Search Criteria: Research Area is "Research Tools: lacZ Expression"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 003474 | B6.129S4-Gt(ROSA)26Sortm1Sor/J | Level 4 |
| Homozygous mice are viable and fertile, with a loxP-flanked DNA STOP sequence preventing expression of the downstream lacZ gene. When crossed with a cre transgenic strain, the STOP sequence is removed and lacZ is expressed in cells/tissues where cre is expressed. These mutant mice may be used as a Cre-reporter strain; to test the tissue/cellular expression pattern of cre transgenic mice. | ||
| 002292 | 129-Gt(ROSA)26Sor/J | Repository- Live |
| Mice heterozygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. Formerly named TgR(ROSA26)26Sor. | ||
| 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 | ||
| 004545 | 129S-Npytm1Rpa/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 brain or adrenal gland tissue. Beta-galactosidase activity assays and in situ hybridization demonstrate similar expression patterns for the lacZ gene and the endogenous wildtype gene. Spontaneous seizures are exhibited by some mice at age 6 to 8 weeks. Homozygous mice are susceptible to seizures induced by GABA antagonist treatment. Mutant mice have an increased sensitivity to leptin treatment which results in a greater initial reduction of food intake and weight loss when compared to wildtype mice. This mutant mouse strain may be useful in studies related to the role of neuropeptide Y in obesity. | ||
| 007199 | 129S-Sgpl1Gt(ROSA)78Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote
..... For more information please see the full phenotype on the strain data sheet | ||
| 004178 | B6.129(Cg)-Tg(CAG-Bgeo/GFP)21Lbe/J | Repository- Live |
| These Z/EG transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being liver and lung tissue. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with enhanced GFP expression in tissues expressing Cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess Cre excision activity in live animals and cells.
As an example, when crossed to a strain expressing Cre recombinase in olfactory sensory neurons (see Stock No. 006668), this mutant mouse strain may be useful in lineage tracing. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved t
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| 006939 | B6.129-Fut1tm1Sdo/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. Alpha(1,2)fucosylated glycans are not detected in the epididymis of homozygotes. Fucosylated glycolipids (fucosyl GA1) are not detected in the pancreatic acinar glands of homozygotes. Homozygotes exhibit delayed maturation of nerve fibers in the glomerular layer of the olfactory bulb due to absence of cell surface carbohydrate, blood group H carbohydrate, expression in primary sensory neurons. The Donating Investigator reports that the beta-galatosidase is expressed. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, and olfactory nerve pathway development. This strain was transferred from the collection of the Consortium for Functional Glycomics. | ||
| 006497 | B6.129-Skiltm2Spw/J | Repository- Live |
| Mice homozygous for this targeted mutation (called "Snoex1" in the primary reference) are viable and fertile with no reported gross morphological defects. Although the deletion of exon 1 leads to complete absence of the mature full-length protein in immunoblots of brain and embryonic tissues, a truncated 3'-end RNA species is derived from downstream coding sequence. Homozygotes exhibit T cell proliferation/activation defects, which can be rescued by treatment with anti-TGF-beta antibodies or exogenous interleukin-2. Homozygous deletion also results in increased sensitivity to TGF-beta and altered growth properties of cultured mouse embryo fibroblasts (MEFs). These mutant mice may be useful in studies of T cell activation, T cell receptor stimulation and TGF-beta signaling. | ||
| 005775 | B6.129P2-Adipor2tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005793 | B6.129P2-Ccr6tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005794 | B6.129P2-Ccr7tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005796 | B6.129P2-Cxcr3tm1Dgen/J | Repository- Live |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 002192 | B6.129S7-Gt(ROSA)26Sor/J | Repository- Live |
| Mice heterozygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. | ||
| 006262 | B6.129X1-Fut2tm1Sdo/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. Homozygous mice have a chinchilla (gray) coat color, while heterozygotes have the typical black coat color expected for the C57BL/6J genetic background. Alpha (1,2) fucosylated glycans are not detected in the uterine epithelia from homozygotes at estrus. Beta galactosidase staining is detected in endocervial and uterine gland mucus secreting cells, stomach foveolar pit cells and chief cells, and colon goblet cells. The pattern of beta galactosidase activity mimics the endogenous expression pattern of the endogenous gene. This mutant mouse strain represents a model of the nonsecretor ABH histo-blood group antigen, which confers resistance to Norwalk virus infection, and may be useful in studies of reproductive biology, gastrointestinal tract epithelium, and the function of fucosylated glycans.
This strain was transferred fr ..... For more information please see the full phenotype on the strain data sheet | ||
| 005085 | B6.Cg-Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
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| 005317 | B6.Cg-Tg(BAT-lacZ)3Picc/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These "BAT-GAL" transgenic mice are a reporter strain that express beta-galactosidase in the presence of activated beta-catenin. The transgene expresses the lacZ gene under the control of a regulatory sequence consisting of seven consensus LEF/TCF-binding motifs upstream of the Xenopus siamois gene minimal promoter. Transgenic mice display beta-galactosidase activity beginning at embryonic day 6.0 in the posterior side of the proximal epiblast. Beta-galactosidase expression is detectable in the posterior primitive streak and node at gastrulation, and progresses to the paraxial mesoderm and notochord. Beta-galactosidase activity in developing and adult nervous tissue mimics the pattern of Wnt signaling. When bred to other mutant strains, this reporter strain may be useful for identifying mutations that affect the Wnt-signalling pa
..... For more information please see the full phenotype on the strain data sheet | ||
| 006055 | B6.Cg-Tg(CAG-Bgeo,-DsRed*MST)1Nagy/J | Repository- Live |
| While mice hemizygous for this Z/RED transgene (on an outbred genetic background, see Stock No. 005438) are reported to be viable and fertile, it has been our experience at The Jackson Laboratory that hemizygous animals are often smaller than littermates and subject to postnatal mortality. Delayed weaning greatly enhances the survival. Although homozygous animals are born, animals have not survived past 5 weeks of age. These transgenic mice express beta-galactosidase (lacZ) under the control of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) immediate early enhancer. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with red fluorescent protein (DsRed*MST) expression in tissues expressing Cre recombinase. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to
..... For more information please see the full phenotype on the strain data sheet | ||
| 006229 | B6.Cg-Tg(DRE-lacZ)2Gswz/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo. | ||
| 003504 | B6;129-Gt(ROSA)26Sortm1Sho/J | Repository- Live |
| Mice with the Gtrosa26tm1Sho targeted mutation are similar to the B6;129-Gtrosa26tm1Sor from Dr. Philippe Soriano, but reported in the literature to be an improved reporter strain for monitoring cre-mediated excisions. The B-galactosidase-neomycin phosphotransferase fusion gene (Bgeo)-trapped reverse orientation splice acceptor Bgeo line 26 (ROSA26) locus was modified by gene targeting such that Bgeo is expressed only after Cre-mediated excision of loxP-flanked DNA sequences. Bgeo from the excised ROSA26 allele is expressed ubiquitously in embryos and adult mice. When mating the reporter strain with cre-expressing transgenic mice, one can see that the loxP-flanked ROSA26 allele is accessible to cre during early embryogenesis, as well as in a specific hematopoietic lineage (T lymphocytes). These mice may prove useful in the study of cell fate and cell migration during embryogenesis through recombinase-activated taggi
..... For more information please see the full phenotype on the strain data sheet | ||
| 006251 | B6;129-Tor1atm1Wtd/J | Repository- Live |
| Homozygous mutant mice have a perinatal lethal phenotype. They fail to feed or vocalize at birth, and typically die within 48 hours. No protein is detected by immunoblot analysis in tissues (liver, brain, spinal cord, mouse embryonic fibroblasts (MEFs)) from homozygous mutant animals. Microscopic and ultrastructural examination of central nervous system neurons from embryonic day 18 homozygous embryos reveals abnormalities including dysmorphic ventral horn neuron nuclei, vesicles in the neuronal nuclear envelope and enlarged endoplasmic reticulum. Neurons within homozygotes appear normal when migrating, but develop nuclear membrane abnormalities upon maturation.
In contrast to homozygous mutant mice, heterozygotes are viable, fertile, normal in size, and do not manifest any gross physical or behavioral abnormalities. Torsin A (TOR1A) protein levels in heterozygous mice are approximately 50% of wildtype levels. This mutant mouse strain may be useful in studies of torsion dystonia 1
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| 002073 | B6;129S-Gt(ROSA)26Sor/J | Repository- Live |
| Mice hemizygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Repository- Live |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 006958 | B6;129S-Nkd1tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd1lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. Northern blot of lung tissue, as well as western blot of embryonic tissue, confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-b-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/b-catenin signaling, these nkd1lacZ mutant mice (as well as the similar nkd2lacZ mutant strain; Stock No. 006960) may be useful as a reporter for Wnt/b-catenin-dependent transcriptional activity during embryonic development or in adult
..... For more information please see the full phenotype on the strain data sheet | ||
| 006960 | B6;129S-Nkd2tm1Kwha/J | Repository- Live |
| Mice homozygous for this nkd2lacZ mutant allele are viable and fertile with slightly reduced mean litter sizes. RT-PCR analysis of homozygous brain tissue confirms that the deleted exons (encoding the Dvl-binding domain) are not expressed in homozygous mutants. However, the endogenous promoter directs expression of the internal ribosome entry site-b-galactosidase (IRES-lacZ) fusion gene in a manner that closely mimics the patterns of the endogenous gene mRNAs. Because the naked cuticle (NKD) genes are considered targets for Wnt/b-catenin signaling, these nkd2lacZ mutant mice (as well as the similar nkd1lacZ mutant strain; Stock No. 006958) may be useful as a reporter for Wnt/b-catenin-dependent transcriptional activity during embryonic development or in adult mice. | ||
| 007204 | B6;129S4-2610005L07RikGt(ROSA)73Sor/J | Repository- Live |
| Mice homozygous for this mutant allele (called BC058969 in the primary publication) are viable and fertile, with greater than 50% embryonic lethality observed in homozygous embryos. Homozygotes occur at a lower than Mendelian ratio (9%) from heterozygote x heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects (sternum and calvarial bones). Notably, 100% incidence of calvarial bones defects is reported. Additionally, homozygotes are reported to have low b-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These BC058969-mutant (2610005L07Rik-mutant) mice may be useful in st
..... For more information please see the full phenotype on the strain data sheet | ||
| 006044 | B6;129S7-Ephb4tm1And/J | Repository- Live |
| Mice homozygous for this targeted mutation show growth retardation and lack of blood flow by embryonic day 9.5-10 (E9.5-10), with lethality occurring around this time. Expression of lacZ occurs exclusively in embryonic vascular endothelial cells and is preferentially expressed on veins. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Arrested cardiac morphogenesis and defective myocardial trabecular extensions are also observed. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation
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| 006465 | B6;CBA-Tg(CAG-lacZ-WGA)330Bbm/J | Repository- Live |
| These ZW transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread, but mosaic, throughout the central and peripheral nervous systems. Purkinje cells display intense beta-galactosidase activity. Approximately 50% of the total neuron population express the transgene, as detected by beta-galactosidase activity. Newborn mice exhibit widespread beta-galactosidase activity. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with wheat germ agglutinin (plant lectin) expression in tissues expressing cre. The double reporter system makes it possible to distinguish a lack of reporter (lacZ) expression from a lack of Cre recombinase expression while providing a means to assess Cre excision activity at the individual cell level. This transgenic mouse strain may be useful in tracing transneuronal or trans-synaptic connections and circuits in brain regions or in the s
..... For more information please see the full phenotype on the strain data sheet | ||
| 006672 | B6;CBA-Tg(Olfr16*,taulacZ)7Mom/MomJ | Repository- Live |
| 006214 | FVB.Cg-Smn1tm1Msd/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Beta-galactosidase staining is found in oocytes of pregnant heterozygous females. Homozygous mice have an early embryonic lethal phenotype, failing to form a blastocoel cavity and do not implant. Abnormal development is observed by 80 hours post conception. By 90 to 100 hours post conception there is massive cellular degeneration and apoptotic cell death. This mutant mouse strain may be useful in studies of spinal muscular atrophy. | ||
| 005024 | FVB.Cg-Tg(SMN2)89Ahmb Smn1tm1Msd/J | Repository- Live |
| Mice that are homozygous for the targeted mutant Smn1 allele and carry the SMN2 transgene exhibit symptoms and neuropathology similar to patients afflicted with type I proximal spinal muscular atrophy (SMA). In the initial characterization by the donating investigator, mice were either stillborn or survived 4-6 days. Mice that died at or shortly after birth were slightly smaller (1.33 g. vs. 1.51 g.) than normal littermates. Mice that survive for several days are indistinguishable from normal littermates in the first 48 hours, after which they exhibit decreased suckling and movement, labored breathing and tremoring limbs. Mice succumbing at this later time point are noticeably smaller than normal littermates (1.47 g vs. 4.59). A bell-shaped trunk is also noticeable in affected mice, presumably from intercostal muscle weakness, a characteristic of type I SMA. Histological analysis indicates that affected mice that survive to day 5 exhibit a loss of motor neurons from spina
..... For more information please see the full phenotype on the strain data sheet | ||
| 005026 | FVB.Cg-Tg(SMN2)89Ahmb Tg(SMN1*A2G)2023Ahmb Smn1tm1Msd/J | Repository- Live |
| Mice that are homozygous for the targeted mutant Smn allele and homozygous for the SMN2transgene and hemizygous for the SMN1*A2G transgenes exhibit symptoms and neuropathology similar to patients afflicted with type III (mild) proximal spinal muscular atrophy (SMA). These same animals with only one copy of the SMN2transgene are 20%-40% smaller than unaffected mice. At 3 weeks of age they become less active and show signs of muscle weakness. The mice have a shortened lifespan (less than a year) near the end of which they exhibit reduced movement, diminished grooming, shallow breathing and considerable weight loss. Immunohistochemical analysis of spinal cord tissue from 1 month-old animals indicates the presence of cytoplasmic SMN protein and intranuclear aggregates (gems) of the SMN protein. The number of gems is however, fewer than the number found in age matched control tissues. Histological analysis of muscle tissue (gastrocnemius, quadriceps, and intercostals mu
..... For more information please see the full phenotype on the strain data sheet | ||
| 005025 | FVB.Cg-Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb Smn1tm1Msd/J | Repository- Live |
| This triple mutant mouse harbors two transgenic alleles and a single targeted mutant. The Tg(SMN2*delta7)4299Ahmb allele consists of a SMA cDNA lacking exon 7 whereas the Tg(SMN2)89Ahmb allele consists of the entire human SMN2 gene. Mice that are homozygous for the targeted mutant Smn allele and homozygous for the two transgenic alleles exhibit symptoms and neuropathology similar to patients afflicted with proximal spinal muscular atrophy (SMA). At birth, triple mutants are noticeably smaller than normal littermates. By day 5, signs of muscle weakness are apparent and become progressively more pronounced over the following week as the mice display an abnormal gait, shakiness in the hind limbs and a tendency to fall over. Mean survival is approximately 13 days. Immunocytochemical analysis indicates that dystrophin expression is normal, however fibers isolated from the gastrocnemius muscle of a 14 day old triple mutant clearly show evidence of atrophy. Importation
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| 002856 | FVB/N-Tg(TIE2-lacZ)182Sato/J | Repository- Live |
| Transgenic mice carry a beta-galactosidase reporter gene under the control of the murine Tek (Tie2) promoter. LacZ is expressed specifically in vascular endothelial cells in embryonic and adult mice. The transgenic line may be useful when crossed with tumor producing strains and the transgene used to visualize neovascularization during tumorigenesis. | ||
| 005878 | NOD.Cg-Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. 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 f
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| 003899 | STOCK Cd44tm1Hbg/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. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. | ||
| 006578 | STOCK Myoz2tm1Eno/J | Repository- Live |
| Mice homozygous for this calsarcin-1 mutant allele are viable and fertile. Immunoblot of homozygous cardiac tissue shows no endogenous protein expression. Strong lacZ expression throughout all cardiac chambers mirrors the expression pattern of the endogenous gene, and marked skeletal muscles known to contain a high proportion of type I (slow) fibers. Homozygotes have skeletal muscle abnormalities in type I (slow) fibers and calcineurin activity. Echocardiography of homozygous mice reveals abnormal heart performance. Absence of gene function activates a cardiac hypertrophic fetal gene program (despite the absence of hypertrophy) and enhanced the cardiac growth response to pressure overload. These mutant mice may be useful in studying growth and gene expression of cardiac and skeletal muscle, as well as the pathogenesis of human cardiomyopathies. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic bac
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| 006882 | STOCK Tg(CAG-Bgeo,-AML1/ETO,-ALPP)1Lbe/J | Repository- Live |
| Mice hemizygous for this "Z/AP-AML1-ETO" transgene (coding for the translocation t(8;21) present in 15% of acute myeloid leukemias (AML)) are viable and fertile. Homozygotes die in utero presumably due to high lacZ expression. Prior to cre-mediated excision of the "floxed" STOP sequence, expression of lacZ is observed in all tissues including bone marrow progenitor cells. When bred to Cre recombinase expressing mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human AML1-ETO fusion protein and placental alkaline phosphatase (ALPP or PLAP) to proceed in the Cre recombinase expressing cells. While pan expression of AML1-ETO leads to embryonic lethality (E7.5), hematopoietic and endothelial expression leads to malignancy in B- and T- lymphoid cells and secondary mutations that closely resemble the association of AML1-ETO with acute myeloid leukemia in humans. These transgenic mice may
..... For more information please see the full phenotype on the strain data sheet | ||
| 006850 | STOCK Tg(CAG-Bgeo,-NOTCH1,-EGFP)1Lbe/J | Repository- Live |
| Mice hemizygous for this Cre-conditional IC-Notch (or Z/EG-Notch) transgene are viable and fertile. Homozygotes die in utero, presumably due to high lacZ expression. Prior to Cre-mediated excision of the "floxed" STOP sequence, high expression of lacZ is observed in cells and tissues. When bred to Cre recombinase expressing mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the intracellular human NOTCH1 (IC-Notch) and EGFP to proceed in the Cre recombinase expressing cells. For example, endothelial expression of IC-Notch using different Cre-transgenic matings is associated with neural, somite and angiogenic defects, infertility in females, and embryonic lethality in the resulting offspring. These transgenic mice may be useful for global expression of lacZ or, when crossed to a Cre recombinase expressing strain, for studying the role of Notch signaling during both embryonic develo
..... For more information please see the full phenotype on the strain data sheet | ||
| 006876 | STOCK Tg(CAG-Bgeo,-TEL/AML1,-EGFP)A6Lbe/J | Repository- Live |
| Mice hemizygous for this Cre-conditional TEL-AML1 (or iZ/EG-TEL-AML1) transgene are viable and fertile. Homozygotes die in utero, presumably due to high lacZ expression. Prior to Cre-mediated excision of the "floxed" STOP sequence, high expression of lacZ is observed in cells and tissues. When bred to Cre recombinase transgenic mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human TEL-AML1 fusion protein and EGFP in all cre-expressing cells. TEL-AML1 transcripts are not observed in adult organ tissues prior to excision of the floxed sequences. Following Cre-mediated deletion of the STOP sequence (by B6.Cg-Tg(Tek-cre)12Flv/J, Stock No. 004128), Western blot analysis reveals that EGFP levels are well correlated with TEL-AML1 transcript levels. While global expression of TEL-AML1 leads to embryonic lethality (E7.5), hematopoieti
..... For more information please see the full phenotype on the strain data sheet | ||
| 006613 | STOCK Tg(CAG-Bgeo,-Tle1,-ALPP)1Lbe/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the mouse transducin-like enhancer of split 1, homolog of Drosophila E(spl) gene, Tle1 (also known as Groucho-related gene 1; Grg1) under the regulation of the chicken beta actin promoter (ACTB) and the cytomegalovirus (CMV) intermediate-early enhancer. An internal ribosome entry sequence (IRES) followed by the human alkaline phosphatase (ALPP) reporter gene inserted downstream of the Tle1 gene directs co-expression of ALPP and TLE1. TLE1 and ALPP co-expression is blocked, however, by the presence of a loxP-flanked Bgeo (beta-galactosidase/neomycin resistance fusion protein) cassette inserted between the ACTB/CMV promoter and the Tle1 coding sequence. In the absence of Cre recombinase, beta-galactosidase activity is detected in all tissues tested including pancreas, lung, kidney, cerebellum, heart, m
..... For more information please see the full phenotype on the strain data sheet | ||
| 003920 | STOCK Tg(CAG-Bgeo/GFP)21Lbe/J | Repository- Live |
| These Z/EG transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being liver and lung tissue. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with enhanced GFP expression in tissues expressing cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess cre excision activity in live animals and cells. Although homozygotes are viable, attempts to breed homozygous mice proved unsuccessful. | ||
| 004623 | STOCK Tg(Fos-lacZ)34Efu/J | Repository- Live |
| These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and
..... For more information please see the full phenotype on the strain data sheet | ||
| 002484 | 129-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 003451 | 129-Smad3tm1Par/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was fo
..... For more information please see the full phenotype on the strain data sheet | ||
| 003310 | 129S-Gt(ROSA)26Sortm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous or homozygous for the Gtrosa26tm1Sor targeted mutation may be used to test the tissue/cellular expression pattern of the cre transgene in any transgenic strain carrying cre under the regulation of a specific promoter. Cre expression results in the removal of a loxP-flanked DNA segment that prevents expression of a lacZ gene. When crossed with a cre transgenic strain, lacZ is expressed in cells/tissues where cre is expressed. The 129-Gtrosa26tm1Sor strain is particularly useful for this purpose because the ROSA26 promoter leads to generalized expression of lacZ during development or in the adult. | ||
| 003383 | 129S-Nogtm1Amc/J | Repository-Cryopreserved |
| Homozygous mice are born but die shortly after birth, exhibiting multiple defects, including an open neural tube, skeletal abnormalities, shortened body axis, and a small vestigial tail. Analysis of early gene expression has shown that the loss of Nog expression in the floorplate, notochord, and roofplate results in a progressive failure of ventral development in the CNS and somites. Nog is also expressed in condensing cartilage in the limb and in the sclerotome of somites so its loss results in defects in cartilage patterning and skeletal morphogenesis. Heterozygous embryos show lacZ reporter expression in pattern consistent with the endogenous gene. | ||
| 005091 | 129S-Pnpla6tm1Blw/J | Repository-Cryopreserved |
| Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic day 8.5. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and are more active than wildtype littermates. A reduced level of protein gene product is detected by immunoprecipitation and Western blot analysis of brain, testes and kidney, but protein levels are not reduced in liver. Beta galactosidase activity in heterozygotes aged embryonic day 13.5 is found in the developing lens and spinal cord. In adult heterozygotes, beta galactosidase activity is detected throughout the brain, especially in the cerebellar Purkinje cells and hippocampus. Beta galactosidase activity patterns mimic the endogenous gene expression pattern. NTE activity in brain tissue is reduced by 40%. Heterozygotes are more sensitive to organophosphate toxicity with increased motor activity and mortality. This mutant mouse strain may be useful in studies of neuropathological hyperactivity, G
..... For more information please see the full phenotype on the strain data sheet | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Repository-Cryopreserved |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 004478 | B6.129-Foxd1tm1Lai/J | Repository-Cryopreserved |
| 005768 | B6.129-Htr5atm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 002938 | B6.129-Kdrtm1Jrt/J | Repository-Cryopreserved |
| Mice homozygous for the Kdrtm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells. | ||
| 004158 | B6.129-Maftm1Gsb/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted allele appear weak, fail to feed and die within a few hours of birth from unspecified causes. Embryos exhibit a slightly foreshortened head and abnormal lens development. No Maf gene transcript is detected. Posterior lens cells from homozygotes fail to elongate. These cells display inappropriately high levels of DNA synthesis and express alpha A crystallin and all of the beta crystallin genes at dramatically reduced levels. Heterozygotes are phenotypically normal. The presence of lacZ in the targeted allele makes it possible to observe Maf expression characteristics. | ||
| 005772 | B6.129P2-Acvrl1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 006431 | B6.129P2-Adam21tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005770 | B6.129P2-Adamts4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005771 | B6.129P2-Adamts5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005773 | B6.129P2-Adcy3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005774 | B6.129P2-Adcy7tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005776 | B6.129P2-Avpr1atm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005777 | B6.129P2-Axltm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005783 | B6.129P2-Cacna1ctm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005780 | B6.129P2-Cacna2d3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005781 | B6.129P2-Cacng3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005782 | B6.129P2-Cacng4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005784 | B6.129P2-Capn5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005785 | B6.129P2-Capn7tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005792 | B6.129P2-Ccr1l1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005779 | B6.129P2-Celsr2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005797 | B6.129P2-Chrna2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005787 | B6.129P2-Ctsctm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005798 | B6.129P2-Drd5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005800 | B6.129P2-Efemp2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005801 | B6.129P2-Esrratm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005802 | B6.129P2-Faim2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005803 | B6.129P2-Fzd1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. Initial reports from Delatagen state that homozygous animals are viable and fertile. However, it is the experience of The Jackson Laboratory that homozygous animals are not recovered from heterozygous matings. More that 100 progeny from heterozygous matings were genotyped. | ||
| 005804 | B6.129P2-Fzd8tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005811 | B6.129P2-Gabra3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005812 | B6.129P2-Gabra4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005810 | B6.129P2-Gabrptm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005809 | B6.129P2-Galr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005816 | B6.129P2-Glra3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005805 | B6.129P2-Gpr151tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005806 | B6.129P2-Gpr37tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005807 | B6.129P2-Gpr6tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005813 | B6.129P2-Grik5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005808 | B6.129P2-Grk5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005814 | B6.129P2-Grm1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005815 | B6.129P2-Grm3tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005817 | B6.129P2-Gsk3btm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005818 | B6.129P2-Hcrtr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005767 | B6.129P2-Htr4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005769 | B6.129P2-Htr7tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005830 | B6.129P2-Kcnq2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005821 | B6.129P2-Lats2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. Homozygous mutant mice die in utero at ~ E12.5. Heterozygous mutant mice exhibit significantly decreased prepulse inhibition when compared with age- and gender-matched wildtype control mice. | ||
| 005822 | B6.129P2-Lmbr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005850 | B6.129P2-Mapkapk2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005824 | B6.129P2-Mmp17tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005825 | B6.129P2-Mtmr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005778 | B6.129P2-Naip1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005826 | B6.129P2-Ntsr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005829 | B6.129P2-Pkd2l2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005828 | B6.129P2-Ppardtm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005831 | B6.129P2-Ppm1ftm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005827 | B6.129P2-Ptch2tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005832 | B6.129P2-Ptprotm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005799 | B6.129P2-S1pr4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005837 | B6.129P2-Scn11atm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005836 | B6.129P2-Scn9atm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005834 | B6.129P2-Sema5atm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005835 | B6.129P2-Sema6ctm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 006432 | B6.129P2-Slc18a1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005839 | B6.129P2-Slc22a12tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005838 | B6.129P2-Slc22a6tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005840 | B6.129P2-Slc40a1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005841 | B6.129P2-Slc6a9tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005842 | B6.129P2-Slc7a8tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005843 | B6.129P2-Slc9a6tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005844 | B6.129P2-Sstr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005847 | B6.129P2-Tgfbr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005845 | B6.129P2-Thbs4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005790 | B6.129P2-Tpp1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005848 | B6.129P2-Trpm5tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005791 | B6.129P2-Xcr1tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 005901 | B6.129S4-Ppardtm2Rev/J | Repository-Cryopreserved |
| Heterozygous mice are viable and fertile. All homozygous mice die in utero. Macrophages homozygous for this mutation have no transcriptional response to very low-density lipoprotein treatment. No evaluation of lacZ expression is published. The donating investigator reports homozygous mice on this background have a similar, albeit earlier, embryonic phenotype as the exon 4 deleted mutants described in other publications (Barak PNAS 2002 99:303-8, Chawla PNAS 2003 100:1268-73, and Lee Science 2003 302:453-7). Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Repository-Cryopreserved |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 003754 | B6.129S4-Shroom3Gt(ROSA)53Sor/J | Repository-Cryopreserved |
| Mice that are homozygous for this mutation survive to term or die very shortly after birth. The gene trap insertion appears to have occurred between the translational start sites of the long and short forms in the 5' portion of the endogenous gene. No gene product (protein or mRNA) is detected in homozygous embryos. Mutant embryos can be distinguished by E9.25 as the lateral edges of the cranial neural folds exhibit a wavy appearance and fail to converge at the dorsal midline. As the embryo develops, the neural folds continue to enlarge and develop away from the dorsal midline, presenting a mushroom-like appearance. By day E14.5, failed neural tube closure results in exencephaly, acrania, and facial clefting. Some mutants exhibit defects in ventral closure resulting in herniation of the intestine and liver. Not all aspects of the phenotype are fully penetrant. Hemizygous mice express a B-galactosidase under the control of the endogenous promoter, with expression variously observed
..... For more information please see the full phenotype on the strain data sheet | ||
| 005119 | B6.129S6-Npas2tm1Slm/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. Altered gene product (protein), lacking the basic helix-loop-helix (bHLH) domain is detected by Western blot analysis of brain lysates, and is not functional. Northern blot analysis of brain tissue detects a lacZ fusion gene product (mRNA), and does not detect an intact transcript containing the bHLH domain. Beta-galactosidase activity is detected in the cortex, hippocampus, striatum, amygdala, thalamus, and in the barrelfield structures of the cortical somatosensory region. Homozygotes display defective complex emotional long-term memory, as assayed by cued and contextual fear tests. Under conditions of constant darkness, homozygotes exhibit a shortened circadian rhythm period of 23.5 hours and increased nocturnal locomotor activity. Mutant mice do not adapt to restricted feeding conditions, and lose weight due to decreased food consumption. This
..... For more information please see the full phenotype on the strain data sheet | ||
| 002741 | B6.129S7-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 005970 | B6.129S7-Atoh1tm2Hzo/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 mutant mice have a perinatal lethal phenotype and die shortly after birth. No gene product (protein) is detected in resting chondrocytes by immunohistochemical analysis of embryonic age 18.5 homozygotes. Beta-galactosidase X-gal staining of neural tissue from embryonic day 14.5 and newborn (postnatal day 0) aged homozygous and heterozygous mice mimicks the endogenous expression pattern. Mice homozygous for this mutation exhibit a phenotype similar to the phenotype observed in mice homozygous for the null (loss of function) targeted mutation. Homozygotes lack cerebellar granule neurons, cochlear and ventricular hair cells, and the pontine nuclei in the brain stem. This mutant mouse strain may be useful in studies of brain and inner ear development. | ||
| 006039 | B6.129S7-Efnb2tm1And/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation show growth retardation and enlargement of the heart at embryonic day 10 (E10), with 100% lethality occurring around E11. Reporter protein expression patterns are consistent with arterial, but not venous, expression of the endogenous gene; prominent lacZ signal is observed in hindbrain and somites, with lower levels in aorta and heart as early as E8.25. Expression in the yolk sac was first detected at E8.5, and is also observed in nephrogenic mesoderm and branchial arches. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Endothelial vessel support cell differentiation of the yolk sac is also defective. Homozygotes lack myocardial trabecular extensions, and capillary ingrowth into the neural tube does not occur. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying
..... For more information please see the full phenotype on the strain data sheet | ||
| 005039 | B6.129X1-Adra1atm1Pcs/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR or RNase protection assay analysis. Total alpha-1 adrenergic receptor binding is reduced by 50% in brain and kidney, and by approximately 30% in heart. Expression of the beta-galactosidase reporter gene under the control of the endogenous gene promoter, is detected in embryonic day 12.5 aged embryos and in adult tissues closely mimicking the endogenous gene expression pattern. The resistance arteries, abdominal aorta, celiac, renal, mesenteric, hepatic, splenic, gastric, testicular, ovarian, iliac, femoral and tail arteries, as well as dermal arterioles, are positive for beta-galactosidase staining. Homozygotes are hypotensive with an 8-12% reduction from wildtype control blood pressure levels, as measured in conscious animals at rest. Administration of an alpha-1 adrenergic receptor specif
..... For more information please see the full phenotype on the strain data sheet | ||
| 006253 | B6.Cg-Ap3b1tm1.1Sms/J | Repository-Cryopreserved |
| Ap3b1 encodes the beta-3A subunit of the adaptor protein complex 3 (AP-3). 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 Ap3b1 mRNA is detected by Northern blot analysis of spleen and kidney tissue, and beta-3A immunoreactivity is absent in monocytes from homozygous mice. In brain tissue from homozygous mutants, expression levels of the AP-3 beta-3B (beta-NAP), mu-3 and sigma-3 subunit proteins are normal, but expression of the delta-3 subunit protein is reduced. In kidney, no sigma-3 protein is detected, and mu-3 and delta-3 subunit proteins levels are greatly reduced.
Homozygotes have a diluted coat color (light gray), which is lighter than the coats of homozygotes carrying the allelic pearl (Ap3b1pe) spontaneous mutation. Cultured melanocytes from homozygous mutant mice have very few pigment granules. Lysosomal-associated membrane
..... | ||
| 003139 | B6.Cg-Tg(DBHn-lacZ)8Rpk/J | Repository-Cryopreserved |
| Transgenic mice carry a beta-galactosidase reporter gene driven by dopamine beta hydroxylase promotor. LacZ expression is seen in neurons of the locus ceruleus and other classic noradrenergic brain stem nuclei, sympathetic ganglion neurons, and adrenal chromaffin cells. LacZ expression is also observed in neurons of the enteric system, the retina, some sensory and all cranial parasympathetic ganglia, and some diencephalic and telencephalic brain nuclei. | ||
| 002982 | B6.Cg-Tg(xstpx-lacZ)32And/J | Repository-Cryopreserved |
| This mutant, when crossed with a cre transgenic, will express lacZ in cells where cre is expressed to remove the STOP of translation section which lies between the 2 loxP sites. LacZ expression is restricted to neural and skeletal muscle tissue and heart by the chicken beta-actin promoter that is driving the reporter. | ||
| 005064 | B6;129-Slc30a3tm1Rpa/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected in brain homogenates by Western blot analysis. Beta-galactosidase activity pattern in homozygotes mimics endogenous gene expression. Total zinc levels in the hippocampus and cortex is reduced by approximately 20%. Histochemically reactive and immunoreactive synaptic vesicle zinc is undetectable. There is no N-(6-Methoxy-8-quinolyl)-p-Toluene-Sulfonamide (TSQ) fluorescence in hippocampal tissues, although it is detected in testis and pancreas. This mutant mouse strain may be useful in studies of zinc transport into synaptic vesicles. | ||
| 005788 | B6;129P2-Cd97tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 006703 | B6;129P2-Gucy2dtm1Mom/MomJ | Repository-Cryopreserved |
| A subset of necklace glomeruli demarcating main and accessory portions of the olfactory bulb are labeled by lacZ driven by an axonally-expressed guanylate cyclase 2d (GC-D) promoter. | ||
| 005833 | B6;129P2-Rgs4tm1Dgen/J | Repository-Cryopreserved |
| This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen. | ||
| 004153 | B6;129S-Mtap7Gt(ROSABetageo)1Sor/J | Repository-Cryopreserved |
| At birth, mice homozygous for the gene-trapped Mtap7 allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. Although trace amounts of a presumably nonfunctional transcript can be detected in testis tissue, no protein product is immunodetectable. Male homozygotes are sterile. Expression of the reporter gene (B-galactosidase from the Bgeo fusion gene) employed by the gene trap vector indicates that the Mtap7 promoter directs expression in various tissues with highest levels seen in the seminiferous tubules. During the first wave of spermatogenesis at 5 weeks of age, deformed spermatids can be observed. Abnormalities are attributed to aberrant microtubule organization. Microtubule aberrations are also observed in Sertoli cells. Gradual loss of germ cells occurs. At three months of age, the testes of homozygous mutants are less than one-third the size of those of heterozygous littermates. | ||
| 007208 | B6;129S4-Axud1Gt(ROSA)80Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Axud1-mutant allele are viable and fertile, with some incidence of perinatal lethality before 2 weeks of age (the Donating Investigator reports 18% of homozygotes die by 2 weeks of age). Homozygotes have abnormalities in palate bone fusion. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. These Axud1-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 003309 | B6;129S4-Gt(ROSA)26Sortm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous or homozygous for the Gtrosa26tm1Sor targeted mutation may be used to test the tissue/cellular expression pattern of the cre transgene in any transgenic strain carrying cre under the regulation of a specific promoter. Cre expression results in the removal of a loxP-flanked DNA segment that prevents expression of a lacZ gene. When crossed with a cre transgenic strain, lacZ is expressed in cells/tissues where cre is expressed. | ||
| 007207 | B6;129S4-Zfp640Gt(ROSA)81Sor/J | Repository-Cryopreserved |
| Mice homozygous for this Zfp640-mutant allele are viable and fertile, with abnormalities in palate bone fusion and increased weight gain observed only in males after adolescence. Homozygotes exhibit defects that affect the same cell types and processes as those controlled by the platelet-derived growth factor (PDGF) pathway, including vasculature, kidney, and skeletal defects. Additionally, homozygotes are reported to have low b-galactosidase activity; in situ hybridization or other sensitive methods may be necessary to detect expression of the lacZ-neo reporter fusion gene. These Zfp640-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 004365 | B6;129S6-Srebf1tm1Mbr/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 targeted mutation results in a total ablation of the SREBP-1c transcript and only a slight redution in levels of the alternate SREBP-1a transcript. There is a 50% increase in level of SREBP-2 transcript and increases in transcripts of enzymes utilized in cholesterol biosynthesis. Liver cholesterol content is increased while plasma cholesterol and plasma triglycerides levels are reduced. There is a reduction of expression of all genes required for fatty acid and triglyceride synthesis. Administration of liver X receptor (LXR) agonist did not result in increased levels of SREBP-1a transcript or in liver triglycerides. This mutant mouse strain represents a model that may be useful in studies of transcriptional control of fatty acid and triglyceride biosynthesis. | ||
| 002317 | B6;129S7-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 003266 | B6;129S7-Epas1tm1Rus/J | Repository-Cryopreserved |
| Mice homozygous for the Epas1tm1Rus targeted mutation develop normally until embryonic day 11.5. Beginning at embryonic day 12.5 the ratio of homozygous embryos begins to decline and by day 16.5 there are no viable mutant embryos. Overall morphological development, including the circulatory system, is normal. Of particular interest however, is a pronounced bradycardia in homozygous mutant mice. Catecholamine levels in homozygous mutant mice are also significantly lower than wildtype controls. Administration of the catecholamine precursor DOPS to pregnant females rescues approximately 40% of mutant embryos. Embryos that survive to birth appear runted, fail to nurse, and die within 24 hours of birth. These results suggest a pivotal role of EPAS1 in catecholamine homeostasis. Heterozygous mice from this strain contain a modified lacZ gene in the targeting construct. This characteristic makes this strain useful as a marker for endothelial cells. | ||
| 003471 | B6;C3H-Tg(CNP-GEO)1Ldh/J | Repository-Cryopreserved |
| This transgenic strain is used to trace glial cell lineage from the early stages throughout their development while simultaneously selecting for oligodendrocytes and Schwann cells. The transgenic mice contain a bacterial b-galactosidase and neomycin phosphotransferase fusion protein (bgeo) under the control of murine 2'3'-cyclic nucleotide 3'-phosphodiesterase (muCNP) promoters I and II. No overt phenotype is observed. | ||
| 006680 | B6;CBA-Tg(Olfr16*,taulacZ)19Mom/MomJ | Repository-Cryopreserved |
| 006671 | B6;CBA-Tg(Olfr16*,taulacZ)5Mom/MomJ | Repository-Cryopreserved |
| 006673 | B6;CBA-Tg(Olfr16,taulacZ)sn2Mom/MomJ | Repository-Cryopreserved |
| 004141 | B6;CBA-Tg(UAS-lacZ)65Rth/J | Repository-Cryopreserved |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of the transgenic lacZ gene is directed by upstream activating sequence (UAS) elements. This strain serves as a reporter for mice employing GAL4/UAS bigenic system for controlled gene expression in the developing CNS. In this system, a transgenic strain expressing the yeast transcriptional activator GAL4 (see Stock No. 003829) is bred to a second transgenic, target strain bearing an UAS-regulated gene. In the double transgenic offspring, an UAS-regulated gene would be selectively expressed in tissues expressing GAL4. | ||
| 002369 | B6;SJL-Tg(c177-lacZ)226Bri/J | Repository-Cryopreserved |
| Transgenic mice show a strong expression of the lacZ gene in round spermatids and subsequent stages of spermatogenesis. These mice can be used as a source of germ cells and transplanted into busulfan treated mice (busulfan (40 mg/kg i.p.) destroys spermatogenic stem cells). LacZ serves as a reporter for the transplanted cells. Following transplantation, spermatogonia with stem cell potential establish themselves on the basal membrane of the recipient seminiferous tubule and begin to replicate. This strain has a higher copy number of the transgene than the TgN(c177lacZ)227Bri strain and may be distinguished from it by a dot blot. Cells from these two lines may therefore be mixed prior to injection and be distinguished from each other in the progeny. | ||
| 002372 | B6;SJL-Tg(c177-lacZ)227Bri/J | Repository-Cryopreserved |
| B6SJLF1/J mice (Stock No. 100012) may be used as controls. These only provide an approximate genetic match to this B6,SJL background. | ||
| 002621 | B6;SJL-Tg(tetop-lacZ)2Mam/J | Repository-Cryopreserved |
| B6;SJL-Tg(tetoplacZ)2Mam transgenic mice serve as reporter/tester mice for transgenic mice expressing the tetracycline-controlled transactivator proteins tTA or rtTA. This strain carries a beta-galactosidase (lacZ) reporter gene under the control of a tetracycline-responsive promoter element (TRE; tetO), consisting of the human cytomegalovirus early promoter fused to tet operator sequences. When these mice are mated with transgenic mice expressing tTA or rtTA, lacZ transcription may be induced by the administration (or withdrawl, if tTA is used) of tetracycline, or its analog, doxycyline. Beta-galactosidase activity is not observed in the absence of tTA or rtTA transgene. | ||
| 003299 | B6;SWJ-Tg(TIMP3-lacZ)7Jeb/J | Repository-Cryopreserved |
| These transgenic mice show no phenotypic defects. LacZ expression is observed in the eye, specifically in the corneal endothelium and ganglion cell layer. LacZ expression is also observed in the kidney, choroid plexus, testes and ovaries, gingiva, bone and the hair follicles of the skin. Transgene expression is developmentally regulated. | ||
| 002865 | B6CBA-Tg(Wnt1-lacZ)206Amc/J | Repository-Cryopreserved |
| These transgenic mice show no phenotypic defects. LacZ is expressed in the dorsal CNS. This strain is useful as a marker for CNS development, specifically for the migrating cranial and trunk neural crest. | ||
| 002955 | C.129S7-Gt(ROSA)26Sor/J | Repository-Cryopreserved |
| Mice hemizygous or homozygous for the ROSA26 retroviral insertion display no distinguishing phenotype. lacZ is expressed in all tissues of the developing embryo and in most tissues of the adult mouse. | ||
| 002754 | C57BL/6-Tg(LacZpl)60Vij/J | Repository-Cryopreserved |
| Homozygous transgenic mice carry multiple copies of the lacZ plasmid construct pUR288. The copy number and size of the construct (5kb) render this transgenic ideal for studies requiring the quantitation of mutation rates in virtually any tissue. This model can be further used to identify specific mutation types including small and large deletions, insertions, and point mutations in vivo. | ||
| 002193 | C57BL/6J-Tg(MTn-lacZ)204Bri/J | Repository-Cryopreserved |
| These lacZ transgenic mice carry no obvious phenotype. The protein product is localized to the cell nucleus. Expression is present in the liver of transgenic mice as a result of the presence of the SV40 large T-antigen nuclear localization signal peptide. Hepatocytes from this strain stain blue with X-gal staining. Expression can be induced up to 10-fold by administration of heavy metal ions. | ||
| 002981 | DBA/2-Tg(xstpx-lacZ)36And/J | Repository-Cryopreserved |
| This test strain is used determine the tissue expression pattern of cre transgenic mice. The transgene is loxP-STOP-of-translation-loxP-lacZ driven by the beta-actin promoter. The lacZ is expressed only in cells where the STOP element has been removed by Cre recombinase. LacZ expression is restricted to neural and skeletal muscle tissue and heart by the chicken beta-actin promoter that is driving the reporter. | ||
| 004127 | FVB-Tg(Nes-rtTA)306Rvs/J | Repository-Cryopreserved |
| Mice that are hemizygous for this transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat nestin intron II enhancer/promoter. According to the donating investigator, expression occurs in the neuroepithelium of the developing nervous system (embryonic days 10-17), in some neuron subsets of the adult mouse (e.g. cerebellum, hippocampal dentate gyrus, subventricular zone, spinal cord) and in adult testes. The rtTA gene is cotranscribed with the lacZ reporter gene Bgeo, which allows verification of the site of rtTA expression. When Tg(Nes-rtTA) hemizygous mice are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycli
..... For more information please see the full phenotype on the strain data sheet | ||
| 003140 | FVB/N-Tg(PAI1-lacZ)1Jjb/J | Repository-Cryopreserved |
| Transgenic mice carry a beta-galactosidase reporter gene driven by human plasminogen activator inhibitor type I (PAI1) promotor. Transgene expression detected in two independent lines was observed only in kidney from embryonic day 13 to adult, and was seen primarily in proximal tubule cells of the outer medulla. Transgene expression and activity was unchanged in response to TGFbeta and remained restricted to kidney. | ||
| 005941 | FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J | Repository-Cryopreserved |
| Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant
..... | ||
| 003315 | FVB/N-Tg(tetORo1-lacZ)3Conk/J | Repository-Cryopreserved |
| Transgenic mice express both Ro1 (Receptor Activated Solely by a Synthetic Ligand (RASSL), opioid, #1) and lacZ under the regulation of tetracycline responsive elements (TRE; tetO)(see Strain Development for more information). When Ro1 is expressed in the heart (by crossing it with strain FVB.Cg-Tg(Myh6-tTA)6Smbf/J - Stock No. 003170), administration of the drug spiradoline produces a dramatic decrease in heart rate. Since Ro1 and lacZ are co-integrated and under tetracycline/doxycycline control, X-gal staining can be used to identify cells in which the tet-inducible system is working. Ro1 activates Gi-signaling in response to spiradoline, and can be used to study the effect of Gi-signaling in many tissues. In the heart, Ro1-mediated activation of Gi-signaling slows heart rate, but in other tissues it is predicted to control diverse physiological events, such as cell proliferation, se
..... For more information please see the full phenotype on the strain data sheet | ||
| 003487 | FVB/NJ-Tg(XGFAP-lacZ)3Mes/J | Repository-Cryopreserved |
| Mice carrying this transgene express beta galactosidase in the nuclei of astrocytes. The donating investigator reports that more recent studies on this particular line indicate low level expression of the lacZ reporter gene in many neuronal populations as well. The transgene integrated on the X chromosome and therefore undergoes X-inactivation. This strain may be useful for cell culture and transplantation studies. | ||
| 006241 | STOCK Hhiptm1Amc/J | Repository-Cryopreserved |
| Mice heterozygous for this targeted mutation are viable and fertile. Homozygotes die from respiratory failure shortly after birth. Expression of the "knocked-in" lacZ gene is detected in a pattern similar to the endogenous transcript (in lung, skeleton, stomach, duodenum, spleen, and pancreas), and serves as a faithful reporter for Hedgehog (Hh) signaling. Because Hh and fibroblast growth factor (Fgf) signaling are abnormal, homozygous mice have defects in many Hh target tissues. Although the primary lung buds form in homozygotes, lung branching morphogenesis is defect beginning at 10.5 days postcoitus (dpc), and fails to generate a complete respiratory tree. The single left lobe also is significantly reduced, and total lung size at birth is diminished 67-75% compared to wildtype. In addition, homozygous mice have delayed mineralization of the endochondral skeleton, as well as impaired pancreas morphogenesis, islet formation and endocrine cell proliferation. These mutant mice ma
..... For more information please see the full phenotype on the strain data sheet | ||
| 005707 | STOCK Rag1tm1Mom Tg(TIE2-lacZ)182Sato/J | Repository-Cryopreserved |
| Mice homozygous for both the targeted mutation and the transgene are viable and fertile. The transgene beta-galactosidase is well expressed, reflects endogenous Tek/Tie2 activity, and is specific to the vascular endothelium. Mice homozygous for the Rag1 mutation are immunodeficient as they lack mature B and T lymphocytes. This double mutant mouse may be useful in studies of cancer, tumor-related angiogenesis, and as a recipient of xenografted tumors. | ||
| 003919 | STOCK Tg(CAG-Bgeo/ALPP)1Lbe/J | Repository-Cryopreserved |
| These transgenic mice constitutively express lacZ under the control of the CMV enhancer/chicken actin promoter. Expression is widespread with notable exceptions being erythrocytes, chondrocytes and adipocytes. Expression is observed throughout all embryonic and adult stages. When crossed with a Cre recombinase-expressing strain, lacZ expression is replaced with alkaline phosphatase expression in tissues expressing Cre. This double reporter system makes it possible to distinguish a lack of reporter expression from a lack of Cre recombinase expression while providing a means to assess cre excision activity at the individual cell level. | ||
| 006674 | STOCK Tg(Olfr16,taulacZ)2030Mom/MomJ | Repository-Cryopreserved |
| Hemizygous mice express a mini-transgene for the olfactory receptor MOR23. Olfactory sensory neurons that express MOR23 co-express the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. These mice may be useful in studies of axon guidance and mechanisms of olfactory receptor specificity in the olfactory bulb. | ||
| 002395 | STOCK Tg(Zfy1-lacZ)218Bri/J | Repository-Cryopreserved |
| LacZ staining is present in the embryonic gonad of both male and female mice (somatic cells, but not germ cells). Staining is less intense in males and is repressed shortly after formation of the testis cords. Staining is also present in the kidney, brain, and spine prior to birth. | ||
| 003274 | STOCK Tg(tetNZL)2Bjd/J | Repository-Cryopreserved |
| In this strain both the lacZ gene with a nuclear localization signal (NZ) and the luciferase gene (L) are driven by a bidirectional, tetracycline-responsive promoter element (TRE). When mated to a strain expressing the tetracycline-controlled activator proteins tTA or rtTA coupled to tissue-specific promoters, lacZ and luciferase will be expressed in the appropriate tissue in a tetracycline-inducible fashion. According to the donating investigator, the express | ||