Search Criteria: Research Area is "Neurobiology Research: lacZ expression in neural tissue"
Additional Register Interest Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 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. | ||
| 017623 | B6.129-Trpv1tm2Bbm/J | Repository- Live |
| The TRVP1 nociceptor is primarily expressed in dorsal root ganglia and peripheral sensory nerve endings. It is also detected in the central nervous system and non-neuronal thermoregulatory tissues. In these knock-in mutant mice, beta-galactosidase (nlacZ) is detected in primary afferent neuron nuclei of the dorsal root ganglion (DRG) and trigeminal ganglia. More than 90% of capsaicin responsive cultured DRG neurons and more than 95% of TRPV1 immunoreactive neurons in DRG sections stain for beta-galactosidase. Beta-galactosidase activity is detected along the midline of the rostral midbrain and caudal hypothalamus. Alkaline phosphatase (ALPP) is detected in cell bodies and axonal processes of the dorsal root ganglion and spinal cord dorsal horn primary afferent terminals. If TRRVP1 nerve fibers are destroyed by capsaicin treatment, no ALPP histochemical staining is detected in the spinal cord. No ALPP staining is detected in the cell bodies of neurons in the brain. Beta-galactosid ..... For more information please see the full phenotype on the strain data sheet | ||
| 018054 | B6.129P2(Cg)-Pitx2tm1.1Dmm/J | Repository- Live |
| In this mutant strain an IRES Tau-lacZ cassette replaces exon 4 of the paired-like homeodomain transcription factor 2 (Pitx2) gene, abolishing expression of all three PITX2 isoforms. PITX2 is a transcription factor expressed in the developing mammillary and retromammillary regions of the hypothalamus. PITX2 is involved in memory processing by regulating neural axonal migration. Heterozygous Pitx2tlz/+ mice are viable and fertile, while homozygous Pitx2tlz/tlz mice exhibit embryonic lethality. Pitx2tlz/+ embryos show lacZ staining in the eye, pituitary, teeth, heart, craniofacial regions, and neural tube. The brains of heterozygous embryos show lacZ staining the hypothalamus and midbrain. Pitx2tlz/tlz embryos exhibit defects of the heart, abdominal viscera, and distal turning. They have improperly bundled and disorganized axonal fibers in the primary mammillary tract which are still ..... For more information please see the full phenotype on the strain data sheet | ||
| 009120 | B6.129P2-Axin2tm1Wbm/J | Repository- Live |
| Homozygous mice are viable and fertile, with the Axin2lacZ (or conductinlacZ) mutation that both abolishes endogenous Axin2 gene function and expresses NLS-lacZ under the control of the endogenous Axin2 promoter/enhancer regions. Homozygous mice exhibit cranial skull defects and malformations of skull structures; a phenotype resembling craniosynostosis in humans. Specifically, homozygous mice show an obvious reduction in head growth within the first 3 weeks after birth, resulting from developmental defects of the cranial skull (premature fusion of cranial sutures) at early postnatal stages. Axin2-deficient mice have abnormal calvarial morphogenesis/osteoblast development. Because Axin2 is a negative regulator of the canonical Wnt pathway that suppress signal transduction by promoting β-catenin degradation, the NLS-lacZ expression in these Axin2lacZ (or conductinlacZ) mutant mice may be useful in monitoring end ..... For more information please see the full phenotype on the strain data sheet | ||
| 009089 | B6.129S1(Cg)-Ndntm2Stw/J | Repository- Live |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Ndn allele, only the paternally inherited Ndn allele is expressed. The Ndntm2Stw (ΔNdn-lacZ or Ndn-lacZ) knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is highest in hypothalamus, but also detected in other central nervous system tissues (pons and medulla, spinal cord), peripheral nervous system (dorsal root ganglia), and some non-neuronal tissues (tongue, cartilage brown fat). Breeding heterozygous females with wildtype m ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 009136 | B6.Cg-Tg(tetO-Kcnj2,lacZ)1Gogo/J | Repository- Live |
| These mice express a potassium inwardly-rectifying channel, subfamily J, member 2 (Kcnj2) cDNA and a tau-β-galactosidase (lacZ) cassette under the direction of tetracycline operator. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of KCNJ2 and lacZ may be regulated with the tetracycline analog doxycycline in the double mutant offspring. Hemizygous mice are viable and fertile. For example, when bred to mice expressing olfactory marker protein (Omp)-tTA, the olfactory sensory neurons in bigenic offspring express KCNJ2 and the taulacZ fusion protein by virtue of IRES-mediated co-translation after dox treatment. Overexpression KCNJ2 hyperpolarizes neurons and inhibits the firing of action potentials, disrupting the formation of the olfactory map. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity. These mice ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 016857 | B6;129-Itga7tm1Burk/J | Repository- Live |
| The α7- (or α7βgal-) mutant allele has exon 1 of the α7 integrin gene replaced by a lacZ/neo cassette; this both abolishes endogenous gene expression and also places β-galactosidase under transcriptional control of the α7 integrin promoter/enhancer regions. No α7 integrin chain RNA expression from the mutant allele is observed in skeletal muscle and cerebral artery. Homozygous mice (α7-/-) show absence of α7 integrin chain protein in skeletal muscle and vascular tissues compared to wildtype controls, while heterozygous mice (α7+/-) show reduced levels. Expression of lacZ from the mutant allele is observed in α7 integrin-expressing cells of the embryonic vasculature, skeletal/non-skeletal musculature and central/peripheral nervous system beginning at embryonic day (E)11.5; significantly increasing out to ~E14.5. Although not detected in embryonic heart, lacZ express ..... For more information please see the full phenotype on the strain data sheet | ||
| 008344 | B6;DBA-Tg(Fos-tTA,Fos-EGFP*)1Mmay Tg(tetO-lacZ,tTA*)1Mmay/J | Repository- Live |
| The TetTag mouse is a bi-transgenic mutant that has tetracycline (or tetracycline analog) inducible expression of beta-galactosidase in activated neurons. Two independently generated transgenic strains were crossed to produce this bi-transgenic TetTag strain. In the first transgenic construct, the tetracycline-controlled transactivator (tTA) protein and a two hour half-life Green Fluorescent Protein (shEGFP) are expressed under the direction of the fos, FBJ osteosarcoma oncogene, minimal promoter. The second transgenic construct expresses a nuclear-localizing beta-galactosidase gene and the doxycycline insensitive tetracycline regulated transactivator (containing point mutation, H100Y), under the control of the tetO, tetracycline-responsive regulatory element. In the absence of tetracycline or a tetracycline analog (such as doxycycline), selective expression of beta-galactosidase is observed in activated neurons. Doxycycline administration prevents expression beta-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 018913 | B6N.Cg-Tg(tetO-GFP,-lacZ)G3Rsp/J | Repository- Live |
| TgGFPtetO7lacZ (TgPtetbi-GFP/lacZ or TRE-lacZ/GFP) mice express both humanized green fluorescent protein (gfph or GFP-H) and β-galactosidase (lacZ) under the control of a bi-directional Tet-responsive element (TRE or tetO7). No GFP-H or β-galactosidase is reported in the absence of tetracycline-controlled transactivator protein (tTA). When bred to other mice expressing tTA or reverse tetracycline-controlled transactivator protein (rtTA), simultaneous GFP-H and β-galactosidase expression in the resulting double mutant offspring can be regulated by tetracycline or its analog doxycycline (dox).
Hemizygous TgGFPtetO7lacZ mice from founder line G3 are viable and fertile, with no reported phenotypic abnormalities. The donating investigator reports TgGFPtetO7lacZ line G3 mice have ~4 copies of the transgene integrated on chromosome 17 (chr17:43,015,611 bp [NCBI37/mm9]). This integration site is near t ..... | ||
| 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 | ||
| 017989 | STOCK Fkbp5tm1Dvds/J | Repository- Live |
| FKBP5 (or FKBP51) functions as a co-chaperone that binds to HSP90 and is involved in regulation of the glucocorticoid receptor. Mutations that increase protein levels of human FKBP5 are associated with depressive disorders, anxiety, bipolar disorders, and post-traumatic stress syndrome. In this strain, the targeting vector includes a lacZ gene and replaces the Fkbp5 first coding exon. Expression of beta-galactosidase is under the control of the endogenous promoter. Expression in the brain increases with age particularly in the upper cortical layers of the forebrain. Homozygous mice are viable and fertile. Aged mice over a year old) exhibit shorter immobility time in forced swim and tail suspension tests, and reduced stress corticosterone levels. This strain may be useful for studying anxiety and depressive disorders. | ||
| 008211 | STOCK Gli1tm2Alj/J | Repository- Live |
| Mice homozygous for the Gli1lz (or Gli1lacZ) allele are viable and semi-fertile, with a "knock-in" of β-galactosidase (lacZ) inserted into the first coding exon (exon 2) and replacing the genomic fragment encoding the entire N-terminal and zinc-finger domains of the targeted locus (exons 2-7); abolishing endogenous gene function even if alternative splicing occurs. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern indistinguishable from wildtype gene mRNA expression. As Gli1 transcription is a readout of high level Hedgehog signaling, these Gli1lz (or Gli1lacZ) mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in axis patterning, proliferation, and cell fate specification of Hedgehog responding cells at different stages of embryogenesis. | ||
| 007922 | STOCK Gli2tm2.1Alj/J | Repository- Live |
| Mice homozygous for this Gli2lzki allele harbor a β-galactosidase "knock-in" (lzki) allele that also abolishes endogenous gene function. As such, homozygous mice die at birth with many defects including absence of Sonic Hedgehog-expressing floor plate cells, reduction of Nkx2.2-expressing V3 interneurons in the spinal cord, and defects in midbrain, cerebellum and lung development. Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern identical to the wild-type gene. Heterozygotes are viable and fertile. These Gli2lzki mice may be useful for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and axis patterning), as well as the role of Gli2 in adult organs. | ||
| 021055 | B6.129S2(Cg)-Bdnftm1Krj/J | Under Development - Now Accepting Orders |
| Brain derived neurotrophic factor is important for survival of neurons, regulates neuronal differentiation and is involved in synaptic plasticity as well as mediation of food intake and body weight. These mice possess loxP sites on either side of exon 5 of the targeted gene, with polyadenylation sequence upstream of the 3' loxP site, and lacZ downstream of the 3' loxP site. Mice that are homozygous for this allele are viable, obese and are poor breeders. The Donating Investigator reports that homozygotes exhibit subtle neurological abnormalities. The phenotype of homozygotes is probably due to disruption by insertion of lacZ and loxP sites into the locus. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 5 deleted and express lacZ in the cre-expressing tissues.
When bred to mice carrying Tg(Wnt1-cre)11Rth (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 018608 | B6N(Cg)-Arrb2tm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Arrb2 (arrestin, beta 2) is expressed in the central nervous system and may play a role in the regulation of synaptic receptors. A beta-galactosidase-containing cassette disrupts the Arrdc1 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 018653 | B6N(Cg)-Bzw2tm1b(KOMP)Mpb/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Bzw2 (basic leucine zipper and W2 domains 2) is involved in neuronal differentiation. A beta-galactosidase containing cassette generates a knockout first reporter allele for the Bzw2 gene (Skarnes et al. Nature 474,337-342;2011). Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the International Knockout Mouse Consortium website. | ||
| 018556 | B6N(Cg)-Cbln3tm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Cbln3 (cerebellin 3 precursor protein) gene is expressed in cerebellar granule cells. A beta-galactosidase-containing cassette disrupts the Cbln3 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 018584 | B6N(Cg)-Dixdc1tm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Dixdc1 (DIX domain containing 1) inhibits cell growth by regulating the TOR signaling. A beta-galactosidase-containing cassette disrupts the Dixdc1 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 018615 | B6N(Cg)-Htr3btm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Htr3b (5-hydroxytryptamine (serotonin) receptor 3B) gene encodes a ligand-gated ion channel which causes depolarizing responses in neurons after activation. A beta-galactosidase-containing cassette disrupts the Htr3b gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 018575 | B6N(Cg)-Ncaldtm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. The Ncald (neurocalcin delta) gene encodes a cytosolic neuronal calcium binding protein which becomes memebrane-associated under conditions of increased intracellular calcium. A beta-galactosidase-containing cassette disrupts the Prom2 gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 018577 | B6N(Cg)-Nefhtm1.1(KOMP)Vlcg/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Nefh (neurofilament, heavy polypeptide) is required for the development of neurofilaments in cells of the nervous system. A beta-galactosidase-containing cassette disrupts the Nefh gene in this strain. Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Regeneron Velocigene website. | ||
| 021750 | B6N(Cg)-Rilpl2tm1b(KOMP)Wtsi/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Rilpl2 (Rab interacting lysosomal protein-like 2) gene is involved in neuronal structure and function. A beta-galactosidase containing cassette generates a knockout first reporter allele for the Rilpl2 gene (Skarnes et al. Nature 474,337-342;2011). Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the International Knockout Mouse Consortium website. | ||
| 021142 | B6N(Cg)-Sh3tc2tm1b(KOMP)Wtsi/J | Under Development - Now Accepting Orders |
| This strain was generated by the Knockout Mouse Phenotyping Program (KOMP2) at The Jackson Laboratory using embryonic stem cells provided by the International Knockout Mouse Consortium. Sh3tc2 (SH3 domain and tetratricopeptide repeats 2) gene, expressed in Schwann cells, has been associated with the onset of autosomal recessive Charcot-Marie-Tooth disease type 4C. A beta-galactosidase containing cassette generates a knockout first reporter allele for the Sh3tc2 gene (Skarnes et al. Nature 474,337-342;2011). Phenotype data is being generated by the JAX KOMP2 program and will be available to the public when complete from the International Mouse Phenotyping Consortium website. For additional information on this mutation, please see the Inter ..... For more information please see the full phenotype on the strain data sheet | ||
| 018626 | STOCK Myf5tm1Pas/J | Under Development - Now Accepting Orders |
| Myf5, myogenic factor 5, is a basic Helix-Loop-Helix transcription factor involved in muscle cell differentiation. These mice carry a targeted mutation in which a beta-galactosidase gene (lacZ) with a nuclear localization signal disrupts the bHLH domain of the protein. Beta galactosidase activity mimics the endogenous expression pattern of the Myf5 gene, and is detected as early as embryonic day 9 in the caudal myotomes and embryonic day 8 in newly differentiated neurons in the mesencephalon.
Mice that are heterozygous for the targeted mutation are viable and fertile. Homozygotes die soon after birth due to respiratory failure. Homozygotes also exhibit delayed myotome formation and truncated ribs. No gene product (mRNA) is detected by in situ hybridization analysis of homozygous embryos. Expression of the adjacent Myf6, myogenic factor 6, is not detected by RT-PCR of skeletal muscle from homozygotes, or by whole mount in situ hybridizati ..... For more information please see the full phenotype on the strain data sheet | ||
| 009348 | B6.129P2(Cg)-Hprttm17(Ple48-lacZ)Ems/Mmjax | Transferred |
| 012572 | B6.129P2(Cg)-Hprttm19(Ple88-lacZ)Ems/Mmjax | Transferred |
| 012574 | B6.129P2(Cg)-Hprttm38(Ple17-lacZ)Ems/Mmjax | Transferred |
| 012575 | B6.129P2(Cg)-Hprttm39(Ple24-lacZ)Ems/Mmjax | Transferred |
| 012576 | B6.129P2(Cg)-Hprttm40(Ple34-lacZ)Ems/Mmjax | Transferred |
| 010805 | B6.129P2(Cg)-Hprttm41(Ple160-lacZ)Ems/Mmjax | Transferred |
| 012331 | B6.129P2(Cg)-Hprttm42(Ple131-lacZ)Ems/Mmjax | Transferred |
| 012577 | B6.129P2(Cg)-Hprttm43(Ple140-lacZ)Ems/Mmjax | Transferred |
| 010709 | B6.129P2(Cg)-Hprttm44(Ple49-lacZ)Ems/Mmjax | Transferred |
| 012333 | B6.129P2(Cg)-Hprttm45(Ple67-lacZ)Ems/Mmjax | Transferred |
| 012733 | B6.129P2(Cg)-Hprttm53(CAG-lacZ)Ems/Mmjax | Transferred |
| 012578 | B6.129P2(Cg)-Hprttm56(Ple25-lacZ)Ems/Mmjax | Transferred |
| 012579 | B6.129P2(Cg)-Hprttm58(Ple119-lacZ)Ems/Mmjax | Transferred |
| 012580 | B6.129P2(Cg)-Hprttm59(Ple123-lacZ)Ems/Mmjax | Transferred |
| 012581 | B6.129P2(Cg)-Hprttm62(Ple153-lacZ)Ems/Mmjax | Transferred |
| 012342 | B6.129P2(Cg)-Hprttm63(Ple12-lacZ)Ems/Mmjax | Transferred |
| 012347 | B6.129P2(Cg)-Hprttm64(Ple170-lacZ)Ems/Mmjax | Transferred |
| 012582 | B6.129P2(Cg)-Hprttm67(Ple238-lacZ)Ems/Mmjax | Transferred |
| 012583 | B6.129P2(Cg)-Hprttm68(Ple127-lacZ)Ems/Mmjax | Transferred |
| 012656 | B6.129P2(Cg)-Hprttm70(Ple240-lacZ)Ems/Mmjax | Transferred |
| 012657 | B6.129P2(Cg)-Hprttm71(Ple155-lacZ)Ems/Mmjax | Transferred |
| 012659 | B6.129P2(Cg)-Hprttm73(Ple142-lacZ)Ems/Mmjax | Transferred |
| 012734 | B6.129P2(Cg)-Hprttm74(Ple232-lacZ)Ems/Mmjax | Transferred |
| 014536 | B6.Cg-Hprttm75(Ple143-lacZ)Ems/Mmjax | Transferred |
| 010707 | STOCK Hprttm37(lacZ)Ems/Mmjax | Transferred |
| 012335 | STOCK Hprttm50(Ple55-lacZ)Ems/Mmjax | Transferred |
| 013764 | STOCK Hprttm57(Ple26-lacZ)Ems/Mmjax | Transferred |
| 012353 | STOCK Hprttm65(Ple53-lacZ)Ems/Mmjax | Transferred |
| 012354 | STOCK Hprttm66(Ple5-lacZ)Ems/Mmjax | Transferred |
| 012584 | STOCK Hprttm69(Ple134-lacZ)Ems/Mmjax | Transferred |
| 016927 | 129-Crmp1tm1Pako Dpysl4tm1Ttq/J | Cryopreserved - Ready for recovery |
| In this strain an IRES-lacZ-neo cassette replaces part of exon 4 of the collapsin response mediator protein 1 (Crmp1) gene, and a second IRES-lacZ-neo cassette replaces exon 3 of the dihydropyrimidinase-like 4 (Dpysl4 or Crmp3) gene. Double homozygotes are viable and fertile. CRMP-1 and CRMP-3 are members of a family of phosphoproteins that are involved in dendritic length and branching, semaphorin signaling pathway, growth cone collapse, and neurite extension after binding with tubulin heterodimers. CRMP-1 is expressed during brain development in the cerebellum, olfactory bulb, hypothalamus, and retina, but is restricted mainly to the hippocampus and olfactory bulb in adults. CRMP-1 single knockout (KO) mice exhibit a decrease in granule cell proliferation, apoptosis, and migration. Also radial migration of cortical neurons is delayed. CRMP-3 is also expressed during brain development, but is restricted to the hippocampus, pontine nuclei, and olivary complex i ..... For more information please see the full phenotype on the strain data sheet | ||
| 016928 | 129;B6-Dpysl5tm1Gosh/J | Cryopreserved - Ready for recovery |
| In this strain an IRES-lacZ-neo cassette replaces exons 2-6 of the dihydropyrimidinase-like 5 (Dpysl4 or Crmp5) gene. Homozygotes are viable and fertile. CRMP-5 is a member of a family of phosphoproteins that are involved in dendritic length and branching, semaphorin signaling pathway, growth cone collapse, and neurite extension after binding with tubulin heterodimers. It is expressed throughout the nervous system after P14 and is specifically involved in filopodia and growth cone morphology in neurons. These mice exhibit abnormally small Purkinje cells in the cerebellum during the period of dendritic branching. They also display long-term depression of excitatory synaptic transmissions. This strain may be useful for studying nervous system developmental disorders. | ||
| 003082 | 129S1/SvImJ-Bcl2tm1Mpin/J | Cryopreserved - Ready for recovery |
| Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2tm1Sjk targeted mutation (Stock No. 002265). | ||
| 010633 | B6(Cg)-Gt(ROSA)26Sortm1(CAG-taulacZ)Bene/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. A loxP-flanked neo cassette prevents transcription of the downstream tau- beta galactosidase (tauLacZ) gene. When bred to mice that express Cre recombinase, the resulting offspring will have the neo cassette deleted in the cre-expressing tissue(s); resulting in expression of taulacZ. Upon histochemical staining with X-gal, the tau beta galactosidase activity is revealed as an intense blue precipitate found in the entire cell, regardless of cell type. When tested with an olfactory sensory neuron specific cre-expressing strain, expression of lacZ labels axon projections. This mutant mouse strain may be useful as a cre reporter. | ||
| 008233 | B6.129-Nrgntm1Kph/J | Cryopreserved - Ready for recovery |
| Homozygous neurogranin-deficient (Ng-/-) mice are viable and fertile (although the donating investigator reports that homozygous females do not nurse their pups as well as wildtype or heterozygous mothers). Homozygotes have no mRNA or protein from the targeted gene observed in brain tissues. Expression of lacZ is observed in a manner consistent with the endogenous gene. Ng-/- mice exhibit impaired spatial learning, altered hippocampal short- and long-term plasticity (including long-term potentiation induction), and decreased activated CaMKII. Heterozygotes show similar, yet milder, effects. These neurogranin- (Ng or RC3)-mutant mice may be useful for neurological studies involving memory and learning, neuronal signaling pathways (including calmodulin, alpha-CaMKII, protein kinase A, protein kinase C, MAPK, and CREB), attention deficit-hyperactivity disorder (ADHD), and schizophrenia. | ||
| 007566 | B6.129P2-Clip2tm1.1Gal/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable and fertile. Female homozygotes adults have lower body weights and smaller body length when compared to wildtype. No gene product (mRNA or protein) is detected by Northern or Western blot analysis of brain tissue. A splice acceptor site introduced into the lacZ reporter cassette results in a hybrid Clip2-lacZ transcript. Beta galactosidase staining is observed primarily in the hippocampus and in other areas of the brain. Homozygotes exhibit a mild growth retardation. The average copus callosum volume is significantly smaller than wildtype. Homozygotes and heterozygotes exhibit abnormal behavior indicative of hippocampal defects. In contextual fear-conditioning tests, mutant mice have a diminished response, although in cued fear-conditioning tests mutant mice exhibit normal behavior. Synaptic plasticity in the CA1 area of the hippocampus is decreased in mutant mice. Both heterozygotes and homozygotes e ..... For more information please see the full phenotype on the strain data sheet | ||
| 016094 | B6.129P2-Git2Gt(XG510)Byg/WeisJ | Cryopreserved - Ready for recovery |
| A targeting vector containing β-galactosidase was randomly inserted downstream of exon 2 of the endogenous G protein-coupled receptor kinase-interactor 2 (Git2) gene. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git2-exon1-2/lacZ fusion protein. Git2 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. GIT2 expression is seen throughout the liver, lungs, spleen, muscle, and the central nervous system. Expression of GIT2 is also seen during absent spermatid differentiation but is absent in mature spermatids. These mice may be useful as a lacZ reporter for Git2 e ..... For more information please see the full phenotype on the strain data sheet | ||
| 012909 | B6.129P2-Klf9tm1Yfk/J | Cryopreserved - Ready for recovery |
| Coding sequence of the Klf9 (Kruppel-like factor 9; also known as BTEB) gene is replaced by lacZ in these targeted mutation mice. Homozygotes show reduced activity levels in rotorod and contextual fear-conditioning tests. They also show a subtle increase in anxiety-like behavior. During development, dentate granule neurons lacking expression of this gene show delayed maturation. Homozygous females exhibit sub-fertility and slightly delayed labor. Homozygous pups are generally smaller at birth but catch up in weight by the time of weaning. This strain may be useful in studies of reproduction, development and behavior. | ||
| 007767 | B6.129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The P2-IRES-tau-lacZ knockin allele has a an internal ribosome entry site and the microtubule-binding protein tau / beta-galactosidase (tau-lacZ) fusion protein downstream of the olfactory receptor 17 gene (Olfr17). Olfactory sensory neurons that express the olfactory receptor 17 also co-express the tau-lacZ 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.
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 of the B6-P2-IRES-tau-lacZ mice could vary from that originally described for P2-IRES-tau-lacZ mice on a mixed B6;129P2 background. We may modify the strain description if necessary as published results become available ..... | ||
| 012723 | B6.129P2-Sptbn2Gt(XK442)Byg/LlpJ | Cryopreserved - Ready for recovery |
| Homozygous Sptbn2-/- mice are viable and fertile, and are prone to a mild nonprogressive ataxia and stimulus-induced seizures. This gene trap mutation abolishes endogenous spectrin beta 3 (Sptbn2) gene function and expresses a β-galactosidase (β-geo) reporter fusion protein. In these mice synapse morphology is altered, and there is a reduction in synapse-associated proteins, EAAT4, EAAT1, GluRδ, IP3R, and NCAM 140, leading to a failure to assemble transporters, receptors, and adhesion molecules. These Sptbn2-/- mice may be useful as a lacZ reporter for Spnb3 expression or as a knockout model for studying glutamate transport dynamics, synaptogenesis, seizures, and neuronal damage. | ||
| 012374 | B6.129S-Artm1Rax/ShahJ | Cryopreserved - Ready for recovery |
| This mutation is on the X chromosome. Homozygous females and hemizygous males are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice possess a reporter cassette, IRES-PLAP-IRES-nlacZ, downstream of the stop codon in the 3' UTR of the targeted locus. Nuclear β-galactosidase (β-gal) labels the nuclei of cells expressing AR, whereas human placental alkaline phosphatase (ALPP or PLAP) labels the cell membrane of such cells. In neurons expressing AR, these reporters label the nuclei and neuronal processes. These mice may be useful to visualize tissues expressing AR. | ||
| 012377 | B6.129S-Cyp19a1tm1.1Shah/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mutant mice possess a reporter cassette, IRES-PLAP-IRES-nlacZ, downstream of the stop codon in the 3' UTR of the targeted locus. Nuclear β-galactosidase (β-gal) labels the nuclei of cells expressing aromatase, whereas human placental alkaline phosphatase (ALPP or PLAP) labels the cell membrane of such cells. These mice may be useful for visualizing aromatase-positive cells to define where testosterone may be converted into estrogen in the mouse brain. | ||
| 007768 | B6.129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The OMP-tau-lacZ knock-in/knockout allele has a microtubule-binding protein tau and beta-galactosidase (tau-lacZ) fusion protein replacing the coding exon of the olfactory marker protein gene (Omp); both abolishing endogenous gene function and placing tau-lacZ expression under direction of the Omp promoter/enhancer regions. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile.
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 of the B6-OMP-tau-lacZ mice could vary from that originally described for OMP-tau-lacZ mice on a mixed B6;129S2 background. We may modify the str ..... | ||
| 016092 | B6.129S4-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Cryopreserved - Ready for recovery |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression is restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent ..... For more information please see the full phenotype on the strain data sheet | ||
| 005119 | B6.129S6-Npas2tm1Slm/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 005970 | B6.129S7-Atoh1tm2Hzo/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous 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. | ||
| 016167 | B6.Cg-ClockGt(P007F12)Wrst/JtJ | Cryopreserved - Ready for recovery |
| A "FlipROSAβgeo" genetrap inserted in intron 2-3 of the Clock (circadian locomotor output cycles kaput) locus disrupts gene expression to create a null allele. Loss of expression (confirmed in hypothalamus, cerebellum, liver and kidney) does not severely attenuate the expression levels and oscillations of other core circadian transcripts. | ||
| 003139 | B6.Cg-Tg(DBHn-lacZ)8Rpk/J | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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. | ||
| 012822 | B6;129-Fzd3tm1Nat/J | Cryopreserved - Ready for recovery |
| Homozygous Fzd3 (frizzled homolog 3 (Drosophila)) targeted mutation mice die at birth due to breathing difficulties which are most likely secondary to central nervous system (CNS) developmental defects. These mice show a complete loss of the thalamocortical, corticothalamic, and nigrostriatal tracts as well as the anterior commissure with variable loss of the corpus callosum. Axonal defects are apparent beginning at embryonic day 13 (E13). Peripheral nerve fibers are mostly or completely unaffected. Extensive cell death in the striatum occurs late in gestation, perhaps due to the complete absence of long-range connections. Beta galactosidase expression replaces that of the targeted gene. This strain may be useful in studies of neurodevelopment. | ||
| 008621 | B6;129-Fzd5tm1Nat/J | Cryopreserved - Ready for recovery |
| These frizzled 5 targeted mutant mice carry a beta galactosidase reporter. Heterozygous embryos show lacZ expression in the neural ridge at the anterior of the neural plate at E8.5, in the telencephalon, optic vesicle, hindgut and midgut at E10.5, and in the retinas at E16.5. Six-week-old animals express lacZ in the parafascicular nucleus and hypothalamus. Homozygous mice have placenta and yolk sac defects, thus die midway through gestation. In situ hybridization has confirmed that transcripts from the targeted gene are absent. | ||
| 012587 | B6;129-Iis1tm3(CAG-Bgeo,-tdTomato/TEVP,-Dlg4,-GFP)Nat/J | Cryopreserved - Ready for recovery |
| A CMV/beta actin (Z/AP) promoter located 2 kb 5' of the Ubb (ubiquitin B) gene drives constitutive expression of a nuclear-localized beta-galactosidase/neomycin resistance protein reporter (NLS-beta-geo) in the absence of Cre-mediated recombination. Following Cre-mediated recombination, the NLS-beta-geo coding region is excised and a downstream open reading frame is expressed. The downstream open reading frame codes for a single large protein (tdTomato/Tobacco etch virus protease (TEVP), a 6xMyc epitope, a TEVP cleavage site, post-synaptic density protein (PSD95) fused to green fluorescence protein (GFP) with a 3xHA epitope) which cleaves itself into two pieces shortly after translation. When Cre-mediated recombination occurs in neurons, the amino terminal piece (tdTomato/TEVP, a 6xMyc epitope, a TEVP cleavage site) labels all axon and dendrites, and the carboxy-terminal portion (PSD95, GFP, 3xHA epitope) labels post-synaptic structures. | ||
| 005064 | B6;129-Slc30a3tm1Rpa/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 009599 | B6;129P2-Adam19Gt(Betageo)1Bbl/J | Cryopreserved - Ready for recovery |
| Heterozygous mice are viable and fertile, while ~80% of homozygous mice die in the first few days after birth with severe heart valve defects. This β-geo secretory trap mutation abolishes endogenous gene function and expresses an ADAM19/LacZ/neo fusion protein. The mutant fusion protein has improper protein folding that keeps the ADAM19 regions of the protein retained in the endoplasmic reticulum by chaperones where they are subsequently degraded. As such, lacZ expression is directed to the same tissues as the wildtype gene. No wildtype ADAM19 protein product is observed from the targeted allele. These Adam19-mutant mice may be useful as a lacZ reporter for Adam19 expression or as a knockout model for studying developmental biology (cardiac morphogenesis). | ||
| 006703 | B6;129P2-Gucy2dtm1Mom/MomJ | Cryopreserved - Ready for recovery |
| 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. | ||
| 006595 | B6;129P2-Olfr17tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The P2-IRES-tau-lacZ knockin allele has a an internal ribosome entry site and the microtubule-binding protein tau / beta-galactosidase (tau-lacZ) fusion protein downstream of the olfactory receptor 17 gene (Olfr17). Olfactory sensory neurons that express the olfactory receptor 17 also co-express the tau-lacZ 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. | ||
| 012850 | B6;129P2-TardbpGt(RRB030)Byg/J | Cryopreserved - Ready for recovery |
| Tardbp+/- mice contain a gene trap targeting vector which inserts a β-geo fusion protein into intron 2 of the endogenous TAR DNA-binding Protein 43 (Tardbp) gene, abolishing gene function. Heterozygous mice are viable, fertile, and normal in size, while homozygous mice die between E3.5 and E8.5. lacZ expression in heterozygous embryos at E9.5 is restricted to neuroepithelium and is prominent in all neural progenitors from E10.5-12.5. By E12.5 expression is seen in spinal cord progenitors, in differentiated motor neurons, and in the dorsal root ganglia. Adult Tardbp+/- mice show widespread expression in various regions of the central nervous system. These mice may be useful as a lacZ reporter for Tardbp expression in neurodegenerative disorders. | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The OMP-tau-lacZ knock-in/knockout allele has a microtubule-binding protein tau and beta-galactosidase (tau-lacZ) fusion protein replacing the coding exon of the olfactory marker protein gene (Omp); both abolishing endogenous gene function and placing tau-lacZ expression under direction of the Omp promoter/enhancer regions. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile. | ||
| 011052 | B6;129S4-Ctbp2Gt(ROSA61)Sor/J | Cryopreserved - Ready for recovery |
| Mice that are heterozygous for the gene trap mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes have an embryonic lethal phenotype, failing to survive past embryonic day 10.5. No gene product (protein) is detected by Western blot analysis of homozygous embryos. Homozygous embryos exhibit extraembryonic vasculature defects, small size, axial truncations, delayed forebrain and midbrain development, dilated pericardium and abnormal heart development. Beta-galactosidase expression and staining mimics the expected endogenous gene expression pattern. | ||
| 017759 | B6;129S7-Cyp46a1tm1Rus/J | Cryopreserved - Ready for recovery |
| A tau-β-galactosidase (lacZ) fusion protein, followed by a neomycin (neo) resistance cassette, replaces the 3' end of exon 1 of the Cyp46a1 gene, abolishing gene function. Cyp46a1 encodes the enzyme cholesterol 24-hydroxylase which is expressed mainly in the brain, with low expression in liver. Cholesterol 24-hydroxylase is involved in cholesterol biosynthesis and turnover, and has also been implicated in the development of amyloid plaques in Alzheimer's disease. Homozygous mice are viable and fertile. In these mice, lacZ staining is evident in the spinal cord, midbrain, and hindbrain at E11.5, with expression decreasing between E11.5 and E13.5. LacZ staining is intensified between E11.5 and E13.5 in cells of the telencephalon, and the cerebral cortex. Beginning at E13.5, expression is restricted to dividing neurons in the neuroepithelium and post-mitotic neurons of the primordial plexiform layer of the telencephalon. These mice display a 4 ..... For more information please see the full phenotype on the strain data sheet | ||
| 003471 | B6;C3H-Tg(CNP-GEO)1Ldh/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 006465 | B6;CBA-Tg(CAG-lacZ-WGA)330Bbm/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 007975 | B6;CBA-Tg(OR8A1-taulacZ)1Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 154 base pairs upstream of the human OR8a1 transcription start site and 146 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for human olfactory receptor expression. Histology shows mosaic expression of LacZ in the main olfactory epithelium. | ||
| 007972 | B6;CBA-Tg(Olfr151-taulacZ)4Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 161 base pairs upstream of the Olfr151 transcription start site and 176 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows LacZ activity spread over a large domain of the dorsal aspect of the medial half-bulb, not coalescing into glomeruli. | ||
| 007973 | B6;CBA-Tg(Olfr16-taulacZ)1Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 148 base pairs upstream of the Olfr116 transcription start site and 154 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows LacZ expressing olfactory neurons projecting diffusely to a large domain centrally in the medial half-bulb, not coalescing into glomeruli. | ||
| 007974 | B6;CBA-Tg(Olfr160-taulacZ)V4-7Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 135 base pairs upstream of the Olfr160 transcription start site and 163 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows mosaic expression of LacZ in the main olfactory epithelium with the expression ventralized compared to the normal pattern of Olfr160 expression. | ||
| 007976 | B6;CBA-Tg(Olfr713-taulacZ)4Mom/MomJ | Cryopreserved - Ready for recovery |
| This transgene encodes tau-linked-LacZ under the control of a minimal promoter comprised of 143 base pairs upstream of the Olfr713 transcription start site and 163 base pairs of the 5' nontranslated exon 1. It does not drive expression of any olfactory receptor sequence. It is useful in mapping promoter elements important for olfactory receptor expression and the related olfactory sensory neuron development. Histology shows mosaic expression of LacZ in the ventral main olfactory epithelium. | ||
| 006743 | B6;CBA-Tg(P-taulacZ)11Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)11Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006793 | B6;CBA-Tg(P-taulacZ)13Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)13Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. | ||
| 006742 | B6;CBA-Tg(P-taulacZ)8Mom/MomJ | Cryopreserved - Ready for recovery |
| The Tg(P-taulacZ)8Mom transgene is expressed in approximately 10% of olfactory sensory neurons, which are also expected to co-express an endogenous olfactory receptor. This transgene is preferentially expressed in olfactory sensory neurons that co-express class II olfactory receptors, with a 100-fold lower expression found in class I expressing neurons. Immunohistochemistry shows expression in NCAM2 staining glomeruli, which are generally dorsally projecting, and a ventral subset of NQO1 staining glomeruli, which are generally ventrally projecting. Expression is absent in glomeruli in the dorsal-medial and anterior-dorsal olfacotry bulb giving an unlabeled butterfly-shaped pattern in a dorsal view. When mice co-express both this transgene and a YFP labelled null allele of Olfr545, a class I olfactory receptor, they label distinct regions; when mice co-express both this transgene and a GFP labelled null allele of Olfr160, a class II olfactory receptor, they label the same reg ..... For more information please see the full phenotype on the strain data sheet | ||
| 004141 | B6;CBA-Tg(UAS-lacZ)65Rth/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002865 | B6CBA-Tg(Wnt1-lacZ)206Amc/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 016095 | C.129P2(B6)-Git2Gt(XG510)Byg/WeisJ | Cryopreserved - Ready for recovery |
| A targeting vector containing β-galactosidase was randomly inserted downstream of exon 2 of the endogenous G protein-coupled receptor kinase-interactor 2 (Git2) gene. Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git2-exon1-2/lacZ fusion protein. Git2 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. GIT2 expression is seen throughout the liver, lungs, spleen, muscle, and the central nervous system. Expression of GIT2 is also seen during absent spermatid differentiation but is absent in mature spermatids. These mice may be useful as a lacZ reporter for Git2 e ..... For more information please see the full phenotype on the strain data sheet | ||
| 016093 | C.129S4(B6)-Git1Gt(FHCRC-GT-S10-12C1)Sor/WeisJ | Cryopreserved - Ready for recovery |
| A targeting vector containing β-galactosidase, a polyadenylation signal, and a PGK Hygromycin selection cassette, was randomly inserted downstream of exon 1 of the endogenous G protein-coupled receptor kinase-interactor 1 (Git1) gene. Heterozygous mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, although some males have decreased fertility. Homozygous mice die within a few days after birth. This β-geo secretory trap mutation abolishes endogenous gene function and expresses a Git1-exon1/lacZ fusion protein. Git1 belongs to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and has been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, neuronal spine formation, and aggregate formation in Huntington's disease. GIT1 expression restricted to some areas of the brain, to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 is absent dur ..... For more information please see the full phenotype on the strain data sheet | ||
| 009062 | C57BL/6-Magel2tm1Stw/J | Cryopreserved - Ready for recovery |
| The mouse locus 7qB4/B5 (syntenic with the Prader-Willi region at chromosome position 15q11-q13 in humans) encompasses the cluster of paternally-expressed imprinted genes Magel2, Ndn, Mkrn3, and Peg12. As maternal imprinting silences the Magel2 allele, only the paternally inherited Magel2 allele is expressed. The Magel2-lacZ knock-in allele abolishes endogenous gene function and expresses a β-galactosidase fusion protein. Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wildtype gene. For example, β-galactosidase expression during embryogenesis is detected in central nervous system (neural tube, forebrain, midbrain and embryonic hypothalamus), peripheral nervous system (dorsal root ganglia and peripheral neurons innervating limb and trunk muscles), and some non-neuronal tissues (genital tubercle, midgut region and placenta). Adult β-galactosidase ..... For more information please see the full phenotype on the strain data sheet | ||
| 004127 | FVB-Tg(Nes-rtTA)306Rvs/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 007225 | FVB.129(B6)-Usp18tm1Dzh/J | Cryopreserved - Ready for recovery |
| Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full phenotype on the strain data sheet | ||
| 008209 | FVB.Cg-Smn1tm1Msd Tg(ACTA1-SMN)69Ahmb Tg(SMN2)89Ahmb/J | Cryopreserved - Ready for recovery |
| As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 low copy line 89 transgene exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the HSA-SMN transgene; with the human alpha-skeletal actin (HSA or ACTA1) promoter directing full-length human SMN expression at high levels in skeletal muscle. When the HSA-SMN transgene is derived from HSA69-SMN founder mice, skeletal muscle-specific SMN expression is preserved, and homozygous SMN2; Smn; HSA69-SMN mutant animals (Stock No. 008209) have the same phenotype as homozygous SMA mice. In contrast, expression of the HSA-SMN transgene derived from HSA63-SMN founder mice is leaky; with hi ..... For more information please see the full phenotype on the strain data sheet | ||
| 008206 | FVB.Cg-Smn1tm1Msd Tg(SMN2)566Ahmb/J | Cryopreserved - Ready for recovery |
| As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and single copy human SMN2 low copy line 89 exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. In contrast to that SMA model, this strain carries the high copy SMN2 (founder line 566) transgene instead of the single copy SMN2 (line 89) transgene. As a result of the high SMN2 copy number, mice homozygous for the Smn1tm1Msd targeted mutation and high copy SMN2 line 566 (16 copies when homozygous) are rescued from all overt features of the severe SMA phenotype. Homozygous Smn; SMN2 high copy line 566 mice have a shorter and thicker tail. These Smn; SMN2 high copy line 566 mutant mice may be useful in neuromuscular studies including spinal muscular atrophy (SMA). | ||
| 003487 | FVB.Cg-Tg(XGFAP-lacZ)3Mes/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 008602 | STOCK Cdontm2Rsk/J | Cryopreserved - Ready for recovery |
| Homozygous CdonlacZ-2 (or CdolacZ-2) mice on a "129/Sv" genetic background are viable and fertile, harboring a beta-galactosidase (lacZ) "knock-in" mutation that also abolishes targeted gene expression. LacZ expression mimics the pattern observed for the endogenous gene. On a 129/Sv background, Cdo-deficient mice exhibit craniofacial midline defects identified as microforms of holoprosencephaly (HPE; a common defect of human forebrain development) with partial penetrance, grossly normal limb development and no perinatal lethality. These CdonlacZ-2 (or CdolacZ-2) mice are a genetic model of HPE and may be useful in studying craniofacial/brain development and the regulation of Sonic Hedgehog (Shh) signaling pathways, as well as for lacZ expression in Cdo-expressing tissues.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background dif ..... | ||
| 007912 | STOCK En1tm2Alj/J | Cryopreserved - Ready for recovery |
| En-1lki (or En1lacZ) mutant mice harbor a β-galactosidase "knock-in" allele that also abolishes endogenous gene function. While heterozygotes are viable and fertile, homozygous mice die at birth (unless when maintained on a C57BL/6 genetic background). Under control of the upstream promoter/enhancer elements, lacZ expression is observed in a pattern almost identical to the wildtype gene. These En-1lacZ mice may be useful for reporter protein expression in En1-expressing tissues in studying engrailed protein function in limb patterning along the dorso-ventral axis, spinal cord V1 interneuron development, embryonic mesencephalon and rhombomere 1 (cerebellum) development, as well as developing somites, and skin. Of note, these mice may also be useful in conjunction with other engrailed mutants (such as Stock No. 007916, Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 007925 | STOCK En2tm5.1Alj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this En2flox-taulacZ (also called En2-floxLacZ, En2tau-lacZ, or En2-tau-lacZ) mutation are viable but may not breed well (reported as "semi-fertile"). These mice harbor a loxP-flanked tau β-galactosidase "knock-in" allele that also abolishes engrailed 2 (En2) gene function. While both the tau-lacZ and En2 transcripts are made, only tau-lacZ is translated to protein. Expression of lacZ mimics that of the endogenous En2 gene. When bred to mice that express Cre recombinase, the resulting offspring will have the lacZ reporter deleted in the cre-expressing tissue(s) with subsequent restoration of En2 translation. These En2flox-taulacZ mutant mice may be useful for conditional reporter protein expression in En2-expressing tissues (including the early mesencephalon and rhombomere 1, and developing cerebellum and jaw muscles), as well as for conditional restoration of ..... For more information please see the full phenotype on the strain data sheet | ||
| 013123 | STOCK Gt(ROSA)26Sortm6(Gli1)Amc/J | Cryopreserved - Ready for recovery |
| These RosaGli1Flag c/c mice contain a floxed-neomycin resistance (neo) cassette and polyadenylation signal, cDNA encoding a FLAG-tagged GLI-Kruppel family member (Gli1) gene, an internal ribosome entry site (IRES), and a Venus yellow fluorescent protein (YFP) under control of the ubiquitous Gt(ROSA)26Sor locus. Breeding these mutant mice to mice that express Cre-recombinase will also result in Floxed-neo-stop excision. When these mice are crossed to mice containing Cre-recombinase under direction of an atonal homolog 1 (Math1) promoter, active in dividing granule neuron precursor cells and medulloblastoma tumors, the mice produce Gli1Flag at levels higher than the endogenous protein in the cerebellum. These mice may be useful for understanding Sonic hedgehog signaling and identifying targets of Gli1 action in developing ventral neural tube. | ||
| 004837 | STOCK Ntrk1tm1Apat/DnJ | Cryopreserved - Ready for recovery |
| 008203 | STOCK Smn1tm1Msd Tg(ACTA1-SMN)63Ahmb Tg(SMN2)89Ahmb/J | Cryopreserved - Ready for recovery |
| As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 low copy line 89 transgene exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the HSA-SMN transgene; with the human alpha-skeletal actin (HSA or ACTA1) promoter directing full-length human SMN expression at high levels in skeletal muscle. When the HSA-SMN transgene is derived from HSA69-SMN founder mice, skeletal muscle-specific SMN expression is preserved, and homozygous SMN2; Smn; HSA69-SMN mutant animals (Stock No. 008209) have the same phenotype as homozygous SMA mice. In contrast, expression of the HSA-SMN transgene derived from HSA63-SMN founder mice is leaky; with hi ..... For more information please see the full phenotype on the strain data sheet | ||
| 006553 | STOCK Smn1tm1Msd Tg(H2-K1-tsA58)6Kio Tg(SMN2*delta7)4299Ahmb Tg(SMN2)89Ahmb/J | Cryopreserved - Ready for recovery |
| This mutant mouse harbors a single targeted mutation and three transgenic alleles. The Smn1tm1Msd targeted mutation eliminates endogenous expression of the targeted gene. The Tg(SMN2*delta7)4299Ahmb transgene consists of a SMA cDNA lacking exon 7, whereas the Tg(SMN2)89Ahmb transgene consists of the entire human SMN2 gene. The Immortomouse transgene (from H-2Kb-tsA58 transgenic founder line 6 (H2ts6)) allows interferon-inducible expression of a thermolabile large tumor antigen (TAg) (and the small tumor antigen) from the SV40 thermosensitive A58 (tsA58) strain directed to widespread tissues by the interferon-inducible Class I antigen promoter from the mouse H-2Kb locus.
The following describes the phenotype of H-2Kb-tsA58 transgenic mice from founder line 6 (H2ts6; also called the Immortomouse): | ||
| 008212 | STOCK Smn1tm1Msd Tg(Prnp-SMN)92Ahmb Tg(SMN2)89Ahmb/J | Cryopreserved - Ready for recovery |
| As described for SMA mice (see Stock No. 005024), mice homozygous for Smn1tm1Msd targeted mutation (Smn null allele) and human SMN2 transgene (SMN2 low copy line 89) exhibit symptoms, neuropathology, and early lethality similar to human type I proximal spinal muscular atrophy (SMA) patients. As an addition to that SMA model, this strain also carries the PrP-SMN transgene; with the mouse prion protein (PrP or Prnp) promoter directing full-length human SMN expression at high levels in neurons (with low expression in skeletal muscle and liver). When the PrP-SMN transgene is derived from PrP92-SMN founder mice, high SMN expression in spinal cord and brain is observed. Homozygous SMN2; Smn; Prp92-SMN mice are rescued from the severe SMA phenotype, have significantly increased lifespan (average of 210 days) and have normal lumbar motor neuron root counts. Homozygous SMN2; Smn; PrP92-SMN mal ..... For more information please see the full phenotype on the strain data sheet | ||
| 006633 | STOCK Vmn1r49tm3Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutation causes a deletion of the coding region of the vomeronasal receptor V1rb2 and encodes two detectable tags. Vomeronasal sensory neurons that express the mutated locus co-express GFP and the taulacZ fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, by immunofluorescence with anti-GFP antibodies, by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. There is a three fold diminution in neurons expressing this disrupted allele relative to those that express a tagged endogenous sequence, and the pattern of innervation of the accessory olfactory bulb differs, with axons failing to converge onto distinct glomeruli. | ||
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