Genetic Background | Generation |
---|---|
|
Allele Type | Gene Symbol | Gene Name |
---|---|---|
QTL | Idd3 | insulin dependent diabetes susceptibility 3 |
Allele Type | Gene Symbol | Gene Name |
---|---|---|
QTL | Idd10 | insulin dependent diabetes susceptibility 10 |
Marker Symbol | Marker Name | |
---|---|---|
D3Mit124 | DNA segment, Chr 3, Massachusetts Institute of Technology 124 | |
D3Mit93 | DNA segment, Chr 3, Massachusetts Institute of Technology 93 |
Allele Name | C57BL/6 |
---|---|
Allele Type | QTL |
Allele Synonym(s) | |
Gene Symbol and Name | Idd3, insulin dependent diabetes susceptibility 3 |
Gene Synonym(s) | |
Strain of Origin | C57BL/6 |
Chromosome | 3 |
General Note | Idd3 and Idd5 appear to interact additively. C57BL/6-derived alleles at Idd3 in combination with C57BL/10-derived alleles at Idd5 partially reverses autoimmune exocrinopathy markers on an NOD genetic background. Idd10 and Idd3 interact to promote disease resistance. Homozygosity for C57BL/6-derived alleles at both Idd10 and Idd3 confers significantly increased resistance to type 1 diabetes. Il2 is a proposed candidate gene for Idd3. The electrophoretic mobility pattern of IL-2 correlates with type 1 diabetes incidence. Resistant strain C57BL/6J displays a heterogenous IL-2 mobility pattern with major protein species ranging from 17-19 kDa while susceptible strains 129 and NOD display a homogenous IL-2 mobility pattern with one major protein species at approximately 21-22 kDa. |
Molecular Note | This allele confers resistance to insulin dependent diabetes compared to NOD. |
Allele Name | C57BL/6J |
---|---|
Allele Type | QTL |
Allele Synonym(s) | |
Gene Symbol and Name | Idd10, insulin dependent diabetes susceptibility 10 |
Gene Synonym(s) | |
Strain of Origin | C57BL/6J |
Chromosome | 3 |
General Note | Idd10 and Idd18 interact to promote disease resistance. Homozygosity for C57BL/6-derived alleles at both Idd10 and Idd18 confers significantly increased resistance to type 1 diabetes. Idd10 and Idd17 interact to promote disease resistance. Homozygosity for C57BL/6-derived alleles at both Idd10 and Idd17 confers significantly increased resistance to type 1 diabetes. Idd10 and Idd3 interact to promote disease resistance. Homozygosity for C57BL/6-derived alleles at both Idd10 and Idd3 confers significantly increased resistance to type 1 diabetes. |
Molecular Note | This allele confers resistance to insulin dependent diabetes compared to NOD. |
Marker Synonym(s) | |
---|---|
Chromosome(s) | 3 |
Marker Synonym(s) | |
---|---|
Chromosome(s) | 3 |
When using the NOD.B6(PL)-(D3Mit93-D3Mit124)/Lt mouse strain in a publication, please cite the originating article(s) and include JAX stock #003853 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
---|---|---|
Homozygous, 1 pair minimum |
Frozen Mouse Embryo | NOD.B6(PL)-(D3Mit93-D3Mit124)/Lt Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | NOD.B6(PL)-(D3Mit93-D3Mit124)/Lt Frozen Embryos | $2595.00 |
Frozen Mouse Embryo | NOD.B6(PL)-(D3Mit93-D3Mit124)/Lt Frozen Embryos | $3373.50 |
Frozen Mouse Embryo | NOD.B6(PL)-(D3Mit93-D3Mit124)/Lt Frozen Embryos | $3373.50 |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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