JAX Mice Database - Endogenous Regulators

Search Criteria: Research Area is "Apoptosis Research: Endogenous Regulators"

JAX^® Mice Strains

Stock Number	Strain Name Phenotype	Standard Supply
002101	B6.129S2-Trp53^tm1Tyj/J	Level 4
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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.
006050	129-Sirt6^tm1Fwa/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-Parp1^tm1Zqw/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)-Rorc^tm2Litt/J	Repository- Live
	Mice homozygous for this Rorc(gt^GFP (or RORgt)^GFP) mutant allele are viable and fertile. While Rorcg mRNA is detected in liver in Rorc(g)t^GFP 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-Ddit3^tm1Dron/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-Bcl2l11^tm1.1Ast/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-Casp3^tm1Flv/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-Thbs1^tm1Hyn/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
006440	B6.129S4-Pten^tm1Hwu/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-Traf1^tm1Tsi/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, Bim_s. 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 ..... For more information please see the full phenotype on the strain data sheet
006236	B6.129S6-Casp6^tm1Flv/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-Casp7^tm1Flv/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.
002994	B6.129X1-Bax^tm1Sjk/J	Repository- Live
	Mice homozygous for the Bax^tm1Sjk 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-Bak1^tm1Thsn/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. *Coat color of Bax^tm1Sjk* mice** The coat color loci tyrosinase (Tyr) and pink-eyed dilution (p) are linked to the Bcl2-associated X pr ..... For more information please see the full phenotype on the strain data sheet
006329	B6;129-Bax^tm2Sjk Bak1^tm1Thsn/J	Repository- Live
	Mice homozygous for both alleles (Bax^fl 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 ( ..... For more information please see the full phenotype on the strain data sheet
008045	B6;129-Trp53^tm2Holl/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-Trp53^tm1Holl/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
006980	B6;129-Trp53^tm2Xu/J	Repository- Live
	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.
002785	B6;129S4-E2f1^tm1Meg/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 A^w-J/A-Aifm1^Hq/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
004597	C;129S4-Pten^tm1Hwu/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 Pten^tm1Hwu/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 Rom1^tm1Mci/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-Trp53^tm1Holl/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
002080	129-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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-Rb1^tm1Tyj/J	Repository-Cryopreserved
	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.
003082	129S1/SvImJ-Bcl2^tm1Mpin/J	Repository-Cryopreserved
	Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2^tm1Mpin 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 Bcl2^tm1Sjk targeted mutation (Stock No. 002265).
003079	B6.129-Calb1^tm1Mpin/J	Repository-Cryopreserved
	Mice homozygous for the Calb1^tm1Mpin 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.
004322	B6.129S1-Mapk10^tm1Flv/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. 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-Mad2l1^tm1Sorg/J	Repository-Cryopreserved
	Mice that are heterozygous for the Mad2l1^tm1Sorg 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-Rb1^tm1Tyj/J	Repository-Cryopreserved
	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.
004069	B6.129S6-Crebbp^tm1Dli/J	Repository-Cryopreserved
	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.
006072	B6.129X1-Mcl1^tm2Sjk/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 ..... For more information please see the full phenotype on the strain data sheet
004853	B6.C3-Tg(KRT14-Birc5)19Gros/J	Repository-Cryopreserved
	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.
002319	B6.Cg-Tg(BCL2)22Wehi/J	Repository-Cryopreserved
	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	Repository-Cryopreserved
	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	Repository-Cryopreserved
	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
004264	B6;129-Cycs^tm1Wlm/J	Repository-Cryopreserved
	Mice homozygous for the Cycs^tm1Wlm 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-E2f2^tm1Zubi/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-Mcl1^tm3Sjk/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 ..... For more information please see the full phenotype on the strain data sheet
002265	B6;129S2-Bcl2^tm1Sjk/J	Repository-Cryopreserved
	Mice homozygous for the Bcl2^tm1Sjk 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.
002103	B6;129S2-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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-Mdm2^tm1Bay/J	Repository-Cryopreserved
	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-H2^a-Tg(H2KmPCC)2939Stoe/J	Repository-Cryopreserved
	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.
004187	B6;SJL-Tg(MCL1)8Caig/J	Repository-Cryopreserved
	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
003221	BALB/cAnBr-Tg(H2KePCC)2403Stoe/J	Repository-Cryopreserved
	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)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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.
002318	C.Cg-Tg(BCL2)22Wehi/J	Repository-Cryopreserved
	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
002427	C3H/He-Tg(LCKprBCL2)36Sjk/J	Repository-Cryopreserved
	Hemizygotes carrying the human LCKprBCL2 transgene display normal architecture of all lymphoid organs to 10 weeks of age. They show an increased percentage of CD3^hi/TCR^hi and CD4^-8⁺ thymocytes with a decreased percentage in CD3^lo 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)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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-Rb1^tm1Tyj/J	Repository-Cryopreserved
	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.
002900	FVB.129S2(B6)-Rb1^tm1Tyj/J	Repository-Cryopreserved
	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)-Trp53^tm1Tyj/J	Repository-Cryopreserved
	Mice homozygous for the Trp53^tm1Tyj mutation show no visible phenotype but most develop tumors (principally lymphomas and osteosarcoma) 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.
002659	FVB/N-Tg(Trp53R172H)8512Jmr/J	Repository-Cryopreserved
	The FVB/NTgN(Trp53R172H)8512Jmr express TRP53 with both dominant-negative and a gain-of function properties, i.e. this mutant is capable of inducing multiple drug resistance(MDR) promoter-driven reporter gene expression in transfection studies performed in p53 null cells. Transgene expression alone exerts no apparent effect on normal mammary gland development. Mice treated with the chemical carcinogen, dimethylbenz(a)anthracine (DMBA) or crossed with mice overexpressing erb-B2 develop tumors with significantly shorter latencies than controls. These tumors are characterized by large pleiomorphic nuclei and genomic instability. Spontaneous tumors are rarely observed in multiply bred animals in the first year of life.
002660	FVB/N-Tg(Trp53R172L)4491Jmr/J	Repository-Cryopreserved
	The FVB/N-TgN(Trp53R172L)4491Jmr express TRP53 with pseudo-wildtype properties capable of inducing p21 and mdm-2 expression. Lobuloalveolar development is altered and apoptosis is increased during late pregnancy. The few normal lobules observed during early lactation did not express the Trp53 transgene suggesting that they arose by clonal expansion of cells not expressing the transgene during mid-pregnancy. Transgenic mice fail to lactate. There is no apparent alteration in ductal development. Mice expressing a dominant negative 172Arg-His mutation do not exhibit any detectable alterations in mammary gland development and have a very low incidence of spontaneous mammary tumors. Mice bearing the 172Arg-Leu transgene and a pituitary isograft displayed a marked increase in apoptosis and a significant delay in DMBA-induced tumorigenesis, while those bearing the 172Arg-His dominant negative p53 transgene were more susceptible to DMBA-induced tumorigenesis.
006085	STOCK Rad9^tm1Lieb/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.
003262	STOCK Tg(Trp53A135V)L3Ber/J	Repository-Cryopreserved
	Mice homozygous for the (Trp53A135V)2Ber transgene are viable and fertile, but show a high incidence of tumors, particularly lung adenocarcinomas, osteosarcomas, and lymphomas. This strain may serve as a model for Li-Fraumeni syndrome.

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New Strains Under Development

(See informational text following listing of strains)

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.

Stock Number	Strain Name Phenotype	Standard Supply
008240	B6.129S6-Eif2ak4^tm1Munn/J	Under Development for Production
Mice homozygous for the GCN2.KO4 mutant locus (also called GCN2.KO4^-, GCN2^-, GCN2.KO4^ex, 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 or cell biology research. Of note, mice with a conditional allele (loxP-flanked exon XII) are also ava ..... For more information please see the full phenotype on the strain data sheet
007218	B6.129S6-Trp53^tm2Xu/J	Under Development for Production
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.
007962	B6.FVB-Tg(MMTV-neu/OT-I/OT-II)CBnel Tg(Trp53R172H)8512Jmr/J	Under Development for Production
These compound transgenic mice carry a rat Erbb2/HER-2/neu oncogene tagged with ovalbumin epitopes OT-I and OT-II, which are recognized by T cell receptors, under the control of the MMTV promoter (termed fusion protein neu^OT-I/OT-II). In addition, this strain carries a mouse Trp53 mini-gene, harboring a G to A point mutation in codon 172 (changing Arg to His; R172H) driven by the rat whey acidic protein promoter. Approximately 85% of compound mutant females develop focal mammary tumors at 6-10 months of age. Both virgin and breeder mice develop tumors. Approximately 37% of tumor-bearing mice develop metastatic disease to the lung. High expression of neu is detected in tumor tissue while very low levels are found in lung and ovary. Female mice carrying only the neu^OT-I/OT-II mutation develop focal mammary tumors at approximately 18 months of age. This strain may be useful in studies of cancer immunotherapy.
008080	B6;C3-Tg(CAG-SAC/EGFP)35Rang/J	Under Development for Production
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
008074	C.129S4-Traf1^tm1Tsi/J	Under Development for Production
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 ( ..... For more information please see the full phenotype on the strain data sheet
008232	FVB/N-Tg(Ins2-IAPP)RHFSoel/J	Under Development for Production
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
008452	STOCK Eif2ak4^tm1Dron/J	Under Development for Production
Mice homozygous for the GCN2.KO4^conditional 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.KO4^conditional 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

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New Strains Under Development
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The 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.
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"
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These strains are designated as: "Under Development for Cryopreservation Repository"
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.
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