Search Criteria: Research Area is "Endocrine Deficiency Research: Thyroid Defects"
Strains from the Research Colonies of Jackson Laboratory Scientists
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002019 | NU/J | Level 3 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full descriiption on the strain data sheet | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when
..... For more information please see the full descriiption on the strain data sheet | ||
| 000711 | CByJ.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full descriiption on the strain data sheet | ||
| 000811 | C57BL/6J-Ptpn6me-v/J | Repository- Live |
| Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo
..... For more information please see the full descriiption on the strain data sheet | ||
| 001743 | STOCK dwg/J | Repository- Live |
| Mice homozgyous for the dwarf grey spontaneous mutation (dwg) are viable but do not breed. Homozygous mutant mice have grey coats, are smaller than littermates, and develop cataracts by 3-4 weeks of age. Additional characteristics include increased numbers of osteoclasts, reduced bone mass, reduced red pulp area of the spleen, and slightly reduced thyroxin levels. | ||
| 003100 | STOCK dwgBayer/J | Repository- Live |
| The dwarf-Bayer mutation (dwgBayer) occurred spontaneously in an embryonic stem cell line during genetic targeting of the insulin receptor gene. The phenotype of the mice resemble drawf grey (dwg, Stock No. 001743) and subsequent characterization determined that the two mutations are allelic. Homozygous mutant mice are grey and smaller in size than wildtype littermates. | ||
| 005543 | B6(129)-Duox2thyd/J | Repository-Cryopreserved |
| 003462 | B6.129S1-Thrbtm1Df/J | Repository-Cryopreserved |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 004858 | B6;129S1-Tshrtm1Rmar/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation exhibit delayed eye opening, are runted by day 21, and will die within 1 week if weaned at day 21. Homozygotes will survive by extending weaning to 28 days but will not reproduce. Homozygotes are viable and fertile when weaned at day 21 and subsequently placed on a hormone replacement therapy diet consisting of a 100ppm desiccated thyroid powder supplement. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of thyroid membranes. Enhanced Green Fluorescent Protein (EGFP) gene product is detected by RT-PCR and Western blot analysis of thyroid tissue. Hypothyroidism is exhibited by mutant mice that have a longer weaning period and a non-supplemented diet, as indicated by low T4 and T3 serum levels, and high thyrotropin (TSH) serum levels. Treatment with exogenous TSH does not result in a thyroid hormone release response. Mutant mice produce uniodinated thyroglobulin and do not accumulate radioactive iodide in
..... For more information please see the full descriiption on the strain data sheet | ||
| 002494 | B6;129S2-Cgatm1Sac/J | Repository-Cryopreserved |
| Mice homozygous for the Cgatm1Sac targeted mutation are viable but both sexes are infertile. They lack TSH, LH, and FSH. Homozygous mutant mice are hypogonadal and exhibit severe hypothyroidism resulting in dwarfism. Development of the thyroid gland was arrested in late gestation. However, gonadotropin releasing hormone (GNRH) neuron migration, development of secondary sex organs, and fetal and neonatal gonadal development are normal. Mice heterozygous for the Cgatm1Sac targeted mutation appear normal. | ||
| 002382 | B6;129S6-Ttrtm1Wsb/J | Repository-Cryopreserved |
| Mice carrying the Ttrtm1Wsb targeted mutation are phenotypically normal, viable and fertile. They have markedly reduced levels of serum retinol, retinol-binding protein and thyroid hormone. The homozygotes can utilize stored retinol despite a defective plasma retinol transport system. | ||
| 000225 | C3FeLe.B6 a/a-Ptpn6me/J | Repository-Cryopreserved |
| Mice homozygous for the motheaten spontaneous mutation (Ptpn6me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to an autoimmune pneumonitis. | ||
| 000936 | CBy.AK-Tgcog/J | Repository-Cryopreserved |
| The Tgcog mutation causes the development of goiters due to failed processing of thyroglobulin. Homozygotes are smaller in overall size by 15 days of age. They display an increase in growth rate at the time of weaning but generally do not attain comparable size with their wildtype littermates. Increased thyroidal volume is apparent at embryonic day 18, and continues enlarging to an average of 5 fold higher than normal at 8 weeks of age and 20 fold normal at 10 months of age. In addition to decreased serum T3 and T4 levels, homozygotes have increased serum thyroid stimulating hormone levels, reduced levels of serum IGFBP-3, IGFBP-4, and IGFBP-2, mild anemia, and hypomyelination restricted to the cerebrum. Tgcog is an outwardly recessive mutation, but microdissection reveals a heterozygous phenotype as well. Thyrofollicular cells of heterozygotes have swollen protein-containing vesicles similar to but more moderate than those found in homozygotes
..... For more information please see the full descriiption on the strain data sheet | ||
| 000805 | CBy.RF-Tshrhyt/J | Repository-Cryopreserved |
| Mice homozygous for the hypothyroid spontaneous mutation (Tshrhyt) are characterized by growth retardation, low thyroid hormone levels, elevated thyroid stimulating hormone (TSH) and hypoplastic thyroid glands. Homozygous mice of both sexes are infertile but fertility as well as growth can be restored by treatment with thyroid hormone. The mice do not respond to exogenous TSH. Homozygous mutant mice also display audiotory defects characterized by morphologic abnormalities of the stereocilia on both inner and outer hair cell systems | ||
| 001723 | CByJ.A-Ttc7fsn/J | Repository-Cryopreserved |
| Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G
..... For more information please see the full descriiption on the strain data sheet | ||
| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository-Cryopreserved |
| This NOD congenic strain contains a targeted H2-Ab1 mutation also carries two transgenes: one expressing human CD4 under the regulation of the mouse Cd4 enhancer and a second expressing human HLA-DQ6. The latter transgene confers dominant protection to development of Type 1 diabetes in humans. These double transgenic, H2-Ab1-deficient mice are viable, fertile, normal in size, and free of both autoimmune diabetes and cardiomyopathy, a phenotype found in an NOD stock expressing an HLA-DQ8 transgene (Elliot JF et al. Proc Natl Acad Sci U S A 2003; 100:13447-52). By 55 weeks of age, 100% of the H2-Ab1-deficient, DQ6 transgenic mice develop thyroiditis and thyroid autoantibodies. Of these, 25% develop thyroid gland enlargement and goiter, and a subset of these animals develops thyroid failure with elevated serum TSH levels.
This model is useful for studying autoimmune thyroid disease and to understand the role of MHC class II in au
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| 003118 | STOCK Es1e Foxn1nu/J | Repository-Cryopreserved |
| Mice homozygous for Es1e are viable and fertile and exhibit no apparent defect. Es1e was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Es1e was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Es1e was shown to be a hypomorphic electrophoretic variant (Soares 1979). The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11<
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| 002549 | STOCK Tgcog/J | Repository-Cryopreserved |
| The Tgncog mutation causes the development of goiters due to failed processing of thyroglobulin. Homozygotes are smaller in overall size by 15 days of age. They have an increase in growth rate at the time of weaning but generally do not attain comparable size with their wildtype littermates. Increased thyroidal volume is apparent at embryonic day 18 and continues enlarging to an average of 5 fold higher than normal at 8 weeks of age and 20 fold normal at 10 months of age. In addition to decreased serum T3 and T4 levels, homozygotes have increased serum thyroid stimulating hormone levels, reduced levels of serum IGFBP-3, IGFBP-4, and IGFBP-2, mild anemia, and hypomyelination restricted to the cerebrum. Tgncog is an outwardly recessive mutation but microdissection reveals a heterozygous phenotype as well. Thyrofollicular cells of heterozygotes have swollen protein-containing vesicles similar to but more moderate than those found in homozygotes.
..... For more information please see the full descriiption on the strain data sheet | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000810 | C57BL/6J-Ptpn6me/J | Research Strain |
| Mice homozygous for the motheaten spontaneous mutation (Ptpn6me) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The lifespan of homozygous motheaten mice is approximately 3 weeks with death attributed to a autoimmune pneumonitis. | ||
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