Search Criteria: Research Area is "Research Tools: Apoptosis Research"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 006050 | 129-Sirt6tm1Fwa/J | Repository- Live |
| Homozygous neonates are smaller than their wildtype and heterozygous littermates. They develop normally until approximately 21 days of age, when they develop an acute and rapid, aging-like degenerative pathology resulting in death by postnatal day 24. Homozygous mutant mice exhibit subcutaneous fat loss, lordokyphosis (hunchbacked spine) with osteopenia (30% loss of bone mineral density), colitis, and severe lymphopenia due to increased lymphocyte apoptosis. At day 12, mice have reduced insulin-like growth factor I (IGF-1) levels in serum, and develop severe hypoglycemia. Mouse embryonic fibroblasts (MEFs) prepared from homozygous embryos exhibit reduced proliferation, defective base excision repair function, as indicated by increased sensitivity to alkylating agents and ionizing radiation, and increased chromosomal aberrations. The donating investigators report that no gene product (mRNA or protein) is detected by RT-PCR or immuoblot analysis of tissues, MEFs or embryonic stem cells f
..... For more information please see the full phenotype on the strain data sheet | ||
| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(gtGFP (or RORgt)GFP) mutant allele are viable and fertile. While Rorcg mRNA is detected in liver in Rorc(g)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcgt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(gt) transcription in the thymi of adult Rorc(gt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcgt-deficient T cells lack tissue-infiltrating proinflammatory T-helper cells (Th17 cells), and are protected from induced autoimmune disease (EAE) on this genetic background. The donating investigator also reports increased thymoma incidence with age in homozygo
..... For more information please see the full phenotype on the strain data sheet | ||
| 005530 | B6.129S-Ddit3tm1Dron/J | Repository- Live |
| 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 or protein) is detected by Northern or Western blot analysis of toxin challenged mouse embryonic fibroblasts (MEFs). MEFs and renal proximal tubular epithelial cells have decreased apoptosis in response to endoplasmic reticulum stress induced by the toxin, tunicamycin. Pancreatic islets cells are more resistant to nitric oxide induced apoptosis. MEFs exhibit a delayed onset of unfolded protein response (UPR) target gene expression when treated with tunicamycin. This mutant mouse strain may be useful in studies of apoptosis and pathogenesis due to endoplasmic reticulum stress. | ||
| 006233 | B6.129S1-Casp3tm1Flv/J | Repository- Live |
| On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r
..... For more information please see the full phenotype on the strain data sheet | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 008076 | B6.129S4-Traf1tm1Tsi/J | Repository- Live |
| Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bims. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el
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| 006236 | B6.129S6-Casp6tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with no gross morphological or behavioral abnormalities. These mutant mice may be useful in studies of mitochondrial events of apoptosis (especially when paired with other executioner caspase mutant models) and lens development. | ||
| 006237 | B6.129S6-Casp7tm1Flv/J | Repository- Live |
| Homozygous mice are viable and fertile with normal appearance, organ morphology, and lymphoid development. Endogenous protein expression is absent in all tissues tested (including brain, thymus, heart, lung, liver, spleen, kidney, and skeletal muscle). Mouse embryonic fibroblasts (MEFs) from homozygotes exhibit a slight survival advantage when treated with apoptosis inducers, but other cell subsets undergo normal apoptosis (including activated T cells death following T cell receptor stimulation, thymocyte apoptosis, and Fas-mediated B cell and hepatocyte cell death). These mutant mice may be useful in studies of mitochondrial events of apoptosis, especially when paired with other executioner caspase mutant models. | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Repository- Live |
| Mice homozygous for both alleles (Baxfl and bak-) are viable and fertile with no reported abnormalities. Splenic and thymic tissues display no Bak1 protein expression. When bred to Cre recombinase expressing mice, the resulting offspring will have exons 2-4 of Bax deleted in the cre-expressing tissues (determined by promoter driving cre expression). The conditional deletion of Bax combined with the Bak1 null allele makes these mice useful in studies of apoptosis regulation, tissue homeostasis, and development in multiple cell lineages.
When bred to a strain with a Bak1 targeted null allele (Stock No. 004183) and to either a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126) or to a strain expressing interferon inducible Cre recombinase (
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| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di
..... For more information please see the full phenotype on the strain data sheet | ||
| 008045 | B6;129-Trp53tm2Holl/J | Repository- Live |
| In this mutant strain, exons 4-9 of the endogenous mouse Trp53 gene have been replaced with the homologous human TRP53 region. Transcription of the human sequence is under the control of the endogenous mouse promoter. The inserted human sequence segment encodes the DNA binding domain and the TRP53 polyproline domain. This latter domain contains a polymorphism at codon 72 that encodes either arginine or proline in human populations. This mutant strain expresses the proline variant at codon 72 and the related strain, 129-Trp53tm1Holl/J (Stock No. 004301) expresses the arginine variant. Mice that are homozygous for this mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Immortalized cell lines derived from primary embryonic fibroblasts harvested from these mice frequently harbor a TRP53 (p53) mutation in the DNA binding domain t
..... For more information please see the full phenotype on the strain data sheet | ||
| 005070 | C57BL/6-Tg(Csf1r-EGFP-NGFR/FKBP1A/TNFRSF6)2Bck/J | Repository- Live |
| These transgenic mice have an inducible Fas suicide/ apoptotic system driven by the mouse Csf1r, colony stimulating factor 1 receptor promoter. The transgene insert contains a mutant human FK506 binding protein 1A, 12kDa (FKBP12) which preferentially binds the dimerization drug AP20187. Enhanced Green Fluorescent Protein (EGFP) fluorescence and transgene expression is detected in 78% of isolated peritoneal cells. EGFP fluorescence is variable among tissues (B- and T-cells do not express EGFP). Administration of the dimerizing reagent, AP20187, induces apoptosis in macrophages and dendritic cells (intravenous injection of dimerizer is recommended, since the intraperitoneal route can elicit peritoneal adhesions). In treated mice, EGFP fluorescing peritoneal and bone marrow macrophage numbers are depleted by more than 90%, and macrophage numbers in blood, spleen, lung and thymus by more than 70%. 7 days after cessation of treatment, the EGFP fluorescing macrophage and dendritic cel
..... For more information please see the full phenotype on the strain data sheet | ||
| 006481 | C57BL/6J-Tg(ACTB-NOTCH1)1Shn/J | Repository- Live |
| Transgenic mice are viable, fertile and behaviorally normal. These "CALSL-NICD (H)" mice (or simply CALSL-NICD) reportedly carry 10-20 copies of the transgene inserted into a single genomic locus. Expression of the transgene-derived intracellular domain of human NOTCH1 is prevented by a "Lox-STOP-Lox" cassette. When transgenic mice are bred to a strain expressing Cre recombinase, the "floxed stop" cassette is excised in the resulting offspring, and human NOTCH1 expression is observed in the cre-expressing tissue(s). These transgenic mice may be useful in studying early neural progenitor cell development and apoptosis, and responses to tissue-specific Notch activation. For example, when crossed to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771), this transgenic mouse strain may be useful in studies of notch signaling during apoptotic cell death. | ||
| 004597 | C;129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 006068 | STOCK Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 004510 | STOCK Rom1tm1Mci/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and normal in size. When heterozygous mice are bred together, homozygous animals occur at a greatly reduced frequency (~6%). No gene product (protein) is detected in retinal tissue from homozygotes by Western blot analysis. Onset of progressive retinal degeneration occurs at 2 months of age beginning with a thinning of the outer nuclear layer of retinal cells. Rod outer segments in 2 month old mice display disorganized arrangement, irregular gaps and amorphous aggregates. At 4 months of age organization of rod outer segments improves. TUNEL assay of mutant retinal tissue show photoreceptor degeneration is due to apoptotic cell death. Ultra structural organization of rod outer segment disks is disorganized, often with patches of enlarged disks. Electroretinogram a-wave analysis of photoreceptor function reveals a diminished maximal photoreceptor response (50% lower than wildtype). This mutant mouse strain may be useful in stu
..... For more information please see the full phenotype on the strain data sheet | ||
| 004301 | 129-Trp53tm1Holl/J | Repository-Cryopreserved |
| In this mutant mouse strain, the endogenous murine sequence for exons 4-9 of the targeted gene, which encode the DNA binding domain of the tumor suppressor protein, have been replaced with the homologous normal human sequence. Transcription is under the control of the endogenous mouse promoter. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice exhibit normal expression and functional activity of the chimeric gene. Homozygous mutant mice have normal immunodetectable levels of p53 protein accumulation in nuclei in response to UV-induced DNA damage. Thymocytes from mutant mice are as susceptible to gamma-irradiation-induced and dexamethaxone-induced apoptosis as wildtype thymocytes. This mutant mouse strain may be useful in studies related to in vivo spontaneous and induced mutation of the human TRP53 gene sequence, and pharmacological agents for alt
..... For more information please see the full phenotype on the strain data sheet | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Repository-Cryopreserved |
| 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). | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches. | ||
| 005517 | B6.129S4-Cyb5r4tm1Hfb/HfbJ | Repository-Cryopreserved |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m
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| 006142 | B6.129S4-Ppargtm1Rev/J | Repository-Cryopreserved |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 004197 | B6.129S6-Rac2tm1Mddw/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu
..... For more information please see the full phenotype on the strain data sheet | ||
| 006072 | B6.129X1-Mcl1tm2Sjk/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice are embryonic lethal. These mutant mice may be useful in studies of immune function, including apoptosis, B and T cell development, and bone marrow cell differentiation. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 006088) and a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126), this mutant mouse strain may be useful in studies of lymphocyte development. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 006088) and a strain expressing interferon inducible Cre recombinase in t
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| 005642 | B6.Cg-Clutm1Jakh/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities. No protein is detected in serum, liver, or brain and in situ hybridization shows no mRNA in heart. This mutant has been studied for different functions on different backgrounds. On the Swiss Black outbred background, aging homozygous mutant mice develop a progressive glomerulopathy characterized by deposition of tubulo-fibrillary immune complexes devoid of inflammation or necrosis. On the FVB/N background, homozygous null mice with chemically induced autoimmune myocarditis show severe and diffuse lesions with postinflammatory functional impairment. Induced skin carcinogenesis is more severe than wildtype. On the C57BL/6 background, homozygotes given a hypoxia-ischemia brain injury (modeling cerebral palsy) had 50% less brain injury compared to wild type. Conversely, mutants have less neuroprotective properties after permanent focal cerebral isc
..... For more information please see the full phenotype on the strain data sheet | ||
| 004264 | B6;129-Cycstm1Wlm/J | Repository-Cryopreserved |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 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 phenotype on the strain data sheet | ||
| 006088 | B6;129-Mcl1tm3Sjk/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. The donating investigator indicates that homozygous males have severely reduced fertility for unknown reasons, while females have normal fertility. Endogenous protein expression is unaffected by the inserted loxP sequences. When bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying global, temporal, or tissue-specific deletion of the endogenous gene, particularly in studies of immune function, including apoptosis, B and T cell development, and bone marrow cell differentiation. When bred to a strain with the targeted null allele (Stock No. 006072) and a strain with a Cd19 null allele and expressing Cre recombinase during th
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| 002536 | B6;129S-Btktm1Wk/J | Repository-Cryopreserved |
| Mice homozygous for the Btktm1Wk targeted mutation are viable and fertile. Homozygous mutant mice show defects in B-cell maturation and activation. This strain has the same phenotype as the spontaneous X-linked immune deficiency mutation (CBA/CaHN-Btkxid/J; Stock No. 001011). See Inbred Strain listing. | ||
| 005937 | B6;129S4-Ucp3tm1Lowl/J | Repository-Cryopreserved |
| Homozygous mice are viable and fertile and do not express full length mRNA in skeletal muscle and brown adipose tissue. In skeletal muscle mitochondria, endogenous protein was undetectable. Skeletal muscle mitochondria from homozygous mice show decreased state 4 respiration. Further, skeletal muscle, but not liver, mitochondria produce more superoxide anions and reactive oxygen species both in vitro (lucigenin-derived chemiluminescence) and in vivo (aconitase activity). Skeletal muscle ATP synthesis under fasting conditions is approximately 4-fold greater in mutant mice. This mouse may be useful in studies of energy metabolism, thermogenesis, aerobic respiration (including mitochondrial respiration coupling), and age-related progressive deterioration of fatty acid homeostasis. | ||
| 005516 | C.129S4-Cyb5r4tm1Hfb/HfbJ | Repository-Cryopreserved |
| Mice heterozygous for the targeted mutation are viable and fertile, glucose tolerant, have normal blood sugar levels, serum lipid profiles and white adipose tissue mass. No protein from the targeted gene was detected by Western Blot analysis of mice homozygous for the allele. Homozygous mice consume more food, have decreased adipose tissue mass and are hyperlipidemic compared to wildtype controls post-weaning. At 4 weeks of age glucose levels are normal but insulin levels are 40% of wildtype controls. At 7 weeks of age clinical diabetes is present in both male and female of homozygous mice. Histological evaluation of pancreas from 21 week old homozygote animals revealed a significant reduction in the number of islets and decreased cytoplasmic to nuclear ratio in the islet cells and there was no insulitis nor phagocytosis of necrotic beta cell fragments. While there is a progressive loss of beta cells in aging homozygous mice, there is no loss of alpha, delta or PP cells. Electron m
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| 005076 | NOD.Cg-Tg(tetO-EGFP/FADD)1Doi/DoiJ | Repository-Cryopreserved |
| Mice hemizygous for this transgenic insert are viable, fertile, normal in size. Diabetes incidence and onset is similar to that observed in NOD inbred mice, but otherwise, the mice do not display any gross physical or behavioral abnormalities. These transgenic mutant mice may be mated to strains carrying either rtTA (reverse tetracycline trans-activator protein) or tTA (the tetracycline trans-activator) transgenes regulated by tissue specific promoters. In the bi-transgenic offspring of such crosses, tissue-specific expression of the EGFP/FADD fusion protein can be either induced (in rtTA transgenic mice) or suppressed (in tTA transgenice mice) by administration of the tetracycline analog, doxycycline (dox). Dox may be administered in the animals? water supply. Double transgenic mice generated by intercrossing Tg(tetO-EGFP/FADD)1Doi transgenic mice with NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ (Stock No. 004602) transgenic mice express
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| 005115 | NOD.FVB-Tg(INS-MT2A,Tyr)1Pne/PneJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset, especially in males, and have coat color pigmentation. Immunohistochemical staining with metallothionein specific antibodies confirms pancreatic islet cell specific expression of the INS-MT2A transgene. There is a 40-fold increase in metallothionein activity in transgenic islets when compared to wild-type controls. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase in ROS florescence in wild-type islets, but a very small increase in transgenic islets. Transgenic beta cells are diabetes resistant to diabetes when treated with streptozotocin. Transgenic beta cells generate less ROS fluorescence when treated with hydrogen peroxid
..... For more information please see the full phenotype on the strain data sheet | ||
| 005113 | NOD.FVB-Tg(INS-SOD2)3Pne/PneJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Immunohistochemical staining with mitochondrial superoxide dismutase specific antibody confirms INS-SOD2 transgene expression localized to the mitochondria of pancreatic islet cell. There is a significant increase in SOD2 activity in transgenic islets when compared to wild-type controls. There is no statistical difference in insulin and DNA content, insulin staining and islet morphology or diabetes development following cyclophosphamide treatment between mutant and wild type NOD mice. Transgenic mice are resistant to diabetes when treated with streptozotocin. Islet beta cells from transgenics generate less ROS when treated with peroxynitrite or superoxide. Untreated mutants do not display accelerated spontaneous diabetes. This model provides a tool for looking at the role of oxidative stress in diabetes. | ||
| 005114 | NOD.FVB-Tg(Ins1-Cat,Tyr)25Pne/PneJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, and normal in size, display accelerated spontaneous diabetes onset in males, and have coat color pigmentation. Northern blot analysis and immunohistochemistry confirm pancreatic islet specific expression of the Ins1-Cat transgene. There is a 50-fold increase in catalase activity in transgenic islets when compared to wild-type controls, which approximates catalase activity normally found in the liver. Insulin and DNA content, insulin staining and islet morphology in transgenic animals is essentially the same as in wild-type controls. Transgenic islets have a similar reactive oxygen species (ROS) level as wild-type controls in normal media. However, after exposure to cytokines there is a significant increase of ROS florescence in control islets, but much smaller increase in transgenic islets. Transgenic mice are resistant to diabetes when treated with streptozotocin or alloxan. Transgenic beta cells generate less ROS fluorescence when treated with
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| 005740 | STOCK Ppiftm1.1Mmos/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Brain architecture and cerebrovasculature are normal. No gene product (protein) is detected by immunoblot analysis of mitochondria isolated from liver tissue of mutant mice. Mitochondria from mutant mice have an increased capacity to retain calcium and fail to swell/rupture in response to CaCl2, suggesting abnormal permeability transition pore (PTP) function. Mouse embryonic fibroblasts (MEFs) derived from mutant mice are less susceptible to oxidative stress induced in vitro by exposure to hydrogen peroxide than MEFs derived from wildtype mice. In a model of ischemic brain injury employing a middle cerebral artery occlusion protocol, mutant mice exhibited a reduced infarct volume (37% in heterozygotes, and 62% in homozygotes) when compared to wildtype mice. This mutant mouse strain may be useful in studies investigat
..... For more information please see the full phenotype on the strain data sheet | ||
| 005737 | STOCK Ppiftm1Mmos/J | Repository-Cryopreserved |
| In this strain loxP sites flank exons 3-5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cre-mediated recombination results in the deletion of the loxP-flanked region. This strain represents an effective tool for generating tissue-specific targeted mutants useful in studies examining the consequences of disrupting Ppif-dependent pathways. | ||
| 006085 | STOCK Rad9tm1Lieb/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Mouse embryo fibroblasts (MEFs) cannot be derived from homozygous embryos. Homozygous null mice have an embryonic lethal phenotype, failing to develop somewhere between embryonic days 9.5 and 12.5. Homozygous mutant embryonic day 8.5 and 9.5 embryos exhibit increased apoptosis and reduced cellular proliferation. This mutant mouse strain may be useful in studies of development, DNA damage and repair, and genomic stability. | ||
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How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
Select the strain name to link to the strain data sheet.
New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
Send questions to our Technical Support team using the Express Technical Support Form.
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