Mouse Genome Informatics
tg
    Tg(INS-MT2A,Tyr)1Pne/0
NOD.FVB-Tg(INS-MT2A,Tyr)1Pne
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
       
homeostasis/metabolism
• treatment of transgenic NOD mice with cyclophosphamide (CYP) accelerated NOD diabetes; 20 days after injection of CYP 93% of transgenic mice are diabetic compared with 7% of treated controls
• transgenic mice on the FVB background do not develop diabetes with the same regimen of CYP treatment as the NOD transgenic mice
• transgenic mice exhibit greater resistance to induced diabetes after treatment with streptozotocin compared with NOD controls

endocrine/exocrine glands
• 8 days after CYP treatment significantly more islets of transgenic NOD mice appear small and disrupted compared to treated NOD controls; percentages of damaged areas (Caspase-3 positive) in islets are 11.7 and 5.5% in transgenic NOD and control NOD mice respectively
• cultured islets of transgenic NOD mice are more sensitive to a mix of cytokines (Il-beta, Tnfa and Ifng) than NOD control islets as revealed by Caspase-3 activity
• beta cell damage is significantly increased in transgenic mice after CYP injection compared to controls; pancreatic insulin content is only 36% of original level after 8 days compared to 76% in control NOD mice

Mouse Models of Human Disease
OMIM IDRef(s)
Diabetes Mellitus, Insulin-Dependent; IDDM 222100 J:108415