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Diabetic Complications Consortium provides data and information relevant to diabetes.
(last updated: Apr 7, 2018)
Disease Information OrganismName | Description | Gene Symbol | Organism |
---|---|---|---|
FVB(Cg)+/+/PneJ | Control litter mates for FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ | mouse | |
DBA/2J-Ins2Akita | Ins2 | mouse | |
B6;SJL-TgN(Myl2-Slc2a1)2Mue | Myl2, Slc2a1 | mouse | |
C57BL/6-Pdx1 +/- | Pdx1 | mouse | |
C57BL/6J-Tg(Alb1-Ren1) | Ren1 | mouse | |
STOCK-Tg(alpha-MHC-Cre) Insrlox/lox | H2-Aa, Insr | mouse | |
KK/HlJ | mouse | ||
CAST/Ei | mouse | ||
C57BL/6j-Gclctm1Neb/+ Leprdb | Gclc, Lepr | mouse | |
FH/IS | mouse | ||
Swiss Webster | mouse | ||
FVB.B6-Ins2Akita/MlnJ | FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type offspring in Mendelian ratios. Litter sizes from crosses using either heterozygous males or females are reduced (5-8 pups/litter) compared to litters from control FVB/NJ mice (10 pups/litter). | Ins2 | mouse |
C57BL/6J-Leprdb | Lepr | mouse | |
(DBA/2J X C57BL/6J)F1 | mouse | ||
CD1-Tg(Kdr-Ager) | Ager, Kdr | mouse | |
SWR/J | SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to lysis following microinjection, and are genetically well-defined. SWR/J mice may also be used as controls for comparison to the autoimmune diabetic NOD/ShiLtJ mice (Stock No. 001976), especially for experiments examining the aberrant immune functions of NOD/ShiLtJ mice. Both NOD and SWR/J mice are derived from Swiss mice. SWR/J are in some cases more suitable than random bred Swiss ICR mice because of their genetic uniformity. Unlike NOD/ShiLtJ mice they are not immunocompromised, and they are genetically very different from NOD. SWR/J mice appear to be the only inbred carrying the allele Soaa (Taster) characterized by avoidance of sucrose octaacetate solutions at low concentrations (< 10-3M). | mouse | |
C57BL6/J-TgN(Nes-Cre) Sod2lox/lox | Nes, Sod2 | mouse | |
NOD.Cg-Prkdcscid Il2rgtm1Wjl/Sz | These mutant mice combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid) and IL2 receptor gamma chain deficiency and wildtype allele for Lepr. | Il2rg, Prkdc | mouse |
STOCK-Insrlox/lox | Insr | mouse | |
DBA/1lacJ-Ptgestm1coff | Targeted disruption of mPges-1 gene (kidney) in DBA/1lacJ mice | Ptges | mouse |
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