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| Nomenclature |
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Symbol:
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Tg(INS-SOD2)3Pne
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Name:
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transgene insertion 3, Paul N Epstein
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MGI ID: |
MGI:3525180 |
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Synonyms: |
IsNOD, MnSOD3 |
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Transgene:
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Tg(INS-SOD2)3Pne
Location:
unknown
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Transgene
origin |
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Transgene
description |
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Transgene
Type: | |
Transgenic (random, expressed) |
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Mutation: | |
Insertion |
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Mutation details: 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 localized to the mitochondria of pancreatic islet cell. (J:97839)
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Phenotypes
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View phenotypes for all genotypes (concatenated display).
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Disease models
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| Find Mice (IMSR) |
Mouse strains and cell lines available from the
International Mouse Strain Resource
(IMSR)
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Notes |
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 approximately 10 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.
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| References |
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Original: |
J:97839
Chen H et al.,
"MnSOD and catalase transgenes demonstrate that protection of islets from oxidative stress does not alter cytokine toxicity."
Diabetes 2005 May;54(5):1437-46
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All: |
3 reference(s)
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Analysis Tools
