NOD.FVB-Tg(Rip-RASA1*)1Wid/Orl
| Status | Available to order |
| EMMA ID | EM:05139 |
| International strain name | NOD.FVB-Tg(Rip-RASA1*)1Wid/Orl |
| Alternative name | NOD-Tg(RIP::N)1Wid |
| Strain type | Transgenic Strains |
| Allele/Transgene symbol | Tg(Rip-RASA1*)1Wid, |
| Gene/Transgene symbol | Tg(Rip-RASA1*)1Wid |
Information from provider
| Provider | Christian Widmann |
| Provider affiliation | Physiology, Lausanne University |
| Genetic information | NOD-Tg(Rip-RASA1*)1Wid (TgN(RIP::N)1Wid) mice bear a transgene containing the rat insulin promoter followed by the cDNA encoding a caspase-resistant form of N-terminal fragment of human RasGAP. |
| Phenotypic information | The NOD background induces auto-immune type 1 diabetes with a 60-80% and 20-30% penetrance in females and males, respectively. The presence of fragment N in pancreatic beta cells of NOD mice increases their resistance towards apoptosis and delays the onset of overt diabetes. |
| Breeding history | The RIP-N transgene from FVB/N-Tg(RIP::N)1Wid mice (strain EM:04569) was backcrossed into NOD mice using speed-congenics (first 5 generations) and conventional backcrossing for 2 subsequent generations. The strain is maintained in the NOD background (currently 2 additional generations). |
| References |
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| Homozygous fertile | not known |
| Homozygous viable | not known |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Institut de Transgenose, INTRAGENE, Orléans, France |
| Animals used for archiving | heterozygous NOD, wild-type NOD |
Literature references
- Expression of the NH(2)-terminal fragment of RasGAP in pancreatic beta-cells increases their resistance to stresses and protects mice from diabetes.;Yang Jiang-Yan, Walicki Jöel, Jaccard Evrim, Dubuis Gilles, Bulat Natasa, Hornung Jean-Pierre, Thorens Bernard, Widmann Christian, ;2009;Diabetes;58;2596-606; 19696184