Search Criteria: Research Area is "Apoptosis Research: Endogenous Regulators"
| Stock Number |
Strain Name Strain Description |
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 | ||
| 002779 | 129S-Parp1tm1Zqw/J | Repository- Live |
| Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although a shortened transcript is generated, no enzymatic activity is detected in tissues. Proliferation of homozygous-null fibroblasts and thymocytes is impaired following gamma-radiation in comparison to cells derived from wild-type mice. Older mice are susceptible to spontaneous development of skin disease. A significant portion of older mice ( ~30%) can be expected to exhibit epidermal hyperplasia. Null mice are also less susceptible to damage induced by the neurotoxin MPTP. | ||
| 007572 | B6.129P2(Cg)-Rorctm2Litt/J | Repository- Live |
| Mice homozygous for this Rorc(γtGFP (or RORγt)GFP) mutant allele are viable and fertile. While Rorcγ mRNA is detected in liver in Rorc(γ)tGFP homozygotes, mRNA and protein for the thymus-specific isoform (Rorcγt) encoded by the targeted allele are not detected in the thymus. EGFP expression reports Rorc(γt) transcription in the thymi of adult Rorc(γt)GFP mice. Homozygous mice exhibit abnormal lymph node, Peyer's patch, and lymphoid tissue inducer (LTi) cell development. Mice with Rorcγt-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 homozygotes. These RorcγtGFP mutant mice may be useful in studying immune system homeostasis, T cell repertoire selection, CD4/CD8 double positive (CD4+/CD8 For more information please see the full phenotype on the strain data sheet | ||
| 009088 | B6.129P2(SJL)-Myd88tm1.1Defr/J | Repository- Live |
| Homozygous mice are viable and fertile. The Myd88-deficient allele encodes a deletion of exon 3 of the myeloid differentiation primary response gene 88 locus. Myd88-deficiency is associated with a number of immune system abnormalities, as well as hematopoietic system, molecular signaling, and apoptotic abnormalities. | ||
| 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. | ||
| 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. | ||
| 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 | ||
| 002101 | B6.129S2-Trp53tm1Tyj/J | Repository- Live |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at three to six months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 007899 | B6.129S4-Casp2tm1Yuan/J | Repository- Live |
| Mice homozygous for this caspase-2 targeted mutation are viable and fertile. As the mutation deletes the QACRG active site and the caspase-2S sequence of the endogenous enzyme, this deletion was shown to inactivate both the long and short form of caspase-2. As such, homozygous mice exhibit defects in regulation of apoptosis; including an enlarged oocyte reserve attributed to a germ cell-intrinsic death defect during prenatal ovarian development (resistance to oocyte cell death following complete cytokine starvation or exposure to an anticancer drug), as well as accelerated motor neuron cell death and defective B lymphoblast apoptosis. In addition, caspase-2-deficient mice exhibit characteristics of premature aging (including shortened maximum lifespan, impaired hair growth, increased bone loss, reduced body fat content, and higher hepatic levels of oxidized proteins). As caspase-2 acts as an upstream regulator of cell death in many cell types, caspase-2-deficient mice may b ..... 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.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to ..... | ||
| 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. | ||
| 008240 | B6.129S6-Eif2ak4tm1.2Dron/J | Repository- Live |
| Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4-, GCN2-, GCN2.KO4ex, or GCN2-KO) are viable, fertile and overtly indistinguishable from wild-type mice, with little if any mRNA expressed from the mutant locus. Homozygous GCN2-deficiency is associated with altered inflammatory responses and altered stress responses, including sensitivity to nutritional deficiencies and aberrant eating behavior. As GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) to reduce global translation and activate stress-related transcription factors (such as NF-kappaB) to alleviate cellular injury or alternatively induce apoptosis, these GCN2.KO4 mutant mice may be useful for such immunology, inflammatory, immunity cell biology, or neurobiology research.
Of note, mice with a conditional allele (loxP-flanked exon XII ..... | ||
| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
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| 002785 | B6;129S4-E2f1tm1Meg/J | Repository- Live |
| Mice homozygous for defective E2f1 are viable and fertile. They show thymocyte maturation defects due to a failure of apoptosis, eventually resulting in increased proliferation and increased tumorigenesis. As mutant mice age, they show exocrine gland dysplasia and testicular atrophy. Mutant mice develop a broad spectrum of cancers, although mammary carcinomas were not observed on this genetic background. Mutant mice are also protected from experimental autoimmune encephalomyelitis (EAE). These mice may be useful in studies of apoptosis, cancer, thymocyte development/selection, diabetes, autoimmunity, and multiple sclerosis. | ||
| 000501 | B6CBACa Aw-J/A-Aifm1Hq/J | Repository- Live |
| Harlequin mice exhibit paucity of fur resulting in near baldness in hemizygous males and homozygous females. Heterozygous females have a patchy absence of hair that is not always obvious, since the degree of hair loss is notably less than 50%. Homozygotes and hemizygous males weigh less than heterozygous or wild type controls. Ataxia is noticeable by 5 months and progresses as the mice age. Initially the ataxia manifests itself as a side-to-side, unsteady gait with a lateral tremor visible at rest. A delayed cerebellar cortical atrophy has been characterized in these mutants, with an apoptotic loss of granule cells beginning at 4 months of age and a necrotic loss of Purkinje cells occurring subsequently. The granule cells re-enter the cell cycle, but the Purkinje cells do not, supporting the postulate that inappropriate cell cycle re-entry of terminally differentiated neurons can induce apoptosis. Cell loss is greater in the caudal lobules of the cerebellum and is extensive by 9 to 11 ..... For more information please see the full phenotype on the strain data sheet | ||
| 008517 | C57BL/6-Gt(ROSA)26Sortm3(CAG-MIR17-92,-EGFP)Rsky/J | Repository- Live |
| Mice homozygous for the "miR-17-92 transgene" conditional allele are viable and fertile, with a loxP-flanked Neo-STOP cassette preventing transcription of the downstream bicistronic sequences (human miR-17-92 cluster (encoding the precursor of seven miRNA molecules; miR-17-5p, miR-17-3p, miR-18a, miR-19a, miR-20a, miR-19b and miR-92) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the human miR-17-92 cluster. Because the synthetic CAG promoter driven miR-17-92 transgene was targeted for insertion into the Gt(ROSA)26Sor locus, expression of the transgene is determined by which tissue(s) express Cre recombinase. EGFP fluorescence, however, is not reported following exposure to Cre recombinase (presumably due to RNaseIII excision of the stem-loop structures encoding individual miRNA destabilizing the EGFP portion of the primary transcript ..... For more information please see the full phenotype on the strain data sheet | ||
| 004597 | C;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.
For example, when crossed to a strain expressing Cre recombinase in astrocytes (see Stock No. 012887), this mutant mouse strain may be useful in studies of neurogenesis. When crossed to a strain expressing Cre recombinase in the central nervous system (see Stock No. 004600), this mutant mouse strain may be useful in studies of glia differentiation and cerebellar development. | ||
| 008232 | FVB/N-Tg(Ins2-IAPP)RHFSoel/J | Repository- Live |
| Mice homozygous for the RIPHAT transgene are viable and fertile, with expression of human islet amyloid polypeptide (h-IAPP) under the regulatory control of the rat insulin II promoter. While h-IAPP RNA from the transgene is observed in pancreas, kidney, and stomach, h-IAPP protein is reported only in pancreas tissues. Hemizygous mice show no symptoms of spontaneous disease. Homozygous males spontaneously develop diabetes mellitus due to beta-cell death, associated with impaired insulin secretion (hypoinsulinemia), hyperglycemia, and abnormal intracellular aggregates of h-IAPP (the donating investigator reports that extracellular aggregates are not found on this strain background). Homozygous male onset is between 4-8 weeks of age with death around 16 weeks of age. Homozygous females exhibit a less severe phenotype. These RIPHAT transgenic mice may be useful in studying the beta-cell destruction and islet amyloid deposition associated with non-insulin-dependent diabetes mellitus (NIDDM ..... For more information please see the full phenotype on the strain data sheet | ||
| 008882 | STOCK Bcl2tm1Irt/J | Repository- Live |
| Mice homozygous for this Bcl2flox conditional allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 2, as well as a loxP site downstream of exon 2 of the Bcl2 (B-cell leukemia/lymphoma 2) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 2 deleted, or both the neo selection cassette and exon 2 deleted. The two latter genotypes result in loss of Bcl2 protein expression and are reported to confer the null phenotype. These Bcl2flox mutant mice may be useful in generating conditional mutations for studying apoptosis, mitochondrial permeability, cell survival signaling, cancer, neurological disorders, and immunity.
For example, when crossed to a strain expressing Cre recombinase in myeloid cell lineages (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 009340 | STOCK Eif2ak3tm1Dron/HotaJ | Repository- Live |
| These mice harbor a targeted mutation of the Eif2ak3 (eukaryotic translation initiation factor 2 alpha kinase 3 [also called Perk]) locus that abolishes endogenous gene expression. To date (Feb 2010), the donating investigator has not been able to generate homozygous mice on a C57BL/6J congenic background. The following phenotype describes mice on a mixed albino Swiss Webster;129/SvEv genetic background. Heterozygous mice are viable and fertile. Homozygous (Perk-/-) mice appear runty within a few days of birth and develop a rapid and progressive decline in endocrine and exocrine pancreatic function. This results in a complex pleiotropic phenotype including hyperglycemia, exocrine pancreatic insufficiency, diabetes, growth retardation, inability to breed, and early mortality. The phenotype of the Perk-/- mice is very similar to that observed in humans with Wolcott-Rallison syndrome; the consistent feature of which is severe diabetes mellitus developing in infancy. Heterozygous mi ..... For more information please see the full phenotype on the strain data sheet | ||
| 004301 | 129-Trp53tm1Holl/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 002080 | 129-Trp53tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 002082 | 129S-Rb1tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. | ||
| 008652 | 129S-Trp53tm2Tyj/J | Cryopreserved - Ready for recovery |
| These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R172H; structural mutant homologous to human p53 codon 175). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein. | ||
| 008651 | 129S-Trp53tm3Tyj/J | Cryopreserved - Ready for recovery |
| These mice carry a conditional point-mutant allele of the transformation related protein 53 gene (p53R270H; contact mutant homologous to human p53R273H). The conditional allele is functionally equivalent to a null mutation. Mice have all the phenotypic issues of p53 knockout mice and therefore have some decreased viability of homozygotes. Cre-mediated recombination leads to deletion of a transcriptional termination sequence (Lox-Stop-Lox) and expression of the oncogenic protein. | ||
| 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). | ||
| 003079 | B6.129-Calb1tm1Mpin/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Calb1tm1Mpin targeted mutation are viable and fertile. Homozygous mutant mice show severe impairment in tests of motor coordination and exhibit ataxia when challenged on a runway. These results suggest functional deficits in cerebellar pathways. Confocal calcium imaging of cerebellar Purkinje cells reveals marked changes of synaptically-evoked postsynaptic calcium transients. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 011026 | B6.129S-Bcl2l11tm3Rjd/J | Cryopreserved - Ready for recovery |
| These mice express a mutated Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) protein in which JNK phosphorylation site Thr112 is replaced with Ala. This mutation suppresses JNK-mediated Bim-induced apoptosis. This mutation does not affect expression of Bim in the spleen. | ||
| 004322 | B6.129S1-Mapk10tm1Flv/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product, mRNA or protein, is detected in brain tissue. Histological and immunohistological examination of the brains of homozygous mutant mice reveal normal development and cellular organization. Mutant mice are resistant to seizures and neuronal apoptosis caused by administration of excitotoxic glutamate-receptor agonist kainic acid. With higher doses of kainic acid, mutant mice display severe tonic-clonic convulsions, but survive the treatment while wildtype mice have 60% mortality. This mutant mouse strain represents a model that may be useful in studies related to neurotoxicity of excitatory amino acids and induced models of Parkinson's disease and stroke. | ||
| 004372 | B6.129S2-Mad2l1tm1Sorg/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the Mad2l1tm1Sorg targeted allele are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygous null mice are embryonic lethal; they fail to develop past embryonic days 6-7 due to catastrophic chromosome missegregation and apoptosis. Histological analysis of heterozygous mutant mice reveal increased germinal center formation in spleen and a higher incidence of lung carcinomas when compared to the wildtype. This mutant mouse strain represents a model that may be useful in studies of the role cell-division checkpoints in tumorogenesis. | ||
| 002102 | B6.129S2-Rb1tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 described. We will modify the strain description if necessary as published results become available. | ||
| 008076 | B6.129S4-Traf1tm1Tsi/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 011028 | B6.129S6-Bcl2l11tm1Rjd/J | Cryopreserved - Ready for recovery |
| This strain carries a single loxP site in intron 4 of the Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) gene and serves as a control strain for mutant strains Bim3SA (Stock No. 11025) , BimT112 (Stock No. 11026), and BimDeltaEL (Stock No. 11027). | ||
| 011025 | B6.129S6-Bcl2l11tm2Rjd/J | Cryopreserved - Ready for recovery |
| These mice express a mutated Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) protein that lacks three sites of phosphorylation by MAP kinases. Ser55, Sere65, and Ser73 were replaced with Ala. The mutated protein (Bim3SA) is not subject to MAP kinase-induced ubiquitination and degradation. This causes a gain-of-function and increased apoptosis. The mutation does not affect the expression of mRNA in the spleen or thymocytes, as determined by immunoblot. | ||
| 011027 | B6.129S6-Bcl2l11tm4Rjd/J | Cryopreserved - Ready for recovery |
| These targeted mutation mice lack exon 3 of the Bim (Bcl2l11, BCL2-like 11 (apoptosis facilitator)) gene. Alternative splicing to include exon 3 is required for expression of the BimEL isoform, lacking in these mice. Other isoforms, including BimL and BimS, are expressed however. These mice represent a model for the analysis of BimEL loss-of-function. | ||
| 011021 | B6.129S6-Bmftm1Rjd/J | Cryopreserved - Ready for recovery |
| Homozygous Bmf (BCL2 modifying factor) targeted mutant mice lack expression of its protein which bears only the pro-apoptotic BH3 domain. Expression in brain, spleen, thymus and lymph node tissues is eliminated. Female homozygotes exhibit an imperforate vagina and hydrometrocolpos (22% penetrance). Male and female mice exhibit increased numbers of B cells. | ||
| 011022 | B6.129S6-Bmftm2.1Rjd/J | Cryopreserved - Ready for recovery |
| These mice express Bmf (BCL2 modifying factor) with a targeted Ser74Ala mutation. They provide a model for defects in JNK(Mapk8)-induced apoptosis mediated by Bmf phosphorylation. This mutation does not affect expression in the spleen. | ||
| 011023 | B6.129S6-Bmftm3.1Rjd/J | Cryopreserved - Ready for recovery |
| These mice express Bmf (BCL2 modifying factor) with a targeted gain-of-function Ser74Asp mutation in the JNK (Mapk8) phosphorylation site. This mutation does not affect expression in the spleen. | ||
| 011024 | B6.129S6-Bmftm4.1Rjd/J | Cryopreserved - Ready for recovery |
| This targeted mutation strain may be used as a control for Bmf S74A (see Stock No. 11022) and S74D (see Stock No. 11023) mutant mice in studies of JNK phosphorylation-induced apoptosis. | ||
| 006236 | B6.129S6-Casp6tm1Flv/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004069 | B6.129S6-Crebbptm1Dli/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Crebbp gene are embryonic lethal, dying at about embryonic day 10.5 exhibiting open neural tube defects. Heterozygous mice though viable and fertile, are subject to early growth retardation, craniofacial abnormalities and often fail to thrive. Heterozygous mice are also subject to age-dependent splenomegaly and irregular hematopoiesis. By three months of age, the abundance of all hematopoietic cell types is significantly diminished. Older mice (10-21 months) are more prone to develop hematologic malignancies than wildtype mice. | ||
| 007218 | B6.129S6-Trp53tm2Xu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and also develop a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events, cancer development and apoptosis. 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 become available. | ||
| 006072 | B6.129X1-Mcl1tm2Sjk/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 004853 | B6.C3-Tg(KRT14-Birc5)19Gros/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development. | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 002319 | B6.Cg-Tg(BCL2)22Wehi/J | Cryopreserved - Ready for recovery |
| Expression of the human BCL2 transgene is restricted to B cell lineage (no T cell expression) in which it enhances cell survival. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. This phenotype is somewhat greater on the BALB/c than on the C57BL/6 background. Hemizygotes on a mixed B6,SJL background (but not on the BALB/c background) develop autoimmune disease characterized by immune complex glomerulonephritis, anti-nuclear antibodies, lymphadenopathy and myocardial infarction. These mice serve as a robust source for the production of B cells and antibodies. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incidence is insignificant. When this transgene is crossed with an Emu-myc transgene bearing strain (Stock ..... For more information please see the full phenotype on the strain data sheet | ||
| 002320 | B6.Cg-Tg(BCL2)25Wehi/J | Cryopreserved - Ready for recovery |
| Expression of the human BCL2 transgene restricted to the T cell lineage (no B-cell expression). Thymocytes, peripheral T-cells and activated T cells from these mice withstand prolonged culture in the absence of growth factors. Cells are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. This transgenic line displays no detectable autoimmunity. These mice serve as a robust source for the production of T-cell lines or hybridomas. Also known as 25Wehi or Emu-bcl-2-25. | ||
| 002321 | B6.Cg-Tg(BCL2)36Wehi/J | Cryopreserved - Ready for recovery |
| Expression of the human BCL2 transgene in both T cell and B cell lineages. This transgenic line combines the characteristics of both Tg(BCL2)22Wehi and the Tg(BCL2)25Wehi lines. Hemizygotes show increased numbers of B lymphocytes, Ig-secreting cells and serum Ig, as well as a heightened and prolonged antibody response to immunization. T-cells withstand prolonged culture in the absence of growth factors and are resistant to killing by gamma-radiation, glucocorticoids, ionomycin, PMA and sodium azide but NOT complement, cytotoxic T cells, or Fas ligand. Hemizygotes have a normal total T-cell count and thymic involution rate but show an enhanced response to immunization. These mice serve as a robust source for the production of B-cells, antibodies T-cell lines or hybridomas. Although mice bearing this allele exhibit a mild increase in spontaneous lymphoma and plasmacytoma occurrence (<10% to 18 months) on a (C57BL/6 x SJL)F2 background, on the BALB/c and C57BL/6 backgrounds tumor incid ..... For more information please see the full phenotype on the strain data sheet | ||
| 006329 | B6;129-Baxtm2Sjk Bak1tm1Thsn/J | Cryopreserved - Ready for recovery |
| 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 ( ..... | ||
| 004264 | B6;129-Cycstm1Wlm/J | Cryopreserved - Ready for recovery |
| 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 | 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 | ||
| 008452 | B6;129-Eif2ak4tm1.1Dron/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the GCN2.KO4conditional allele (also called GCN2.KO4c) are viable and fertile, with loxP sites flanking exon XII of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (containing amino acid residues 606-648 encoding the critical lysine 618 required for kinase activity) deleted in the cre-expressing tissue(s). GCN2 is a protein kinase that phosphorylates eIF2 (eukaryotic initiation factor 2) in response to environmental stresses (amino acid starvation, proteasome inhibition and UV irradiation) resulting in a reduction of global translation and activation of stress-related transcription factors (such as NF-kappaB). These GCN2.KO4conditional mice may be useful in studies related to eIF2 phosphorylation in response to environmental stresses. Of note, mice with a traditional "knockout" (deletion of exon XII) are also available (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 006088 | B6;129-Mcl1tm3Sjk/J | Cryopreserved - Ready for recovery |
| 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 ..... | ||
| 006980 | B6;129-Trp53tm2Xu/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. They carry two phosphorylation site disruptions: Ser18 to Ala (S18A), and Ser23 to Ala (S23A). Trp53-dependent apoptosis is essentially abolished in thymocytes. These mice develop spontaneous tumors at approximately 1.5 years of age and a range of malignancies that are distinct from those found in animals carrying either a single S23A mutation or a complete knockout of the gene. This mutant mouse strain may be useful in studies of phosphorylation events in cancer development and apoptosis. | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... 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. | ||
| 008191 | B6;129S2-Trp53tm1Tyj Nf1tm1Tyj/J | Cryopreserved - Ready for recovery |
| These mice carry Trp53 and Nf1 targeted mutations (in cis) on chromosome 11. These mutations are approximately 10 Mbp apart and may segregate independently of one another. Double homozygotes are embryonic lethal. Double heterozygotes survive an average of five months and exhibit a significant increase in the percentage of soft tissue sarcomas compared with mice of other genotypes (Nf1 +/-, 5%; p53, 57%; Nf1/Trp53 trans, 36%; Nf1/Trp53 cis, 81%). Furthermore, although Nf1/Trp53 trans mice exclusively develop osteo-, fibro-, rhabdomyo-, and hemangiosarcomas, about 30% of tumors from the Nf1/Trp53 cis animals stain positively for S100 (consistent with glial cell origin) and exhibit classic histological features of malignant peripheral nerve sheath tumors (MPNSTs). This strain may be useful in studies of astrocytomas/glioblastomas and tumor suppressor genes. | ||
| 002103 | B6;129S2-Trp53tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 002968 | B6;129S7-Mdm2tm1Bay/J | Cryopreserved - Ready for recovery |
| Mice homozygous for a null mutation in Mdm2 die early in gestation, but are rescued in the absence of Trp53. Mdm2/Trp53-double null mice share the same phenotype as Trp53 mice. | ||
| 003240 | B6;B10.A-H2a-Tg(H2KmPCC)2939Stoe/J | Cryopreserved - Ready for recovery |
| PCC transgenic mice are viable and fertile. Pigeon cytochrome c was engineered for expression in lymphoid tissues of transgenic mice in two forms: one in which it is expressed as a type II plasma membrane protein (mPCC), and a second in which it was targeted to the mitochondria after cytoplasmic synthesis (ePCC). This strain carries the mPCC construct. (For mice carrying the ePCC construct, see strain 003221.) PCC is expressed in thymus, spleen and LPS stimulated B cells in both strains of mice. mRNA expression levels are higher in mPCC mice than in ePCC mice. However, tolerance is induced in the thymus of both strains, regardless of antigen compartmentation. | ||
| 008080 | B6;C3-Tg(CAG-SAC/EGFP)35Rang/J | Cryopreserved - Ready for recovery |
| Hemizygous SAC transgenic mice have normal fertility, viability, and aging. Widespread expression of the transgene is observed in all tested tissues (with some differential tissue-specific regulation of transgene expression or protein stability reported). The SAC-GFP fusion protein is composed of the cancer-specific proapoptotic effector domain (or SAC domain) of the Par-4 gene fused to an enhanced green fluorescent protein (EGFP). As a result, SAC-GFP transgenic mice have increased resistance to spontaneous liver/spleen and TRAMP-induced prostate tumor development. The protective nature of the transgene appears to be linked to inhibition of NF-kappaB activity and induction of apoptosis. Cells derived from SAC transgenic mice grow normally in short-term culture and presence of the SAC transgene prevents oncogene-mediated cellular transformation. The donating investigator reports that EGFP expression is appropriate for immunoblots, but not sufficient enough for fluorescence of flow cyto ..... For more information please see the full phenotype on the strain data sheet | ||
| 004187 | B6;SJL-Tg(MCL1)8Caig/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the human MCL1 under the direction of the human MCL1 promoter. Expression of the human MCL1 protein was immunodetectable. Mice hemizygous for the transgene exhibited human MCL1 in bone marrow, lymph node, thymus and spleen (both B- and T-cell populations). Low levels of transgene expression was found in kidney, small intestine, uterus, lung and liver. The majority of the transgenic mice had enlarged spleens, with an increased total splenocyte number (both B- and T-cell). Transgenic mice displayed an increase of myeloid cells relative to lymphoid cells in bone marrow, and an enhanced viability of hematopoietic and lymphoid cells (B, T and myeloid) at immature and mature stages of development. In transgenic mice from 6 to 11 months of age, 27% displayed lymph node enlargement. Transgenic mice had an 88% probability of developing pathologic lymph node disease, and a 60% probability of developing disseminated disease from 6 months to 2 years of a ..... For more information please see the full phenotype on the strain data sheet | ||
| 009685 | B6N.129S1(Cg)-Tnkstm1.1Yjc/J | Cryopreserved - Ready for recovery |
| Homozygous (TANK1-/-) mice are viable and fertile with no reported developmental or gross physical abnormalities. As exon 1 is deleted from the targeted allele, no full length protein (TANK1) is detected in thymus, testis or spleen tissues. Because the deletion does not encompass the potential alternative promoter between exons 4-5, an alternative transcript and subsequent low molecular weight protein (TANK1a) is expressed in testis (but not in other assayed tissues). These TANK1-mutant mice may be useful for studying the post-translational modification of proteins associated with cell cycle, mitosis, telomere length maintenance/aging, DNA replication/repair, cellular senescence, apoptosis, tumorigenesis, vesicle trafficking, and insulin responses. These TANK1-mutant mice may also be used along with TANK2-mutant mice (Stock No. 006200). | ||
| 003221 | BALB/cAnBr-Tg(H2KePCC)2403Stoe/J | Cryopreserved - Ready for recovery |
| PCC transgenic mice are viable and fertile. Pigeon cytochrome c was engineered for expression in lymphoid tissues of transgenic mice in two forms: one in which it is expressed as a type II plasma membrane protein (mPCC), and a second in which it was targeted to the mitochondria after cytoplasmic synthesis (ePCC). This strain carries the ePCC construct. (For mice carrying the ePCC construct, see strain 003240). PCC is expressed in thymus, spleen and LPS stimulated B cells in both strains of mice. mRNA expression levels are higher in mPCC mice than in ePCC mice. However, tolerance is induced in the thymus of both strains, regardless of antigen compartmentation. | ||
| 002526 | C.129S2(B6)-Trp53tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomaa) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. 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 the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008074 | C.129S4-Traf1tm1Tsi/TsiPryhJ | Cryopreserved - Ready for recovery |
| 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 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 elicit enhanced Th2 responses in vivo. BALB/c-TRAF1-/- T cells exhibit elevated nuclear expression of NFAT-interacting protein (NIP45) and also induce significantly more intense pulmonary inflammation and higher airway hyper-responsiveness in OVA allergic inflammation models. Pulmonary leukocyte recruitment is attenuated following inhalation of lipopolysaccharide in BALB/c-TRAF1-/- mice. Homozygous mice on a C57BL/6 congenic background ( ..... | ||
| 002427 | C3H/He-Tg(LCKprBCL2)36Sjk/J | Cryopreserved - Ready for recovery |
| Hemizygotes carrying the human LCKprBCL2 transgene display normal architecture of all lymphoid organs to 10 weeks of age. They show an increased percentage of CD3hi/TCRhi and CD4-8+ thymocytes with a decreased percentage in CD3lo T cells. CD8+ cells and the total percentage of T cells are increased in the spleen and lymph nodes. Mice are resistant to apoptosis induced by glucocorticoid treatment, by radiation treatment, or by anti-CD3 treatment. Malignant lymphoma develop in hemizygotes at approximately 18 months of age. | ||
| 002547 | C3Ou.129S2(B6)-Trp53tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 002546 | C3Ou.129S2-Rb1tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 described. We will modify the strain description if necessary as published results become available. | ||
| 010800 | C57BL/6-Tg(Thy1-PTGS2)300Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These moderate overexpressing C57BL/6J COX-2 transgenic line 300 mice have PGE2 levels that are ~10-12-fold greater than non-transgenic controls (compared to ~25-40-fold overexpression in line 303; see Stock No. 010703). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic m ..... For more information please see the full phenotype on the strain data sheet | ||
| 010703 | C57BL/6-Tg(Thy1-PTGS2)303Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. 010800). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhib ..... For more information please see the full phenotype on the strain data sheet | ||
| 002900 | FVB.129S2(B6)-Rb1tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. 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 described. We will modify the strain description if necessary as published results become available. | ||
| 002899 | FVB.129S2(B6)-Trp53tm1Tyj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Trp53tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and sarcomas) at 3-6 months of age. Heterozygous mice develop tumors at about 10 months of age. These mice model some of the features of human Li-Fraumeni syndrome, a form of familial breast cancer with mutations in TRP53. Homozygous mice may produce a litter before succumbing to tumors. | ||
| 006085 | STOCK Rad9tm1Lieb/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 004510 | STOCK Rom1tm1Mci/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 014547 | FVB/N-Tg(tetO-Fasl)BDepa/J | Under Development - Now Accepting Orders |
| Mice hemizygous for the (tetOp)7-FasL transgene (TetOp-FasL transgenic mice) are viable and fertile with no reported phenotypic abnormalities. The (tetOp)7-FasL transgene has the Tet response element (TRE or tetO) upstream of a murine Fas ligand (FasL) coding sequence. When bred with other mice expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), FasL overexpression in the resulting double mutant offspring can be regulated with tetracycline or its analog doxycycline (dox). FasL overexpression leads to Fas/FasL receptor-mediated death-signaling pathway activation and results in cell apoptosis.
The donating investigator reports that transgenic mice from founder line B (TetOp-FasL transgenic line B) exhibit very high FasL overexpression levels in the presence of rtTA and 0.01 mg/ml Dox (low FasL levels are achievable by titrating Dox even lower). The donating investigator rep ..... For more information please see the full phenotype on the strain data sheet | ||
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