periodic updates on the status of the colony AWAITING TRANSFER
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
Send questions to our Technical Support team using the Express Technical Support Form.
(5.1)