Search Criteria: Research Area is "Internal/Organ Research: Spleen Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 003008 | B6;129S-Tnftm1Gkl/J | Level 4 |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet | ||
| 013039 | 129S-Spictm1Kmm/J | Repository- Live |
| In these mutant mice a loxP-flanked neomycin resistance (neo) cassette replaces exons 2-5 of the Spi-C transcription factor (Spi-1/PU.1 related) gene (Spic), abolishing gene function. Heterozygous mice are viable and fertile, while homozygotes are born at a frequency lower than the expected Mendelian ratio and they have small litters. Spi-C is highly expressed in red pulp macrophages which are a distinct splenic subset required for red blood cell recycling and iron homeostasis. These Spi-C-/- mice exhibit a defect in the development of red pulp macrophages, which fail to efficiently phagocytose red blood cells trapped in the spleen. They also develop an iron overload localized selectively to splenic red pulp. These mice may be useful for studying the development and function of red pulp macrophages. | ||
| 007750 | B6(C)-Mir150tm1Rsky/J | Repository- Live |
| Mice homozygous for this targeted allele (miR150-/- or MiR-150-/-) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19+B220loCD5+CD43+CD23-; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (inc ..... For more information please see the full phenotype on the strain data sheet | ||
| 005540 | B6.129S-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet | ||
| 004525 | B6.129S1-Bcl2l11tm1.1Ast/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No full length gene product (protein) is immunodetected in spleen cells from homozygous mutant mice. Homozygous mice have lympho-myeloid hyperplasia and reduced platelet number. Lymphocytes are insensitive to certain apoptotic stimuli. Both homozygous and heterozygous mice exhibit progressive systemic autoimmune disease. This mutant mouse strain may be useful in studies of apoptosis, degenerative and autoimmune diseases, including lupus erythematosus and autoimmune kidney disease. | ||
| 006848 | B6.129S2(C)-Cxcr2tm1Mwm/J | Repository- Live |
| The donating investigator reports that homozygous mice are viable and fertile but few pups are produced, and they need a gnotobiotic facility to thrive. Homozygous mice have several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. Homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studies of inflammation and immunology and cancer biology.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results becom ..... | ||
| 013547 | B6.129X1-Hip1tm4Tsr/J | Repository- Live |
| In the Hip1LSP-H/P strain, a floxed-STOP cassette causes termination of the endogenous huntingtin interacting protein 1 (Hip1) gene and a human HIP1/PDGFbR (H/P) cDNA fused to another polyA site and a neomycin resistance (neo) cassette, replace endogenous exons 2-7. Heterozygous mice are viable, fertile, and normal in size. These mice exhibit gross micro-ophthalmia and cataracts. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s), resulting in H/R fusion protein overexpression in cre-expressing cells. The overexpression of H/P mimics the human chromosomal translocation, t(5;7)(q33;q11.2), leading to constitutively active PDGFbR signalling and chronic myelomonocytic leukemia (CMML) development in humans. For example, H/P is able to transform hematopoietic cells to factor-independent growth in culture. When Hip1LSP-H/P mice are bred to mice tha ..... For more information please see the full phenotype on the strain data sheet | ||
| 013071 | B6;129-Hbatm1(HBA)Tow Hbbtm2(HBG1,HBB*)Tow/Hbbtm3(HBG1,HBB)Tow/J | Repository- Live |
| These mice may harbor several knockin mutations: 1) the Hbatm1(HBA)Tow mutation (also called hα ; designed with the human hemoglobin α gene replacing the endogenous mouse α-globin), as well as 2) the Hbbtm2(HBG1,HBB*)Tow mutation (also called -1400 γ-βS ; designed with the human hemoglobin gamma (Aγ) gene and the human sickle hemoglobin beta (βS) gene replacing the endogenous mouse major and minor β-globin), and/or 3) the Hbbtm3(HBG1,HBB)Tow mutation (also called -383 γ-βA ; designed with the human hemoglobin gamma (Aγ) gene and the human wildtype hemoglobin beta (βA) gene replacing the endogenous mouse major and minor β-globin). --Of note, these mice should not harbor any wildtype allele at the Hbb locus.--
Mice homozygous at the ..... | ||
| 003092 | BALB/cNctr-Npc1m1N/J | Repository- Live |
| Mice homozygous for the recessive NIH allele of the Niemann Pick type C1 gene (Npc1m1N) show a dual deficiency of sphingomyelinase and glucocerebrosidase activity. The overall phenotype resembles the sphingomyelinosis condition seen in mice homozygous for the sphingomyelinosis allele (Npc1spm, Stock No. 002760). Sphingomyelinosis mutant mice begin to lose weight and to show tremor and ataxic gait at about 7 weeks of age. Weight loss continues and tremor and ataxia become more severe until death at about 12 to 14 weeks of age. The liver and spleen are also enlarged and Purkinje cells in the cerebellum are severely depleted. Sphingomyelin and free cholesterol are markedly elevated in liver and spleen but not in brain. Sphingomyelinosis closely resembles that of human Niemann-Pick Type C disease patients. | ||
| 002724 | C.129S2(B6)-Cxcr2tm1Mwm/J | Repository- Live |
| Mice homozygous for the this targeted mutation are viable and fertile although the reproductive rate is lower than normal wildtype siblings. Homozygous mutant mice have splenomegaly, lymphadenopathy, and impaired neutrophil migration. Formerly referred to as Cmkar2, chemokine (C-X-C) receptor 2; also called Il8r, interleukin 8 receptor. | ||
| 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 phenotype on the strain data sheet | ||
| 007082 | CByJ.129S(B6)-Tnftm1Gkl/J | Repository- Live |
| Mice homozygous for the Tnftm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet | ||
| 013043 | SJL.129S2(C)-Cxcr2tm1Mwm/RmraJ | Repository- Live |
| Homozygous mice are viable but fail to thrive (few pups are produced). Maintaining homozygous mice in a gnotobiotic vivarium may enhance strain breeding performance. Heterozygous mice are viable and fertile with no reported needs for special husbandry. The donating investigator reports that Cxcr2-deficient mice on the SJL/J genetic background are resistant to experimental autoimmune encephalomyelitis (EAE) protocols compared to susceptible SJL/J wildtype mice. Cxcr2-deficiency on other genetic backgrounds is associated with several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. In addition, homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studying inflammation, immunology, cancer biology, demyel ..... For more information please see the full phenotype on the strain data sheet | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Cryopreserved - Ready for recovery |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 005730 | 129S6.CB(B6)-Del(1)1Brk Gpi1b/Gpi1c/BrkMdfJ | Cryopreserved - Ready for recovery |
| Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood. | ||
| 004608 | B6(Cg)-Htra2mnd2/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the recessive Htra2mnd2 mutation have a basal ganglia disorder initially described as an early onset motor neuron disease. This is first outwardly evident by 21 to 24 days of age as an unsteady gait with extended hind limbs, repetitive movements and episodes of sudden arrests. This progresses to include severe muscle atrophy, hunched posture, increased imbalance, chorea, dystonia, and progressive akinesis. A failure to gain weight becomes evident shortly after the onset of the other symptoms and by 35 days of age wildtype littermates are twice as heavy as the mutants. Body fat is not detectable at necropsy. Both the spleen and the thymus drop from normal weights at 23 days of age to 10% of normal at 30 days of age and the thymic corticomedullary junction is lost. Death usually occurs within two weeks of disease onset, by 40 days of age. The growth retardation is not the primary cause since disease is not delayed by intragastric feeding. For more information please see the full phenotype on the strain data sheet | ||
| 004068 | B6.129-Iduatm1Clk/J | Cryopreserved - Ready for recovery |
| At birth, mice that are homozygous null for the Idua gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No alpha-L-iduronidase enzyme activity or mRNA is detected. By three weeks of age, homozygous null mice develop a flattened facial profile and a thickening of digits. Defective bone formation is noticeable by fifteen weeks, characterized by a broadening and thickening of long bones. Evidence of lysosomal storage disorder is apparent in cells of the reticuloendothelial system at four weeks. By eight weeks progressive evidence of lysosomal storage is seen in Kupffer cells, splenic sinusoidal lining cells, chondrocytes, glial and Purkinje cells. This animal model is suitable for use in studies investigating the lysosomal storage disorder mucopolysaccharidosis type I (MPS I). | ||
| 003947 | B6.129P2-Epb4.2tm1Llp/LlpJ | Cryopreserved - Ready for recovery |
| Homozygotes have mild hereditary spherocytosis with significant reduction of red blood cell counts and hematocrits. There is a reduction of the mean corpuscular volume, increase in mean corpuscular hemoglobin concentration, and an approximately 2 fold increase in the percentage of reticuloctyes and spleen weight, but white blood cell counts are normal. Red blood cell membranes are deficient in band 3, although the membrane skeleton appears qualitatively normal by elecron microscopy. Red blood cells of homozygotes also have increased K+ and decreased Na+ resulting in red blood cell dehydration. Heterozygotes have both normal and intermediate, cup-shaped red blood cells with a lower than normal deformability index, but not as low as in homozygotes. | ||
| 003233 | B6.129P2-Fastm1Osa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Tnfrsf6tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively. | ||
| 012768 | B6.129S1-Gnai2tm1.1Rneu/J | Cryopreserved - Ready for recovery |
| A G184S point mutation was created in the Gnai2 (guanine nucleotide binding protein (G protein), alpha inhibiting 2; also called Gαi2) gene which disrupts interactions with regulator of G protein signaling (RGS) proteins that normally deactivate Gα G protein signals. A complex phenotype affecting multiple organ systems (heart, myeloid, skeletal, and central nervous system) can be observed. Homozygous mice and their cardiocytes exhibit enhanced muscarinic (M2) but not adenosine (A1) receptor-mediated responses. Isoproterenol-stimulated beating rates of heterozygous and homozygous hearts are significantly more sensitive to inhibition to carbachol than are those of wildtype mice.
Homozygous mice show slightly reduced adiposity. Unlike females, males placed on a high-fat diet are resistant to weight gain and have decreased body fat as compared to wildtype mice. Both males and females exhibit enhanced insulin sensitivity (protected f ..... | ||
| 002771 | B6.129S2-Tlx1tm1Sjk/J | Cryopreserved - Ready for recovery |
| 010572 | B6.129S2-Tnfsf13btm1Msc/J | Cryopreserved - Ready for recovery |
| Homozygous (BAFF-/- or BAFF KO) mice are viable and fertile. The BAFF knockout mutation has a tailless human CD2 reporter gene inserted into the Tnfsf13b (BAFF) locus that abolishes endogenous BAFF expression. Homozygous mice exhibit abnormal B cell development and function, resulting from significant loss of mature B cell (B220+) populations in lymph nodes, peripheral blood and bone marrow, as well as attenuated antibody responses to both T cell-dependent and T cell-independent type II antigens. Homozygous also have splenic deficiencies (mass, marginal zone B cells and follicular B cells), and decreased total serum immunoglobulin in each subclass (with the exception of immunoglobulin A [IgA] which was only moderately reduced). No loss of marrow pre-B cells, marrow pro-B cells, or CD3+ T cells are reported with BAFF-deficiency. Heterozygous mice have moderately reduced serum IgG subclasses and IgM. These BAFF-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 005643 | B6.129X-Gusbtm1Sly/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable but have reduced neonatal survival. Homozygotes are infertile, but fertility can be restored with enzyme replacement therapy. No residual enzyme activity is observed. Homozygous mice are indistinguishable from heterozygous and wild type mice at birth, but show distinct growth retardation, shortened extremities, and facial dysmorphism observable at wean and increasing in severity with age. Long bones of the lower extremities are shortened, broad, and sclerotic. Compared to wild-type, this model has increased urinary glycosaminoglycan and secondary elevation of other lysosomal storage enzymes. Further, homozygous mice show abundant lysosomal storage in liver, kidney, leptomeningeal cells, cornea, spleen, neurons, and retinal pigment epithelium. The phenotype exhibited by this mutant mouse strain is more severe than that observed in a similarly constructed mutant (Stock No. 005644) which bears a L175F point ..... For more information please see the full phenotype on the strain data sheet | ||
| 006199 | B6.129X1-Fzd9tm1Uta/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical abnormalities. Endogenous transcripts are absent in skeletal muscle and testis. Homozygotes exhibit abnormal B-cell development, reduced survival, lymphadenopathy secondary to accumulation of plasma cells, splenomegaly, and accelerated thymic atrophy. Mutant mice do not exhibit any obvious features of Williams-Beuren syndrome (WBS). These mice may be useful in studies of hematopoietic/lymphoid development and function (including B-cell and T-cell development), plasma cell homeostasis, and the Wnt/frizzled signaling pathway. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally published. We will modify the strain description if necessary as ..... | ||
| 000450 | B6.C3-Spna1sph/BrkJ | Cryopreserved - Ready for recovery |
| Homozygotes have spherocytic hemolytic anemia and neonatal jaundice. Erythrocytes have diminished biconcavity, a smaller than normal diameter, increased density, an appearance of exovesiculation, and a short lifespan. At birth homozygotes are very pale then become yellow during the first few hours of life and die generally within a day of being born. Although it is rare for a spherocytosis homozygote to survive beyond one day of birth on the C57BL/6J or WB/Re (stock #000454) congenic background, homozygotes on the (C57BL/6J x WB/Re)F1 background are much more robust and the majority survive to adulthood. Those that make it to wean age are expected to have a reasonable lifespan, sometimes living as long as a year. Thus, most studies of this mutation in the adult have been done on the (C57BL/6J x WB/Re)F1 background. These homozygotes display diminished hematocrit, decreased red blood cell count, very elevated red blood cell protoporphyrin levels, increased erythropoiesis, reticulo ..... For more information please see the full phenotype on the strain data sheet | ||
| 006407 | B6.Cg-Gusbmps/BrkJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the "mps" (mucopolysaccharidosis type VII or MPS VII) mutation are devoid of expression of the lysosomal enzyme beta glucuronidase. Homozygous animals are viable, but females have a deficiency in lactation. Skeletal and connective tissue anomalies in both males and females are believed to prevent successful breeding. As this mutation is recessive, heterozygous mice are phenotypically similar to wildtype. Homozygotes exhibit short and thickened long bones (smaller than heterozygous or wildtype littermates), "pug type" appearance of the nose, hepatomegaly, splenomegaly, corneal clouding, and deafness. These mice have the H2b haplotype typical of inbred C57BL/6 mice. MPS VII mice are a model of the beta glucuronidase enzyme deficiency in humans called Sly Disease. They may be useful in developing new therapies (enzyme replacement, cell transplantation, gene therapy) broadly applicable to other lysosomal storage diseases. | ||
| 003780 | B6.Cg-Sgshmps3a/PstJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the Sgshmps3a mutation have only 3-4% of the wild type level of sulfamidase activity. This results in extensive lysosomal accumulation of heparin sulfate most prominently in neuronal tissue and liver and, to a lesser degree, in the spleen. GM2 ganglioside accumulation is also found. The outward phenotype of scruffy coat, hunched posture, and reduced activity is usually seen by 6 to 7 months of age. Corneal opacity is also found at approximately 7 months of age. Death occurs between 7 and 10 months of age, on average, and autopsy reveals brain lesions, hepatosplenomegaly and a distended bladder containing turbid urine. The homozygotes have thicker skullcaps, vertebral deformation, thickening of the urinary bladder wall, and bladder blockage that leads to severe bladder distention as they age. Sgshmps3a /Sgshmps3a mice provide a model for the human disease mucopolysaccharidosis 3A (MPSIIIA), also known as S ..... For more information please see the full phenotype on the strain data sheet | ||
| 006210 | B6.Cg-Spna1ihj/LlpJ | Cryopreserved - Ready for recovery |
| Although normal in appearance at birth, homozygotes are smaller than normal by 2 days of age and there is a high rate of neonatal death and death during the first weeks of life and at wean age with some homozygotes surviving to adulthood. Those that survive to adulthood generally do not survive beyond one year. Pups have delayed hair growth such that the coat does not come in until 8 to 10 days of age. The skin, nails and mucosa have an orange pallor that persists throughout life and the feces are soft and also orange in color. Central phenotypes include hemolytic anemia, microspherocytosis, anisopoikilocytosys, polychromatophily, bilirubinemia, and splenomegaly with mild follicular hyperplasia. Although the spleen is of normal size at birth, at death adult splenic weight is three times normal and the architecture is disrupted. This is sometimes accompanied by hepatomegaly. The kidneys are discolored and have mild tubulonephrosis. Female homozygotes rarely become pregnant and do ..... For more information please see the full phenotype on the strain data sheet | ||
| 004338 | B6;129-E2f2tm1Zubi/J | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 002265 | B6;129S2-Bcl2tm1Sjk/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Bcl2tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle. | ||
| 002273 | B6;129S2-Tlx1tm1Sjk/J | Cryopreserved - Ready for recovery |
| 000209 | B6C3Fe a/a-Dh/J | Cryopreserved - Ready for recovery |
| A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain. | ||
| 000182 | B6C3Fe a/a-Eef1a2wst/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the wasted spontaneous mutation (Eef1a2wst) can be recognized at 20 days of age by tremor and uncoordinated body movements. Homozygous mutant mice develop progressive paralysis and do not survive beyond 30 days. They have marked lymphoid hypoplasia in the spleen, thymus, lymph nodes, and peripheral blood. Wasted mice have a severely reduced number of IgA plasma cells in the entire large and small intestines, but the number of such cells in the spleen and the level of serum IgA are normal. Neuronal degeneration occurs in the brain and spinal cord. Spinal cord abnormalities are preceded by gliosis following along a rostrocaudal gradient. Thoracic/abdominal muscles exhibit a progressive denervation of muscle fibers, with progressive asynchronous retraction of motor nerve terminals. (Newbery HJ, et al. 2005) | ||
| 000290 | B6C3Fe a/a-Sox10Dom/J | Cryopreserved - Ready for recovery |
| 003922 | BALB/cByJ-Clcn1adr-mto2J jgl/GrsrJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the jagged tail-like (jgl) mutation are easily characterized by their kinked tails that are recognizable by 10 days of age. Full body X-rays revealed exostosis of the vertebrae near the tail tip and in the phalanges of all 4 feet and abnormal vertebral bodies were also reported in two 5 month old homozygotes. Both female and male reproductive organs are smaller than normal with the males showing severe atrophy of the seminiferous tubules and hyperplasia of Leydig cells. Although most homozygotes are not fertile, a few have produced litters. Homozygotes also have atrophic spleens, particularly the white pulp. | ||
| 002662 | C.Cg-Fechm1Pas/J | Cryopreserved - Ready for recovery |
| Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age. | ||
| 000225 | C3FeLe.B6 a/a-Ptpn6me/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004109 | C57BL/6J-Glra1nmf11/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for Glra1nmf11 entry. | ||
| 010825 | C57BL/6J-Ptpn6me/SzJ | Cryopreserved - Ready for recovery |
| Mice homozygous for the motheaten spontaneous mutation (Ptpn6me) develop severe autoimmune disease. Characteristics include 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. | ||
| 004765 | C57BL/6J-nmf148/J | Cryopreserved - Ready for recovery |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf148 entry. | ||
| 002760 | C57BLKS/J-Npc1spm/J | Cryopreserved - Ready for recovery |
| The sphingomyelinosis mutation (Npc1spm) arose in the C57BLKS inbred strain. Homozygous mutant mice begin to lose weight and to show tremor and ataxic gait at about 7 weeks of age. Weight loss continues and tremor and ataxia become more severe until death at about 12 to 14 weeks of age. The liver and spleen are also enlarged and Purkinje cells in the cerebellum are severely depleted. Sphingomyelin and free cholesterol are markedly elevated in liver and spleen but not in brain. Sphingomyelinosis closely resembles that of human Niemann-Pick Type C disease patients. A dual deficiency of sphingomyelinase and glucocerebrosidase activity has been described in BALB/c mice (npc1N) with resemblance to the sphingomyelinosis condition. | ||
| 003234 | MRL.129P2(B6)-Fastm1Osa/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Tnfrsf6tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively. | ||
| 004083 | NOD.129(B6)-Prkdcscid Iduatm1Clk/J | Cryopreserved - Ready for recovery |
| At birth, mice that are homozygous null for the Idua gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No alpha-L-iduronidase enzyme activity or mRNA is detected. By three weeks of age, homozygous null mice develop a flattened facial profile and a thickening of digits. Defective bone formation is noticeable by fifteen weeks, characterized by a broadening and thickening of long bones. Evidence of lysosomal storage disorder is apparent in cells of the reticuloendothelial system at four weeks. By eight weeks progressive evidence of lysosomal storage is seen in Kupffer cells, splenic sinusoidal lining cells, chondrocytes, glial and Purkinje cells. This animal model is suitable for use in studies investigating the lysosomal storage disorder mucopolysaccharidosis type I (MPS I). | ||
| 001743 | STOCK Gtg1dwg/J | Cryopreserved - Ready for recovery |
| Mice homozgyous for the dwarf grey spontaneous mutation (Gtg1dwg) 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. | ||
| 003534 | STOCK Inpp5dtm1Dmt/J | Cryopreserved - Ready for recovery |
| Inpp5d (commonly called SHIP) -deficient mice are viable and fertile. However, fertility rate is 10% lower in homozygotes and lifespan is shortened in comparison to controls. Inpp5d -deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy and myeloid infiltration of vital organs. Histological and flow studies demonstrate a substantial increase in granulocyte-macrophage/monocyte populations in bone marrow, spleen and lymph nodes. Spleens and lymph nodes are severely enlarged compared to wildtype. The difference in spleen size is apparent as early as 4 weeks of age, and by 16 weeks of age, spleens from null mice are 10 fold greater than those of wildtype mice. Neutrophils and bone marrow-derived mast cells from these mice appear to be less susceptible to apoptotic stimuli. | ||
| 000454 | WB.C3-Spna1sph/BrkJ | Cryopreserved - Ready for recovery |
| Homozygotes have spherocytic hemolytic anemia and neonatal jaundice. Erythrocytes have diminished biconcavity, a smaller than normal diameter, increased density, an appearance of exovesiculation, and a short lifespan. At birth homozygotes are very pale then become yellow during the first few hours of life and die generally within a day of being born. Although it is rare for a spherocytosis homozygote to survive beyond one day of birth on the WB/Re or C57BL/6J (stock #000450) congenic background, homozygotes on the (C57BL/6J x WB/Re)F1 background are much more robust and the majority survive to adulthood. Those that make it to wean age are expected to have a reasonable lifespan, sometimes living as long as a year. Thus, most studies of this mutation in the adult have been done on the (C57BL/6J x WB/Re)F1 background. These homozygotes display diminished hematocrit, decreased red blood cell count, very elevated red blood cell protoporphyrin levels, increased erythropoiesis, reticulo ..... For more information please see the full phenotype on the strain data sheet | ||
| 005027 | B6.129S2-Il10rbtm1Agt/J | Under Development - Now Accepting Orders |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of ES cells. After 12 weeks of age, approximately 60% of mutant mice develop chronic colitis and increased numbers of splenocytes resulting in splenomegaly. Bone marrow-derived macrophages, splenocytes and peritoneal cells derived from homozygotes do not respond to IL-10. Mutant mice housed in non-SPF conditions do not breed well. This mutant mouse strain may be useful in studies of the role of interleukin-10 in inflammatory diseases such as chronic colitis. | ||
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