Search Criteria: Research Area is "Cancer Research: Increased Tumor Incidence (Lymphomas: thymic)"
Strains from the Research Colonies of Jackson Laboratory Scientists
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full descriiption on the strain data sheet | ||
| 002753 | 129S6/SvEvTac-Atmtm1Awb/J | Repository- Live |
| Mice homozygous for the Atmtm1Awb targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma between 2 and 4 months of age. Heterozygous mice display no abnormalities through eight months of age. | ||
| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 004848 | NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/SzJ | Repository- Live |
| Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1tm1Mom/J (Stock No. 003729). Although an increased number of DX5+CD122+ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho
..... For more information please see the full descriiption on the strain data sheet | ||
| 001737 | B6.A-H2-T18a.HRS-Hrhr/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. In an attempt to offer alleles on
..... For more information please see the full descriiption on the strain data sheet | ||
| 004338 | B6;129-E2f2tm1Zubi/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model
..... For more information please see the full descriiption on the strain data sheet | ||
| 002922 | D2.HRS-Hrhr/J | Repository-Cryopreserved |
| 000673 | HRS/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an ather
..... For more information please see the full descriiption on the strain data sheet | ||
| 001103 | HRS/J-Hrhr Esdb/+ Esdb/J | Repository-Cryopreserved |
| Mice homozygous for the hr mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of statified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. | ||
| 002335 | SKH2/J | Repository-Cryopreserved |
| Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. Black juvenile hair coa
..... For more information please see the full descriiption on the strain data sheet | ||
| 000147 | WLHR/LeJ | Repository-Cryopreserved |
| WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by v
..... 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 |
| 002313 | NOD.Cg-Prkdcscid Emv30b/Dvs | Research Strain |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full description on the strain data sheet | ||
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