Search Criteria: Research Area is "Diabetes and Obesity Research: Type 1 Diabetes (IDDM)"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
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 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 wk 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, which exhibit impaired glucose tolerance in the presence
..... For more information please see the full phenotype 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 Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Akita 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 have essentially no subcutaneo
..... For more information please see the full phenotype 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. | ||
| 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 phenotype on the strain data sheet | ||
| 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 phenotype 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. | ||
| 004947 | NOD.129S2(B6)-Casp1tm1Sesh/LtJ | Repository- Live |
| Casp1tm1Sesh homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Casp1 in spleen by northern blot analysis or by RT-PCR of peritoneal exudate cells, brain, lung, heart, liver, adrenal gland, kidney, testis, and thymus (Li et al, 1995). Cultured LPS stimulated bone marrow derived macrophages from homozygous NOD.129S2(B6)- Casp1tm1Sesh /LtJ animals secrete 4-fold less IL1 beta, 30% less IL1 alpha, and IL18 is undetectable when compared with hemizygous and wild-type controls. Diabetes frequency of Casp1tm1Sesh deficient animals is equivalent to NOD/Lt, heterozygote and wild-type controls. Weanling Casp1tm1Sesh homozygous animals injected with Complete Freund's adjuvant and young pre-diabetic males treated with multiple low dose streptozotocin behave similarly to control (wild type, heterozygote, or NOD/Lt) a
..... For more information please see the full phenotype 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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| 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 phenotype on the strain data sheet | ||
| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Repository- Live |
| Mice homozygous for the Faslgld spontaneous mutation are viable and fertile. 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. | ||
| 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 phenotype on the strain data sheet | ||
| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository- Live |
| 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. (2003).Proc Natl Acad Sci U S A 100(23):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 autoimmunity. | ||
| 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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| 007769 | NOD.FVB-Tg(Igh-6-Cd80)1Gjf/JbsJ | Repository- Live |
| 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, Igh-6 (IgM), 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, indicating feature
..... For more information please see the full phenotype on the strain data sheet | ||
| 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 phenotype on the strain data sheet | ||
| 003727 | B6.129P2-Cd38tm1Lnd/J | Repository-Cryopreserved |
| Mice homozygous for Cd38tm1Lnd are viable, fertile and appear to be free from gross defects. Cd38 transcripts and protein product are not detected in these animals, nor are B lymphocytes responsive to the proliferative effects of anti-CD38 antibodies. NAD+ glycohydrolase activity in spleen, liver and brain is either markedly reduced or absent and a decrease in hapten-specific IgM, IgG1 and IgE responses is observed. Kato et al. recently published a targeted disruption in exon 1 of the Cd38 gene (J Biol Chem 274:1869-1872, 1999). Homozygous mutant mice show impairments in glucose-induced increases in ADP-ribosyl cyclase/cyclic ADP-ribose (cADPR), intracellular calcium concentration, and insulin secretion. These results support an essential role for CD38 in intracellular calcium mobilization by cADPR for insulin secretion. CD38 deficient mice are unable to mount an innate immune response to bacterial pathogens such as Streptococcus pneumoniae. In ad
..... For more information please see the full phenotype on the strain data sheet | ||
| 005517 | B6.129S4-Cyb5r4tm1Hfb/HfbJ | Repository-Cryopreserved |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m
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| 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 phenotype 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 phenotype on the strain data sheet | ||
| 005516 | C.129S4-Cyb5r4tm1Hfb/HfbJ | Repository-Cryopreserved |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m
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| 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 phenotype on the strain data sheet | ||
| 005863 | C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J | Repository-Cryopreserved |
| Hemizygous mice are viable and fertile with no anatomic abnormalities. Transgene expression is observed in aorta, heart, and brain. Transgenic dimethylarginine dimethylaminohydrolase (DDAH) activity is reflected in a reduction of plasma asymmetric dimethylarginine (ADMA). Nitric oxide synthase (NOS) activity is significantly increased in transgenic skeletal and cardiac muscle. Transgenic mice have lower blood pressure and higher heart rate. Transgenic mice may be useful in studies of atherosclerosis, hypertension, hyperlipidemia, hypercholesterolemia, hyperhomocystinemia, diabetes mellitus, stroke, renal failure, preeclampsia, and other conditions associated with vascular pathophysiology and/or cardiovascular disease. | ||
| 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 phenotype on the strain data sheet | ||
| 005020 | NOD-Tg(Igh-6/Igh-V281)3Jwt/JwtJ | Repository-Cryopreserved |
| 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. | ||
| 005356 | NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ | Repository-Cryopreserved |
| 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 | ||
| 005347 | NOD.129(B6)-Cd38tm1Lnd Art2atm1Fkn Art2btm1Fkn/Lt | Repository-Cryopreserved |
| 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. | ||
| 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 phenotype on the strain data sheet | ||
| 004311 | NOD.129P2(B6)-Cd38tm1Lnd/LtJ | Repository-Cryopreserved |
| NOD/Lt mice homozygous for the Cd38tm1Lnd mutation are viable, fertile and exhibit accelerated Type 1 diabetes onset in females and males. This acceleration has been correlated with further impairment of an already subnormal immunoregulatory network. Regulatory T-cells from these mice are more sensitive to NAD-mediated apoptosis when compared to NOD/Lt controls. Similarly, NOD-characteristic reductions in NKT cell numbers are further exacerbated in homozygous NOD.Cd38tm1Lnd mutant mice. Although CD38 is reportedly required for normal pancratic beta cell responses to glucose, this was not confirmed in congenic, doubly homozygous NOD.PkrdcscidCD38tm1Lnd mutant mice. NOD.129P2(B6)-Cd38tm1Lnd/LtJ mice are valuable for understanding how systemic NAD metabolism can be used to alter immunoregulatory networks. | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| 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) | ||
| 004352 | NOD.129S1(B6)-Ifngr2tm1Pbro/DvsJ | Repository-Cryopreserved |
| Although Ifngr2 deficient mice on the NOD/Lt background are defective in Ifng induced gene expression, they exhibit no significant difference in leukocyte subset (CD4 positive T cells, CD8 positive T cells, B cells, macrophages, dendritic cells, and granulocutes) as compared to NOD/Lt controls. Upon stimulation of cultured T cells in vitro with anti-CD3, Ifngr2 deficient NOD mice produce more IFNG and significantly more Il4 than NOD controls. Ifngr2 mutant mice develop IDDM at a similar rate as NOD/Lt controls (85% female incidence after 30 weeks in mutant mice versus 100% female incidence in standard NOD/Lt controls). (Serreze et al 2000) | ||
| 004761 | NOD.129S2(B6)-Cd28tm1Mak/JbsJ | Repository-Cryopreserved |
| NOD mice heterozygous for the Cd28tm1Mak mutation are viable, fertile; exhibiting diabetes onset and incidence similar to NOD. NOD mice homozygous for Cd28tm1Mak experience rapid onset Type 1 diabetes in both males and females. When stimulated with anti-Cd3 mAB, T cells from CD28 deficient NOD mice proliferate poorly when compared with wildtype controls. Nor do T cells proliferate in culture after the mice have been immunized with ovalbumin (OVA) in complete Freund’s adjuvant. The IL-2 level of T-cells from mice that have been stimulated with either anti-Cd3 or OVA was significantly reduced. However, when challenged with GAD the CD28 deficient mice produced normal levels of IL-2. RT-PCR indicates a dramatic increase in the amount of IFNgamma and decreased IL4 compared to heterozygous controls. 1.5% of CD4 T cells from homozygous mice express CD25, while 6.5% of the CD4 T cells express CD25 in their wildtype cohorts.
This model is useful for
..... | ||
| 005513 | NOD.129S2(B6)-Cd8atm1Mak/DvsJ | Repository-Cryopreserved |
| Mice homozygote for the Cd8atm1Mak targeted mutation are deficient in functional cytotoxic T-cells; however helper T-cell development and function is comparable to normal. NOD.129S2(B6)-Cd8atm1Mak/DvsJ mice are homozygous for linkage markers delineating all known Idd loci of NOD origin and strongly diabetes resistant (1/17 females diabetic by 30 weeks of age). Survival of allogeneic skin grafts in NOD.129S2(B6)-Cd8atm1Mak/DvsJ mice treated with an anti-Cd40 ligand specific mAb and donor specific transfusion (DST) is significantly shorter (MST=21days) than in B6.129S2-Cd8atm1Mak/J (MST=101days) and (NODXB6)F1-Cd8atm1Mak (MST=35days) mice. Homozygous mutant mice are strongly, but not completely diabetes resistant (<3% in females) and insulitis is strongly, but not completely repressed.
This model is useful for sorting out the genetic mechanism(s) involved in transplant tolerance and for
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| 004639 | NOD.129S2(B6)-Igh-6tm1Cgn/DoiJ | Repository-Cryopreserved |
| NOD mice homozygous for the Igh-6 tm1Cgn allele do not express membrane-bound IgM. Igh-6 deficient mice lack mature B-cells, although some B-cells may be produced using a C gene other than mu. These mice are virtually free of insulitis: at most, presence of only perivascular/periductal leukocytes is detected. No intra-islet infiltrates are found. Results indicate that insulin dependant diabetes mellitus (IDDM) is not delayed, but prevented because of a lack of B cell autoreactive T cell responses. Therefore, the elimination of B lymphocytes by congenic transfer of the Igh-6 tm1Cgn mutation is sufficient to block IDDM development in an otherwise susceptible NOD mouse strain. (Kitamura 1991, Serreze 1996) | ||
| 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 phenotype on the strain data sheet | ||
| 004672 | NOD.129S2(Cg)-Stat6tm1Gru/JbsJ | Repository-Cryopreserved |
| 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. | ||
| 004671 | NOD.129S2-Stat4tm1Gru/JbsJ | Repository-Cryopreserved |
| Stat4tm1Gru homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. NOD female mice homozygous for the Stat4tm1Grumutation are reported to exhibit significantly decreased diabetes, approximately 20% diabetic by 30 weeks of age, compared to Approximately 45% of the female NOD controls (Chatenoud et al, 2001). There is no detectable STAT4 protein in purified splenocytes. IL12 mediated interferon-gamma secretion, natural killer cytolytic function and Th1 cell differentiation are defective. Analysis by ELISA indicates reduction of interferon gamma and IL2 when compared to diabetic and non-diabetic NOD. Phenotype of this stock is similar to the Yang et al, model reported to have a shorter congenic interval on Chromosome 1 including an NOD-derived Idd5. This model is useful for looking at the role of IL12 in diabetes development. | ||
| 004762 | NOD.129S4-Cd86tm1Shr/JbsJ | Repository-Cryopreserved |
| The NOD.129S4-Cd86tm1Shr/JbsJ homozygous mice fail to produce functional protein in T cells. Mice carrying this allele are protected from diabetes. Some homozygote mice have delayed onset peri-insulitis, which does not progress to severe insulitis. Beginning at 20 weeks of age, homozygous mice begin developing spontaneous autoimmune peripheral polyneuropathy marked by symmetrical mild hind limb paralysis. By 32 weeks of age 100% female and 30% males are severely affected with hind limb paralysis and moderate foreleg paralysis. Histological evaluation shows severe inflammation and mononuclear infiltrates in the peripheral nervous system. Skeletal muscle of severely affected mice showed focal neurogenic atrophy, but no cellular infitration. No detectable lesions were found in the brain or spinal cord. This phenotype has not been observed on C57BL/6 or 129 backgrounds (Salomon et al, 2001). NOD.129S4- Cd86tm1Shr /JbsJ provides a useful model for studyin
..... For more information please see the full phenotype on the strain data sheet | ||
| 003090 | NOD.129S6(B6)-Cd4tm1Knw/DvsJ | Repository-Cryopreserved |
| 004482 | NOD.B6-(D6Mit254-D6Mit339)/CarJ | Repository-Cryopreserved |
| 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 | ||
| 005616 | NOD.C-(Ptprc-D1Mit262)/WehiJ | Repository-Cryopreserved |
| 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. | ||
| 004644 | NOD.Cg Prkdcscid-Tg(CSF2)2Ygy Tg(IL3)1Ygy Tg(KITLG)3Ygy/YgyJ | Repository-Cryopreserved |
| Tg(IL3)1Ygy, Tg(CSF2)2Ygy, and Tg(KITLG)3Ygy encode porcine interleukin 3 (IL3), Porcine granulocyte macrophage-colony stimulating factor (CSF2, commonly designated GM-CSF) and soluble Porcine stem cell factor (KITLG, commonly designated sSCF) respectively. All three are individually driven by the human cytomegalovirus promoter. These three transgenes were co-injected and they co-segregate. RT-PCR detects transgenic expression of porcine IL-3, CSF2 and KITLG in bone marrow and spleen in NOD.Cg Prkdc scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy mice. Porcine IL3, CSF2, and KITLG are present in the serum of these mice in levels that can be detected by ELISA. NOD.Cg Prkdc scid-Tg(IL3)1Ygy Tg(CSF2)2Ygy Tg(KITLG)3Ygy/YgyJ not only provide a system in which long-term porcine tissue and stem cell engraftment can be achieved (Abe et al, 2002) but also is a useful tool for evaluating donor-specific tolerance induction by mixed chimerism across xenogeneic ba
..... For more information please see the full phenotype on the strain data sheet | ||
| 005345 | NOD.Cg-Cd38tm1Lnd Prkdcscid/LtJ | Repository-Cryopreserved |
| 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 | ||
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Repository-Cryopreserved |
| 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. | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Repository-Cryopreserved |
| 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. | ||
| 004606 | NOD.Cg-Prkdcscid H2-Ab1tm1Doi Tg(HLA-DQA1,HLA-DQB1)1Dv/SzJ | Repository-Cryopreserved |
| This strain which is MHC II deficient and has no functional T or B cells expresses a humanized transgenic HLA-DQ8 molecule that has been linked to IDDM development. This model is a valuable genetic tool for identifying the role of HLA-DQ8 in Type 1 Diabetes. | ||
| 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. | ||
| 005019 | NOD.Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ | Repository-Cryopreserved |
| 005018 | NOD.Cg-Tg(Igk-C/Igk-V125)1Jwt/JwtJ | Repository-Cryopreserved |
| 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. | ||
| 003869 | NOD.Cg-Tg(Ins2-E3)1Dvs/DvsJ | Repository-Cryopreserved |
| 004937 | NOD.Cg-Tg(Ins2-tTA)1Doi/DoiJ | Repository-Cryopreserved |
| Tg(Ins2-tTA)1Doi encodes the tetracycline regulatable transactivator (tTA) 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 mice are mated to a second transgenic strain carrying the target gene regulated by the tetO responsive elements, expression of the target gene is turned off by the tetracycline analog, doxycycline (dox). Dox can be administered orally in the food or water. This strain provides a Tet-Off tool that permits the inducible expression of genes in the pancreatic beta cells during various stages of diabetes development. | ||
| 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. | ||
| 004226 | NOD/ShiLtDvs-Tg(Ins2-E3*309)5Dvs/DvsJ | Repository-Cryopreserved |
| 004227 | NOD/ShiLtDvs-Tg(Ins2-E3*704)2Dvs/DvsJ | Repository-Cryopreserved |
| 004968 | NOD/ShiLtDvs-Tg(Ins2-E3*734)3Dvs/DvsJ | Repository-Cryopreserved |
| 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 | Repository-Cryopreserved |
| 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 phenotype on the strain data sheet | ||
(70 stocks) Back to Top
IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002574 | NOD.129P2(B6)-Il4tm1Cgn/Dvs | Research Strain |
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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
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