Search Criteria: Research Area is "Immunology and Inflammation Research: Autoimmunity (Type 1 Diabetes)"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001976 | NOD/ShiLtJ | Level 1 |
| Diabetes in NOD/ShiLtJ mice is characterized by insulitis, a leukocytic infiltrate of the pancreatic islets. Marked decreases in pancreatic insulin content occur in females at about 12 weeks of age and several weeks later in males. Onset of diabetes is marked by moderate glycosuria and by a non-fasting plasma glucose higher than 250 mg/dl. Diabetic mice are hypoinsulinemic and hyperglucagonemic, indicating a selective destruction of pancreatic islet beta cells. Susceptibility to IDDM in NOD/ShiLtJ mice is polygenic, and environment, including housing conditions, health status, and diet, exerts a strong effect on penetrance. NOD/ShiLtJ females are more widely used than males because the onset of IDDM symptoms occurs earlier and with a higher incidence (90-100% by 30 weeks of age). NOD/ShiLtJ males develop IDDM at a frequency of between 40-60% by 30-40 weeks of age. Male mice are useful for certain applications, including pharmaceutical studies, "accelerated transfer" of IDDM, and some <
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..... For more information please see the full descriiption on the strain data sheet | ||
| 006411 | B6.129-Gasttm1(INS)Ez/J | Repository- Live |
| 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). | ||
| 006860 | B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Repository- Live |
| Mice homozygous for the targeted mutation and heterozygous for the Ins2Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Ins2Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants
..... For more information please see the full descriiption on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 006864 | B6.Cg-Tg(Ins1-EGFP)1Hara/J | 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 Enhanced Green Fluorescent Protein (EGFP) under the control of the 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 adulthood. The fluorescence expression pattern is similar to the patterns seen in other stocks (see Stock No. 006784 and Stock No. 006866). MIP-GFP transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone (hGH) sequence in the transgenic insert enhances expression of the EGFP, but hGH is not expressed. This mutant mouse strain may be useful in studies of diabetes and pancreatic beta islet
..... For more information please see the full descriiption on the strain data sheet | ||
| 003548 | C57BL/6-Ins2Akita/J | Repository- Live |
| Mice heterozygous for the Akita spontaneous mutation (Ins2Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes. Aged mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as 12 weeks after the onset of hyperglycemia. Retinal complications include increased vascular permeability, alterations in the morphology of astrocytes and microglia, increased apoptosis and thining of the inner layers of the retina. (Barber AJ, et al., 2005) The mean lifespan of diabetic male mice on the C57BL/NJcl background (305 days) was significantly shorter than that of nondiabetic males in anothe
..... For more information please see the full descriiption on the strain data sheet | ||
| 005432 | C57BL/6-Tg(Ins2-OVA)307Wehi/WehiJ | Repository- Live |
| Immunohistochemistry does not detect ovalbumin in the islet beta cells of the pancreas. The double transgenic resulting from a cross of this transgenic stock with C57BL/6-Tg(Tcra Tcrb)1100MjbJ (OT-1) exhibit early onset of spontaneous diabetes with islet infiltration; implying that the beta cells express OVA. One of 60 irradiated Tg(Ins2-OV)307 mice receiving a 1:4 mixture (OT-1 transgenic mice:C57BL/6-Thy1.1 congenic) of bone marrow become diabetic when followed for 10 weeks post transfer. Histolocigal evaluation indicates 22% of the islets are mildly infiltrated 15-21 weeks post transfer. This stock only exhibits antigen presentation in the draining lymph node when the pancreatic islets have been damaged. This ovalbumin expressing model is a tool for assessing antigen ignorance and is used in tumor immunity studies and tissue damage studies. | ||
| 005433 | C57BL/6-Tg(Ins2-OVA)59Wehi/WehiJ | Repository- Live |
| Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The pancreatic islets exhibit weak ovalbumin- (OV-) specific immunohistologic staining and OV is detectable in the islets by Western blot analysis. These mice develop diabetes following adoptive transfer of activated, but not naive, CD8+ T lymphocytes from mice bearing Tg(TcraTcrb)1100Mjb (OT-1). Both CD8+ T-cells and CD4+ T cells from these transgenic animals are tolerant to ovalbumin. This model provides a tool for assessing the requirements of peripheral T-cell deletion. | ||
| 005431 | C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ | Repository- Live |
| Ins2-TFRC/OVA (commonly referred to as RIP-mOVA) line 296-1B hemizygote transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immunohistochemical analysis detects strong expression in pancreatic beta cells and kidney proximal tubular cells and weak expression in testes. When C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ is mated to C57BL/6-Tg(TcraTcrb)1100Mjb/J (commonly referred to as OT-1 and recognizes OVA specific T-cells, Stock No. 003831) thymic deletion of OT-1 cells is observed in double transgenic mice, suggesting very low levels of thymic expression. OVA specific CD-8+ T-cells activated by cross presentation infiltrate the pancreas causing beta cell destruction resulting in diabetes. However, these cells do not infiltrate the kidney. Proliferating OT-1 T-cells appeared specifically in the lymph nodes draining the pancreas (PLN's) and kidney (RLN's) on day
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| 007562 | D2.B6-Ins2Akita/MatbJ | Repository- Live |
| DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.
Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as
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| 006867 | FVB.B6-Ins2Akita/MlnJ | Repository- Live |
| FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type offs
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..... For more information please see the full descriiption on the strain data sheet | ||
| 008063 | NOD-Chr 17NZM2328/McdfJ | Repository- Live |
| 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 | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 006611 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 008224 | NOD.129S2(B6)-Cd74tm1Doi/LwnJ | Repository- Live |
| Mice homozygous for the Cd74 targeted mutation are viable and fertile. Cd74 deficiency affects CD4 T cell development; therefore these mice have very few CD4+ T cells. Antigen presenting cells have reduced, though not abolished, ability to present MHC class II antigens, such as GAD. These mice are protected from diabetes. This stock is important for investigation of MHC class II molecule associated self-antigen selection and the importance of self-peptide in CD4 T cell selection and development. | ||
| 005036 | NOD.129S2(B6)-Ins2tm1Jja/GseJ | Repository- Live |
| Ins2tm1Jja heterozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. RT-PCR detects no expression of Ins2 in the thymus or pancreas of Ins2tm1Jja homozygous mice and Insulin Autoantibody Assays (IAA) indicate that by four weeks of age insulin auto-antibodies were significantly higher than NOD controls. Diabetes incidence occurs in 100 percent of the homozygous females by 15 weeks of age compared with 77% wildtype females by 27 weeks of age. While 100 percent of the homozygote males are diabetic by 22 weeks old compared to 28 percent of the wildtype males by 27 weeks of age. Histological evaluation found extensive islet infiltration in 8 week old homozygous mice compared to wildtype mice in which a minority of islets were infiltrated. NOD.129S2(B6)-Ins2tm1Jja/GseJ is useful for studying insulin autoantigens and their role in the autoimmune process leading
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| 007931 | NOD.A-Idd3A/J/MrkJ | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 007934 | NOD.B6(PL)-Idd3C57BL/6/MrkTacJ | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 006809 | NOD.B6-(D11Nds1-D11Mit41)/J | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 007932 | NOD.CAST-Idd3CAST/EiJ/MrkJ | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 007933 | NOD.CZI-Idd3CZECHI/EiJ/MrkTacJ | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 006608 | NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ | Repository- Live |
| NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Igh-6-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Igh-6-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Igh-6-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 Igh-6-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Igh-6-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Igh-6-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
..... For more information please see the full descriiption on the strain data sheet | ||
| 006956 | NOD.Cg-Vdrtm1Ska/CmatJ | Repository- Live |
| Heterozygous mice are viable, fertile, and phenotypically indistinguishable from wildtype siblings. Homozygous mutant mice are viable but infertile. No VDR mRNA is detected by RT-PCR in samples from the intestine or kidney or from homozygous mutant embryo. Increased expression of CTP27B1 and reduced expression of CYP24A1 and calbindin-D9k is detected by RT-PCR in samples from VDR-deficient kidneys. Although mice homozygous for this targeted mutation are viable, shortly after weaning they exhibit dysmorphic features including a flat face and short nose, alopecia, growth retardation, and skeletal defects including hypocalcaemia, decreased bone mineral density, widened growth plates with hypomineralization, less trabeculae and thicker osteo seams. Homozygous mutant mice exhibit metabolic imbalances including abnormally high and low levels of 1,25(OH),2D3 and 25(OH)D3, respectively and abnormal cytokine and chemokine profiles.
Homozygous mice exhibit normal pancreatic islet archite
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| 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 kenetics 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
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| 008056 | NOD.L-(Csf2-D11Mit339)/McdfJ | Repository- Live |
| 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. | ||
| 008060 | NOD.L-(D11Mit314-D11Mit339)(D11Mit132-D11Mit42)/McdfJ | Repository- Live |
| 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. | ||
| 008054 | NOD.L-(D11Mit314-D11Mit339)/McdfJ | Repository- Live |
| 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 | Repository- Live |
| 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
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| 008061 | NOD.L-(D7Mit253-D7Mit242)/McdfJ | Repository- Live |
| 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 | Repository- Live |
| 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 descriiption on the strain data sheet | ||
| 007930 | NOD.SWR-Idd3SWR/J/MrkJ | Repository- Live |
| 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. | ||
| 005328 | NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J | Repository- Live |
| 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 | Repository- Live |
| 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. | ||
| 006604 | NOD/ShiLtDvs-Tg(HLA-A/H2-D/B2M)1Dvs/J | Repository- Live |
| 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
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| 006866 | STOCK Tg(Ins1-DsRed*T4)32Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-RFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the DsRed.T4 variant of Enhanced Red Fluorescent Protein under the control of mouse insulin I promoter (MIP). 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 adulthood. Transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the sequence is not expressed in a similarly constructed transgenic strain (see Stock No. 006864). This mutant mouse strain may be useful in studies of pancreatic development and pancreatic b
..... For more information please see the full descriiption on the strain data sheet | ||
| 006784 | STOCK Tg(Ins1-ECFP)24Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-CFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cerulean variant of Enhanced Cyan Fluorescent Protein under the control of mouse insulin 1 promoter (MIP). 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 fluorescence expression pattern observed in this strain is similar to the patterns seen in other stocks that express fluorescent proteins from the MIP promoter (see Stock No. 006864 and Stock No. 006866). The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the seque
..... For more information please see the full descriiption on the strain data sheet | ||
| 005500 | B6.C-Tg(Ins2-GP)34-20Olds/MvhJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) glycoprotein(GP) or nucleoprotein (NP) under the control of the rat insulin promoter. Ins2-GP expression was determined only in the pancreas by RT-PCR (von Herrath et al 1994). Tg(Ins2-GP)34-20Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.C -Tg(Ins2-GP)34-20Olds mice (H2b) exhibit a rapid (10-14 days) onset of IDDM compared to C.B6-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or B6.C -Tg(Ins2-NP)25-3Olds mice (H2b) (30-120 days) (Oldstone et al.,1991; von Herrath et al.,1994). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.C -Tg(Ins2-GP)34-20Olds transplanted into nude hosts produce a primary CTL response when challenged with LCMV. CD8 T cells are required for IDDM development in both glycoprotein
..... For more information please see the full descriiption on the strain data sheet | ||
| 004826 | B6.Cg-Tg(Ins2-NP)25-3Olds/MhvJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) or glycoprotein(GP) under the control of the rat insulin promoter. Northern blot analysis identifies a 3kb band expected of the transgene and SV40 processing signals in the pancreas (Oldstone et al., 1991). Ins2-NP expression was determined in the pancreas and thymus by RT-PCR (von Herrath et al 1994). Tg(Ins2-NP)25-3Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.Cg -Tg(Ins2-NP)25-3Olds mice (H2b) exhibit a slower (30-120 days) onset of IDDM than the C.Cg-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or the B6.Cg -Tg(Ins2-GP) 34-20Olds mice (H2b) (10-14 days) (Oldstone et al.,1991, Homann et al.,1999). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.Cg-Tg(Ins2-NP)25-3Olds transplante
..... For more information please see the full descriiption on the strain data sheet | ||
| 004827 | C.Cg-Tg(Ins2-NP)25-3Olds/MvhJ | Repository-Cryopreserved |
| Transgenic mice were created with the Lymphocytic choriomeningitis virus (LCMV) nucleoprotein(NP) or glycoprotein(GP) under the control of the rat insulin promoter. Northern blot analysis identifies a 3kb band expected of the transgene and SV40 processing signals in the pancreas (Oldstone et al., 1991). Ins2-NP expression was determined in the pancreas and thymus by RT-PCR (von Herrath et al 1994). Tg(Ins2-NP)25-3Olds untreated mice rarely develop insulin-dependent diabetes mellitus (IDDM). When challenged with LCMV they develop IDDM. The B6.Cg -Tg(Ins2-NP)25-3Olds mice (H2b) exhibit a slower (30-120 days) onset of IDDM than the C.Cg-Tg(Ins2-NP)25-3Olds mice (H2d) (10-21 days) or the B6.Cg-Tg(Ins2-GP) 34-20Olds mice (H2b) (10-14 days) (Oldstone et al.,1991, Homann et al.,1999). Thymic expression of nucleoprotein has been shown to be responsible for this delayed onset of IDDM. Thymi from newborn B6.Cg-Tg(Ins2-NP)25-3Olds transplanted
..... For more information please see the full descriiption on the strain data sheet | ||
| 005739 | NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 004673 | NOD.129(B6)-Rag1tm1Mom Cd80tm1Shr/JbsJ | Repository-Cryopreserved |
| 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. | ||
| 005075 | NOD.129(B6)-Tnfsf4tm1Shr/DoiJ | Repository-Cryopreserved |
| Tnfsf4tm1Shrhomozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Tnfsf4 on activated dendritic cells, T-cells and B-cells derived from spleen or lymph nodes by FAC analysis or ELISA. Additionally, the number of B-cells, T-cells, T-cell subsets and expression of CD25 and CD69 in spleen and lymph nodes are comparable to NOD controls. All Tnfsf4 homozygous mice are completely protected from diabetes and histological evaluation seldom shows insulitis when compared to wild-type controls, which exhibit a normal NOD like diabetes incidence and onset. This model is useful for studying co-stimulation, dendritic cell function and the role of Tnfsf4 on CD4 positive T cell responses in Type 1 Diabetes. | ||
| 005352 | NOD.129-(D19Mit10-D19Mit54)/GseJ | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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). | ||
| 005080 | NOD.129-Ica1tm1Mdos/MdosJ | Repository-Cryopreserved |
| Ica1tm1Mdos homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Ica1 by western blot analysis. Ica1tm1Mdos homozygous animals develop mild salivary gland infiltrations with progression of disease 55%-65% slower than progression of submandibular gland monouclear foci in wildtype and heterozygote controls. Dacryodenitis was undetectable in 35-40 week old male Ica1tm1Mdos homozygous mice compared to 64% of wildtype and 58% of heterozygotes similarly aged (Winer et al., 2002). Development of spontaneous diabetes is slightly delayed in this stock (by 4 weeks) and incidence is modestly diminished (65% incidence in females after 36 weeks versus 85% in wild-type NOD females). Ica1tm1Mdos homozygous females are significantly protected from cyclophosphomide (CY) induced diabetes (10% in females post CY treatment ve
..... For more information please see the full descriiption on the strain data sheet | ||
| 005035 | NOD.129S2(B6)-Ins1tm1Jja/GseJ | Repository-Cryopreserved |
| Ins1tm1Jja homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Ins1 in the pancreas by RT-PCR and similar levels of insulin auto-antibodies develop in NOD.129S2(B6)-Ins1tm1Jja homozygotes as are found in NOD controls. However, neither homozygous nor heterozygous males develop diabetes, compared with >20% of wild-type littermates, and less than 5% of the Ins1tm1Jja homozygous females and 40% of the heterozygous females become diabetic compared with >80% of wild-type females when followed for 1 year. Histological evaluation found 48 week old homozygous and heterozygous males to have either minimal periinsulitis or no insulitis. Heterozygous females had more extensive insulitis than heterozygous males and homozygous females had minimal intra-ductal infiltrates and no insulitis, whereas wild type littermates had severe insul
..... For more information please see the full descriiption on the strain data sheet | ||
| 006351 | NOD.129S4(B6)-Icam1tm1Jcgr/J | Repository-Cryopreserved |
| Homozygous mutant mice are diabetes resistant. No membrane bound ICAM-1 is detectable in homozygous mutant mice. Histological examination shows no or only mild peri-insular infiltration at 330-410 days of age, By comparison, 64% of their wild-type and 44% of their heterozygote cohorts become diabetic by 310 days of age. In contrast to wild-type, 110-day-old ICAM-1 deficient females do not develop severe insulitis 10 days post cyclophosphamide treatment. Protection is associated with suppression of destructive insulitis as well as a deviation to a T-helper 2 cytokine mRNA expression pattern (Martin et al 2001).
Both the C57BL/6 contaminated strain, Stock No. 5983 - NOD.129S4(B6)-Icam1tm1Jcgr/SmtnJ, and this non contaminated strain are completly diabetes resistant at 30 weeks of age when evaluated in a comparative diabetes incidence study. Fine mapping data may be viewed at GQC of Icam1 c
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| 005073 | NOD.ABH-(D18Mit19-D18Mit4)/TrmJ | Repository-Cryopreserved |
| 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. | ||
| 007573 | NOD.B6-(D6Mit254-D6Mit289)/CarJ | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 005512 | NOD.B6-Tg(HLA-A2.1)1Enge/DvsJ | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 006610 | NOD.B6-Tg(ML5sHEL)5Ccg/DvsJ | Repository-Cryopreserved |
| 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. | ||
| 004304 | NOD.CBALs-Tyr+/LtJ | Repository-Cryopreserved |
| 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 Chr 7 slightly supresses spontaneous T1D development which is an asset when these females are used as blastocyst recipients. | ||
| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository-Cryopreserved |
| 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
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| 006698 | NOD.Cg-Il4tm1Lky/JbsJ | Repository-Cryopreserved |
| 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. | ||
| 005273 | NOD.Cg-Rag1tm1Mom Cd86tm2Shr Cd80tm1Shr/JbsJ | Repository-Cryopreserved |
| Mice homozygous for the Cd80tm1Shr and Cd86tm2Shr mutations are deficient in both CD80 and CD86. NOD mice defiecient for CD80, CD86 and Rag1 are viable and fertile, fail to produce T or B cells, and exhibit no signs of diabetes due to the absence of lymphocytes. In an immunocompetent NOD background, the Cd86tm2Shr and Cd80tm1Shr mutations exacerbate diabetes onset as well as a variety of other autoimmune diseases including thyroiditis, sialitis, exocrine pancreas disease and neuropathy when compared to normal NOD controls. These mice have also been observed, by the donating investigator, to be Treg-deficient. NOD.129(B6)-Rag1tm1Mom Cd86tm2ShrCd80tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation and Treg function as they relate to autoimmune diseases and organ transplantation. | ||
| 005853 | NOD.Cg-Tg(HLA-A2/H2-K)1Scr/ShrmJ | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 005524 | NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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. | ||
| 005115 | NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 005113 | NOD.FVB-Tg(INS-SOD2)3Pne/PneJ | Repository-Cryopreserved |
| 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. | ||
| 005114 | NOD.FVB-Tg(Ins1-Cat,Tyr)25Pne/PneJ | Repository-Cryopreserved |
| 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
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| 005870 | NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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
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| 006778 | NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ | Repository-Cryopreserved |
| 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. | ||
| 006777 | NOD/ShiLt-Tg(Ins2-Cd274)2Mdos/MdosJ | Repository-Cryopreserved |
| 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. | ||
| 003074 | NOD/ShiLt-Tg(Ins2-GAD2)1Lt/LtJ | Repository-Cryopreserved |
| 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
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| 005282 | NOD/ShiLtJ-Tg(Ins1-EGFP/GH1)14Hara/HaraJ | Repository-Cryopreserved |
| 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-Igh-6tm1Cgn Tg(Igh-VB1-8/Igh-6)2Mjsk/FswJ | Repository-Cryopreserved |
| Transgenic mice carrying the Igh-6tm1Cgn 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-Igh-6tm1Cgn 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-Igh-6tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ (Stock No. 005306). | ||
| 005306 | NODCaj.Cg-Igh-6tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk/FswJ | Repository-Cryopreserved |
| Transgenic mice carrying the Igh-6tm1Cgn 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-Igh-6tm1Cgn 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% Igh-6tm1Cgn female controls and 0% Igh-6tm1Cgn 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 Igh-6tm1Cgn Tg(Igh-VB1-8/Igh-6m)1Mjsk mice stimulated with lipopolysaccharide (LPS) respond normally. NODCaj.Cg-Igh-6tm1Cgn Tg(Igh-VB1-8/Igh-6 )2Mjsk/Fsw like NOD.129S2(
..... For more information please see the full descriiption on the strain data sheet | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 004257 | NOD.Cg-Prkdcscid Tg(TcrLCMV)327Sdz/Dvs | Research Strain |
| These mice do not develop diabetes; The presence of the T cell receptor expressing transgene does not alter the resistance to type 1 diabetes conferred to the NOD background by homozygosity for the scid mutation. | ||
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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 Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe 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. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
- 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 Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. 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.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
Send questions to our Technical Support team using the Express Technical Support Form.
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