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Type Congenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered Mutant Mice. Mating System +/+ sibling x Hemizygote (Female x Male) Species laboratory mouse Background Strain NOD Donor Strain FVB H2 Haplotype g7 Donating Investigator Paul Epstein, University of Louisville Description
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.
Development
NOD.FVB-Tg(INS-SOD2)3Pne/PneJ expresses the full-length human mitochondrial superoxide dismutase cDNA controlled by the human insulin promoter. The transgene was first inserted into FVB oocytes. Founder line 3, maintained by Epstein et al., has been backcrossed to NOD for at least 8 generations. A genome wide scan confirmed that all known Idd markers were homozygous for the NOD allele. In 2004, The Jackson Laboratory received NOD.FVB-Tg(INS- SOD2)3Pne/PneJ at generation N8F7.
| Control | ||
|---|---|---|
| Noncarrier | ||
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
Strains carrying other alleles of INS
005115 NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ View Strains carrying other alleles of INS (1 strain)
View Related Disease (OMIM) Terms
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
Tg(INS-SOD2)3Pne/0
NOD.FVB-Tg(INS-SOD2)3Pne
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype (MGI Ref ID J:108415)
- treatment of transgenic NOD mice with cyclophosphamide (CYP) does not affect the rate of onset of diabetes compared to NOD controls
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains (NOD Transgenics)
Immunology and Inflammation Research
Autoimmunity (Type 1 Diabetes)
Research Tools
Apoptosis Research
| Allele Symbol | Tg(INS-SOD2)3Pne | ||
|---|---|---|---|
| Allele Name | transgene insertion 3, Paul N Epstein | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | IsNOD; MnSOD3; | ||
| Mutation Made By | Paul Epstein, University of Louisville | ||
| Strain of Origin | FVB | ||
| Expressed Gene | SOD2, superoxide dismutase 2, mitochondrial, human | ||
| Promoter | INS, insulin, human | ||
| General Note |
Five transgenic lines were generated on an FVB background. This line expressed the highest SOD2 activity. Transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is an approximately10 fold 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. | ||
| Molecular Note | The transgene expresses the full-length human mitochondrial superoxide dismutase cDNA controlled by the human insulin promoter. Immunohistochemical staining with mitochondrial superoxide dismutase specific antibody confirms transgene expression localizedto the mitochondria of pancreatic islet cell. [MGI Ref ID J:97839] | ||
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Optimizing PCR Protocols
Chen H; Li X; Epstein PN. 2005. MnSOD and catalase transgenes demonstrate that protection of islets from oxidative stress does not alter cytokine toxicity. Diabetes 54(5):1437-46. [PubMed: 15855331] [MGI Ref ID J:97839]
Tg(INS-SOD2)3Pne relatedLi X; Chen H; Epstein PN. 2006. Metallothionein and Catalase Sensitize to Diabetes in Nonobese Diabetic Mice: Reactive Oxygen Species May Have a Protective Role in Pancreatic {beta}-Cells. Diabetes 55(6):1592-604. [PubMed: 16731821] [MGI Ref ID J:108415]
Colony Maintenance
Breeding & Husbandry This strain is maintained as hemizygote x wildtype and reciprocal. Mating System +/+ sibling x Hemizygote (Female x Male) Diet Information LabDiet® 5K52/5K67
| Pricing for USA, Canada and Mexico shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $1900.00 Cryopreserved Embryos Fee $1600.00
| Pricing for International shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $2470.00 Cryopreserved Embryos Fee $2080.00
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
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| Supply Notes |
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| Control | ||
|---|---|---|
| Noncarrier | ||
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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