Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(INS-Il10)#Sar transgene insertion #, Nora Sarvetnick MGI:3622661 |
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| Summary |
7 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 60% of deficient transgenic mice develop diabetes by 5 weeks (blood glucose measuring >300 mg/dl), while 100% develop diabetes by 10 weeks compared to 0% of nontransgenic littermates
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• mice are considered diabetic after a blood glucose measure of >300 mg/dl
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 100% of deficient transgenic animals develop diabetes by 5 weeks (blood glucose >300 mg/dl), while only 60% of non-transgenic littermates develop diabetes by 24 weeks
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• mice are considered diabetic after a blood glucose measure of >300 mg/dl
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• only 11% of animals develop diabetes by 5 weeks of age (blood glucose >300 mg/dl), while 50% of wild-type transgenic animals develop diabetes, but the overall incidence by 12 weeks is the same for both
• mice are considered diabetic after a blood glucose measure of >300 mg/dl
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| type 1 diabetes mellitus | DOID:9744 |
OMIM:222100 |
J:64051 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• islets of transgenic mice show extensive leukocytic infiltration compared to Fas-sufficient transgenic mice
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• mice of the N3-4 and N8-9 NOD backcross develop accelerated diabetes with most developing diabetes by 10 weeks of age while lpr-deficient NOD mice are free from spontaneous insulitis and diabetes
• mice are considered diabetic after a blood glucose measure of >300 mg/dl
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• islets of transgenic mice show extensive leukocytic infiltration compared to Fas-sufficient transgenic mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice
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• wild-type transgenic NOD mice readily develop diabetes starting at 5 weeks (blood glucose >300 mg/dl), while ICAM-I deficient transgenic NOD mice have not developed diabetes at 12 weeks (n=4) or 16 weeks (n=5); nontransgenic ICAM-I deficient mice do not develop diabetes over the same period
• transfer of concanavalin A treated splenocytes from 8 week old Tg(TcraBDC2.5)1Doi Tg(TcraBDC2.5)1Doi female mice expressing an islet-specific TCR transgene to irradiated ICAM-I deficient NOD or deficient transgenic NOD mice does not induce diabetes in recipients
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• ICAM-I deficient transgenic mice develop periinsulitis but not insulitis as do wild-type transgenic NOD mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| NOT | type 1 diabetes mellitus | DOID:9744 |
OMIM:222100 |
J:98583 |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• transgenic NOD.scid mice receiving splenocytes from 12 week old nondiabetic Il10-nNOD mice develop diabetes (blood glucose level >300 mg/dl) by 4 weeks posttransfer (blood glucose >300 mg/dl), while no nontransgenic NOD.scid mice are affected over the same period;
• adoptive transfer of splenocytes from diabetic NOD mice into transgenic NOD.scid mice induces clinical disease with faster kinetics compared to nontransgenic NOD.scid mice
• transfer of splenocytes from prediabetic 8 week old NOD mice to transgenic NOD.scid mice caused diabetes after 4 weeks, while nontransgenic NOD.scid recipients didn't develop diabetes until 7 weeks posttransfer
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Tg(INS-Il10)#Sar/0 mice accumulate imflammatory cells within exocrine pancreatic tissue
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• pancreas inflammation is first observed at 1 week of age with the majority of invading cells being macrophages; at 2 months, lymphocytes dominate the inflammation
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• in transgenic mice, the islets of Langerhans are surrounded by infiltrates of inflammatory cells: focal accumulations of mononuclear cells are observed at 4-6 weeks of age, increasing by 2-3 months of age
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• exocrine tissue of pancreas is inflamed with the acini being replaced by dense sheets of inflammatory cells, necrotic tissue
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• islets of Langerhans are surrounded by leukocytes and necrotic exocrine tissue
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• pancreas inflammation is first observed at 1 week of age with the majority of invading cells being macrophages; at 2 months, lymphocytes dominate the inflammation
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• in transgenic mice, the islets of Langerhans are surrounded by infiltrates of inflammatory cells: focal accumulations of mononuclear cells are observed at 4-6 weeks of age, increasing by 2-3 months of age
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• in transgenic mice at 1 week of age, vessels in the pancreata are larger in diameter than in non-transgenic littermates; in older transgenic mice, the vessels demonstrate areas of inflammation only; endothelial cells lining the small vessels are plump and cuboidal compared to the cells in non-transgenic littermates
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• exocrine tissue of pancreas is inflamed with the acini being replaced by dense sheets of inflammatory cells, necrotic tissue
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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