Search Criteria: Research Area is "Research Tools: Neurobiology Research"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 002052 | B6.129P2-Apoetm1Unc/J | Level 2 |
| Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged apoE-deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Additional studies indicate that apoE-deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage. | ||
| 004337 | 129(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain represents a model that may be useful in studies of telencephalic development. | ||
| 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. | ||
| 009575 | B6(129S4)-Et(cre/ERT2)119Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 012688 | B6(129S4)-Et(cre/ERT2)13866Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of a a CreERT2 fusion gene (Cre recombinase fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), the donating investigator reports CreERT2 activity for this line is the same with or without tamoxifen exposure. Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
nice staining in amygdala, with some cells in ventral striatum, hypothalamus, pallidum, and midbrain. No staining in other tested tissues is reported. When these enhancer trap lentiviral transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducibl ..... For more information please see the full phenotype on the strain data sheet | ||
| 009581 | B6(129S4)-Et(cre/ERT2)1642Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)1642Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 009582 | B6(129S4)-Et(cre/ERT2)1645Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 009585 | B6(129S4)-Et(cre/ERT2)2047Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 009577 | B6(129S4)-Et(cre/ERT2)296Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)296Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010689 | B6(129S4)-Et(cre/ERT2)6959Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)6959Rdav images). The Cre- ..... | ||
| 010690 | B6(129S4)-Et(cre/ERT2)7089Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)7089Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010696 | B6(129S4)-Et(icre/ERT2)10596Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind th ..... | ||
| 012689 | B6(129S4)-Et(icre/ERT2)14163Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
only in hypothalamus (perhaps arcuate nucleus only), no Cre recombinase activity is observed prior to tamoxifen exposure, no Cre recombinase activity in other tested tissues.
When these ..... For more information please see the full phenotype on the strain data sheet | ||
| 012690 | B6(129S4)-Et(icre/ERT2)14208Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in the neocortex, hippocampus, amygdala, striatum, thalamus, hypothalamus, midbrain, pons, medulla, and many cerebellar granule cells. No Cre recombinase activity is observ ..... For more information please see the full phenotype on the strain data sheet | ||
| 012694 | B6(129S4)-Et(icre/ERT2)14915Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in all areas of the brain; with high density of staining in granule cell layer. Dentate Gyrus projections are very obvious. No Cre recombinase activity is observed prior t ..... For more information please see the full phenotype on the strain data sheet | ||
| 012687 | B6(129S4)-Tg(SYN1-icre/mRFP1)9934Rdav/J | Repository- Live |
| Mice hemizygous for this lentiviral transgene are viable and fertile, with expression of a codon-improved Cre recombinase/monomeric red fluorescent protein fusion protein (iCre/mRFP1) under control of the human synapsin I promoter. The donating investigator reports Cre recombinase activity in brain tissues as widespread, with no staining in other tested tissues. The donating investigator did not characterize fluorescent expression of the mRFP1 portion of the fusion protein. When these transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. | ||
| 010774 | B6(Cg)-Calb2tm1(cre)Zjh/J | Repository- Live |
| The Cr-IRES-Cre (Calb2-IRES-Cre) allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the Calb2 (calbindin 2; also called calretinin or CR) locus. As such, cre expression is directed to calretinin interneurons in the brain and cortex by the endogenous Calb2 promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cr-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Calb2-expressing cells of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Calb2 expression pattern with highly efficient recombination). The donating investigator did not examine cre expression in tissues other than brai ..... | ||
| 013730 | B6(Cg)-Calb2tm2.1(cre/ERT2)Zjh/J | Repository- Live |
| The CR-CreER (or CR-CreERT2) knock-in allele was designed to both abolish Calb2 (calbindin 2; also called calretinin or CR) gene function and expresses CreERT2 fusion protein from the Calb2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when CR-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the CR-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the phenotype of CR-CreER homozygous mice has not been assessed. However, CR-CreER homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene on a similar genetic background (impaired motor coordination, abn ..... | ||
| 012710 | B6(Cg)-Ccktm2.1(cre/ERT2)Zjh/J | Repository- Live |
| The Cck-CreER (or Cck-CreERT2) knock-in allele both abolishes cholecystokinin (Cck) gene function and expresses the CreERT2 fusion protein from the Cck promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes may be expected to have a phenotype similar to other null mutations of this gene and may exhibit metabolic abnormalities of the endocrine/exocrine glands (increased pancreatic amylase).
Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Cck-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Cck-expressing cells of the offspring. These Cck-CreERT2 mice may be useful in studying brain anatomy, physiology and behavior. The donat ..... | ||
| 012704 | B6(Cg)-Crhtm1(cre)Zjh/J | Repository- Live |
| The CRH-ires-CRE allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the corticotropin releasing hormone locus (Crh). As such, cre expression is directed by the endogenous Crh promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When CRH-ires-CRE mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Crh-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Crh expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in CRH positive neurons (some interneurons), and may not have examined cre expression in tissues other than brain.
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| 010705 | B6(Cg)-Dlx5tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Dlx5-CreERT2 knock-in allele both abolishes Dlx5 gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Dlx5 promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit prenatal/perinatal death with craniofacial and nervous system abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Dlx5-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Dlx5-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Dlx5 expression pattern with highly efficient inducibility). They report tamox ..... | ||
| 013048 | B6(Cg)-Etv1tm1.1(cre/ERT2)Zjh/J | Repository- Live |
| The ER81-CreER (or ER81-CreERT2, Etv1-CreER, Etv1-CreERT2) knock-in allele was designed to both abolish ets variant gene 1 (Etv1) gene function and expresses CreERT2 fusion protein from the Etv1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when ER81-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Etv1-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Although mice homozygous for other null mutations of this gene on a similar genetic background exhibit neuromuscular abnormalities, ataxia and premature lethality, the donating investigator reports that ER81-CreER homozygous mice show no gross abnormalities. ER81 mRNA or protein expression fr ..... | ||
| 008242 | B6(Cg)-Gt(ROSA)26Sortm1(Ikbkb)Rsky/J | Repository- Live |
| Mice homozygous for the R26StopFLikk2ca conditional allele are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of the downstream bicistronic sequences (a FLAG-tagged, constitutively active form of IKbkb (IKK2ca) and EGFP). When bred to mice that express Cre recombinase, the resulting offspring will have the STOP cassette deleted in the cre-expressing tissue(s); resulting in expression of the IKK2ca as well as EGFP fluorescence. Expression of IKK2ca leads to constitutively active NF-kappaB transcription factor activity. These R26StopFLikk2ca mice allow inducible expression of an activated form of Ikbkb (IKK2 or IKK-beta) and subsequent activation of the NF-kappaB transcription factor pathways.
For example, when bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 006785), this ..... | ||
| 010776 | B6(Cg)-Lhx6tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Lhx6-CreERT2 knock-in allele both abolishes Lhx6 (LIM homeobox protein 6) gene function and expresses the CreERT2 fusion protein (creERT2 fusion protein) from the Lhx6 promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit neurological abnormalities and death within a few weeks of birth. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Lhx6-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Lhx6-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Lhx6 expression pattern, but with low efficiency of induction. They report tamoxifen-induc ..... | ||
| 010777 | B6(Cg)-Pvalbtm1(cre/ERT2)Zjh/J | Repository- Live |
| The Pv-CreERT2 (Pvalb-CreERT2) knock-in allele both abolishes Pvalb (parvalbumin; also called PV or Pva) gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Pvalb promoter/enhancer elements. Homozygous mice are viable and fertile. Homozygotes are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit muscle contractile, mitochondrial, and/or Purkinje cell abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Pv-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Pvalb-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Pvalb expression pattern, but with low efficiency of induction. The ..... | ||
| 010708 | B6(Cg)-Ssttm1(cre/ERT2)Zjh/J | Repository- Live |
| The Sst-CreERT2 (or SOM-CreERT2) knock-in allele both abolishes Sst gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Sst promoter/enhancer elements. Heterozygous mice are viable and fertile. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit nervous system and metabolic abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Sst-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Sst-expressing cells of the offspring.
The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Sst expression pattern, but with low efficiency of induction. They report tamoxifen-inducible Cre recombinase activity is observed ..... | ||
| 008355 | B6.129(Cg)-Slc6a4tm1Kpl/J | Repository- Live |
| Mice that are homozygous for the serotonin transporter targeted mutation (SERT-/- or 5-HTT-/-) are viable and fertile with a superficially unremarkable behavioral phenotype through early adulthood. Serotonin uptake is completely absent in homozygous mice. SERT-deficiency is pleiotropic (many different phenotypic traits). Homozygotes and, to a lesser extent, heterozygotes exhibit diminished responses to serotonin receptor agonists and other classes of drugs (including MDMA, SSRIs, 8-OH-DPAT, and DOI). SERT-mutant mice are also reported to have increased anxiety-like behaviors, altered neuroendocrine and sympathoadrenal responses to even minor stress, diminished aggression, altered emotional learning, substantially increased rapid eye movement (REM) sleep time, reduced brain excitability, increased body temperature, increased colonic motility, reduced spinal reflex to injury, reduced bladder response to stretching, blood pressure responses, diminished bone and muscl ..... For more information please see the full phenotype on the strain data sheet | ||
| 008471 | B6.129(SJL)-Oxtrtm1.1Wsy/J | Repository- Live |
| Mice homozygous for the Oxtrflox allele are viable and fertile, with loxP sites flanking exons 2-3 of the targeted gene. Expression and receptor binding distributions from the Oxtrflox targeted allele are reported to be normal when compared to wild-type. When Oxtrflox mice are bred to mice that express Cre recombinase, the resulting offspring will have the floxed region deleted in the cre-expressing tissue(s). These Oxtrflox mice may be used for spatial and temporal inactivation of the oxytocin receptor in studying (for example) parturition and lactation, as well as social, behavioral, and learning disorders such as autism and anxiety.
These Oxtrflox mice may also be useful along with the Oxt/EGFP AI03 transgenic mice (Stock No. 006043) or oxytocin targeted mutant mice (Stock No. 002713) from the same ..... | ||
| 007741 | B6.129-Arg1tm1Rki/J | Repository- Live |
| Homozygous AI-mutant mice completely lack hepatic arginase (AI) activity, exhibit hyperagrininemia, severe symptoms of hyperammonemia (ncluding decerebrate posture, lethargy, and high-frequency tremor of the extremities, particularly the tail) and die between 10-14 days after birth. Neural stem cells (NCSs) isolated from homozygous mice exhibit abnormal proliferation and differentiation. In addition, haploid germ cells carrying the disrupted AI allele may be less fit/less effective in forming zygotes compared to wild-type spermatozoa. Heterozygotes are viable and fertile. These AI-mutant mice may be useful in studying metabolic defects of arginase I deficiency, urea cycle (excretion of excess nitrogen), and neuronal development and function. | ||
| 012942 | B6.129-Gabra2tm1.1Geh/J | Repository- Live |
| These mutant mice carry substitutions of serine to histidine at amino acid position 270 and leucine to alanine at amino acid position 277 of exon 9. The point mutations confer alcohol and anesthesia insensitivity, while retaining near-normal GABA sensitivity. Approximately half of the homozygous mutant mice (from heterozygous crosses) die between birth and weaning. Homozygotes that survive to adulthood are fertile, normal in size and do not display any gross physical abnormalities. Mutant gene product (mRNA) is detected by RT-PCR analysis of whole brain total RNA. The alpha2 subunit protein levels did not differ between mice homozygous for the mutation and wildtype mice in the cortex and hippocampus. Homozygotes exhibit enhanced fear conditioning, reduced sensitivity to anesthesia (isoflurane), increased alcohol consumption without typical conditioned taste aversion, reduced ethanol induced stimulation of motor activity, and recover more slowly from ethanol?induced hypnosis. Den ..... For more information please see the full phenotype on the strain data sheet | ||
| 007251 | B6.129-Mapttm1Hnd/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 RT-PCR analysis of total brain RNA, Western blot analysis of total brain homogenates or immunostraining of coronal brain sections. Hippocampal neurons from homozygous embryos, in primary culture, have delayed axonal extension and shorter total dendritic length when compared to wildtype controls. Mitochondria in the primary culture cells cluster at the distal end of axons. The frequency and velocity of mitochondrial anterograde movements is increased. This mutant mouse strain may be useful in studies of neuronal development, axonogenesis, and organelle movement. | ||
| 009666 | B6.129-Ppargc1atm2Brsp/J | Repository- Live |
| These mice possess loxP sites on either side of exons 3-5 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 3-5 deleted in the cre-expressing tissue(s). When bred to a strain expressing Cre recombinase specifically in the liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatic heme biosynthesis and porphyrias. When bred to a strain expressing Cre recombinase specifically in skeletal muscle, this mutant mouse strain may be useful in studies of neuromuscular junction physiology and muscular dystrophy. | ||
| 004146 | B6.129-Tg(Pcp2-cre)2Mpin/J | Repository- Live |
| These transgenic mice express a cre gene inserted into exon 4 of a Pcp2 gene. Mice homozygous for the insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is observed in most Purkinje cells and some retinal bipolar neurons. Small amounts of activity are observed in an unidentified population of cells of the central nervous system tissue. Recombination is first observed around postnatal day 6 and is fully established 2 to 3 weeks after birth.
View cre expression characterization. | ||
| 008451 | B6.129P(Cg)-Ptprca Cx3cr1tm1Litt/LittJ | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprca) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul ..... For more information please see the full phenotype on the strain data sheet | ||
| 005582 | B6.129P-Cx3cr1tm1Litt/J | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.
Of note, CX3CR1-GFP mice are also avail ..... | ||
| 006084 | B6.129P2(Cg)-Foxg1tm1(cre)Skm/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Foxg1 locus. Forkhead box G1 is required for telencephalon development and is expressed specifically in the telencephalon and discrete head structures. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in the telencephalon, anterior optic vesicle (developing lens and retina), otic vesicle, facial and head ectoderm, olfactory epithelium, mid-hindbrain junction and pharyngeal pouches. Mice that are homozygous for the targeted mutation die perinatally. Heterozygous mutant mice are viable, fertile, normal in size. On the C57BL/6 background, forebrain volume in heterozygotes is substantially reduced especially in the cerebral cortex (40.7%), striatum (29.7%), and hippocampus (18.6%). In the adult, the thalamus is reduced in volume by 21.6%. This mutant mouse strain represents a model that ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 011008 | B6.129P2(Cg)-Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 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 | ||
| 008513 | B6.129P2-Gt(ROSA)26Sortm1(Trpv1,ECFP)Mde/J | Repository- Live |
| A loxP-flanked neomycin cassette blocks expression of the rat Trpv1 (transient receptor potential cation channel, subfamily V, member 1) gene driven by the Gt(ROSA)26Sor gene in this targeted mutation/knock-in strain. Upon crossing to a tissue-specific Cre-expressing strain, TRPV1 and enhanced cyan fluorescent protein (ECFP) is expressed from the ROSA locus. Cells expressing TRPV1 are sensitive to capsaicin and similar chemical agonists. Treatment of mice or cells that have undergone Cre excision to remove the neomycin cassette can induce strong inward currents, trigger action potentials and activate stereotyped behaviors, allowing cell-type specific chemical genetic control of neuronal activity in vitro and in vivo. Mice that are homozygous for the floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
When bred to a strain with widespread expression of Cre recombinase (see Stock No. > ..... | ||
| 016523 | B6.129P2-Htttm2Detl/200J | Repository- Live |
| As early as 9 weeks of age heterozygous mice exhibit cytoplasmic aggregation foci of HTT (huntingtin) protein, and by 20 weeks of age exhibit striatal neuronal intranuclear inclusions (NIIs). By 40 weeks of age, the striatal aggregation foci are perinuclear and exhibit increased immunoreactivity for ubiquitin and autophagosome marker LC3. Heterozygotes exhibit impaired balance and diminished motor coordination by 50 weeks of age, and abnormal gait by 60 weeks. By 80 weeks of age, heterozygotes display loss of grip strength, striatal and cortical astrogliosis, and a loss of approximately 50% of striatal dopamine receptor binding with increased glial fibrillary acidic protein immunoreactivity. Increased glial fibrillary acidic protein immunoreactivity is present in the striatum and ubiquititin- and huntingtin-positive neuronal intranuclear inclusions (NIIs) are detected throughout the dorsal striatum, nucleus accumbens and to a lesser extent other regions of the brain. Mutant CAG/poly ..... For more information please see the full phenotype on the strain data sheet | ||
| 016524 | B6.129P2-Htttm2Detl/250J | Repository- Live |
| HdhQ250 mutant mice exhibit a visibly abnormal phenotype at an earlier age as compared to the HdhQ150 strain (STOCK no. 004595 ), but have yet to be fully characterized. Mutant CAG/polyQ repeat expression is slightly lower than wildtype levels as detected by Western blot analysis and qRTPCR of brain tissue. Mutant mice may be noticeably smaller than wild-type littermates. Mice homozygous for the targeted allele are viable and fertile. Onset of symptoms occurs earlier for homozygotes than for heterozygotes. After 20 weeks of age mutant mice may become infertile. The Donating Investigator reports that homozygotes do not breed well.
This strain is one of a set of different CAG/polyQ repeat length mutants derived from HdhQ150 (STOCK no. 004595 ). The set includes, STOCK numbers: 016521, For more information please see the full phenotype on the strain data sheet | ||
| 013595 | B6.129S-Atoh1tm6.1Hzo/J | Repository- Live |
| These Atoh1FLAG mice contain three c-terminal FLAG tags fused to the 3' end of the atonal homolog 1 (Atoh1) gene. Homozygous mice are viable and fertile. Atoh1FLAG expression is evident evident in all Atoh1 expressing cells including cerebellar granule neuron precursors (GNPs) where it binds the active transcriptional enhancer region of the GLI-Kruppel family member GLI2 (Gli2) gene. These mice may be useful for studying postnatal cerebellar development and regulation of Sonic Hedgehog-induced medulloblastoma. | ||
| 012377 | B6.129S-Cyp19a1tm1.1Shah/J | Repository- Live |
| 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. | ||
| 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 | ||
| 006600 | B6.129S1-Mnx1tm4(cre)Tmj/J | Repository- Live |
| Mice heterozygous for this HB9cre targeted mutation are viable and fertile, with cre expression replacing HB9 (Hlxb9 or Mnx1) expression. Under control of the endogenous upstream elements, cre expression is directed to motor neurons. In heterozygotes, cre expression coincides with HB9 expression. Homozygous HB9cre mice die at or soon after birth, with expression of Cre recombinase likewise directed to motor neurons but no expression of endogenous HB9. When these HB9cre mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination in the resulting offspring leads to deletion of the flanked sequences in Mnx1/HB9 expressing cells; making them useful in neurodevelopmental studies of homeobox genes, motor neuron function and differentiation, and the central nervous system. | ||
| 005628 | B6.129S2-Emx1tm1(cre)Krj/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain expresses Cre recombinase from the endogenous Emx1 locus. Western blot analysis of cortical brain tissue does not detect reduced endogenous gene product (protein). When crossed with a strain containing a loxP-site flanked sequence, Cre-mediated recombination results in tissue-specific deletion of the flanked sequence. Recombination occurs in approximately 88% of the neurons of the neocortex and hippocampus, and in the glial cells of the pallium, mimicking the pattern of expression of the endogenous gene. Further, the donating investigator reports that Cre recombinase is also expressed in a subset of male germline cells, thus some offspring from a cre; floxed male will have the floxed allele recombined in all cells. This mutant mouse strain represents a model that may be useful in studies of forebrain development and f ..... For more information please see the full phenotype on the strain data sheet | ||
| 014156 | B6.129S4(Cg)-Cdk5tm1.1Lht/J | Repository- Live |
| These Cdk5 floxed mutant mice possess loxP sites flanking exons 1-5. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice that express Cre recombinase, resulting offspring lack detectable Cdk5 in the cre-expressing tissues. | ||
| 013720 | B6.129S6(Cg)-Ntrk1tm2Ddg/J | Repository- Live |
| A targeting vector was designed to place a FLAG tag upstream of exon 1 of the neurotrophic tyrosine kinase receptor, type 1 (Ntrk1 or TrkA) gene. Mice homozygous for the TrkAFlag allele are viable, fertile, and normal in size. | ||
| 015840 | B6.129S6-Itga8tm1.1Rdav/J | Repository- Live |
| Mice homozygous for this f(α8) conditional allele are viable and fertile, with loxP sites flanking the last two coding exons (exons 29-30) of the Itga8 gene (also called integrin alpha 8, alpha8-integrin, or α8-integrin). When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the transmembrane and the cytoplasmic domains deleted in the cre-expressing tissue(s). These f(α8) mutant mice may be useful in generating conditional mutations for studying the role of Itga8 transmembrane cell adhesion receptors in neuronal function in the developing and adult central nervous system, including intracellular signaling, behavior, synaptic plasticity, and memory formation.
For example, when f(α8) mice are bred to mice expressing Cre recombinase in forebrain neurons (see Stock No. 005359 for example), the double mutant offspring may exhibit impa ..... | ||
| 006852 | B6.129S6-Per2tm1Jt/J | Repository- Live |
| Mice homozygous for this "mPer2Luc" mutation are viable and fertile with no developmental or morphological differences compared to wildtype littermates. Expression of PERIOD2::LUCIFERASE (or mPER2::LUC) fusion protein during peak periods is similar to endogenous pPER2 patterns. Homozygous mice have normal entrainment and circadian behaviors. These mPer2Luc knock-in mice may be useful as a real-time reporter of circadian dynamics in different tissues. | ||
| 010670 | B6.129S7-Gfaptm1Mes/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. No gene product (mRNA) is detected by Northern blot analysis of whole brain from homozygotes. No protein is detected by immunohistochemistry of the hippocampus from homozygotes. Homozygous mutant mice show subtle changes in astrocyte morphology, CNS physiology, and enhanced LTP of both population spike amplitude and EPSP slope compared to control mice. Homozygotes are also hypersensitive to traumatic cervical spinal cord injury and axonal regeneration is delayed after peripheral nerve injury. Homozygotes display less striatal neuron lesion volume and an increase in striatal neuron projections in response to damage induced by 3-nitroproprionic acid (3-NP) or excitotoxin quinolinic acid (QA) relative to wild-type. Basal levels of glial cell derived neurotrophic factor (GDNF) are increased in homozygotes. These mice may be useful in studies dealing with transplantation, CNS injury, astrocyte biology, neural developmen ..... For more information please see the full phenotype on the strain data sheet | ||
| 008818 | B6.129S7-Itga3tm1Rdav/J | Repository- Live |
| Mice homozygous for this f(α3) conditional allele are viable and fertile, with loxP sites flanking exons 11-18 of the Itga3 (integrin alpha 3 (or alpha3-integrin (α3-integrin)) gene. When bred to mice that express Cre recombinase, the resulting offspring will have the floxed region deleted in the cre-expressing tissue(s): such deletion leads to a non-sense mutation from direct splicing of exon 10 to exon 19 and results in a truncated peptide that is predicted to be missing more than half of the wild-type sequence, including those that encode the transmembrane and the cytoplasmic domains. These f(α3) mutant mice may be useful in generating conditional mutations for studying the role of Itga3 transmembrane cell adhesion receptors in neuronal functions in the developing and adult central nervous system, including synaptic plasticity and memory formation.
When bred to a strain expressing Cre recombinase in the hippocampal CA1 pyramidal cells ..... | ||
| 016187 | B6.BTBR-Tg(Per1-luc,Per1)1Jt/J | Repository- Live |
| This compound transgenic strain was created by co-injecting a BAC clone encoding the entire mouse Per1 locus and a transgenic vector in which the Per1 promoter drives expression of luciferase (Per1:luc). The expression of Per1:luc oscillates in the suprachiasmatic nuclei (SCN) as well as peripheral tissues in ex vivo cultures (unlike most other Per1:luc transgenic strains which have weak rhythms in peripheral tissues). | ||
| 006965 | B6.Cg-Gt(ROSA)26Sortm1(rtTA*M2)Jae/J | Repository- Live |
| Homozygotes are viable, fertile, normal in size and do not display any behavioral abnormalities. These targeted mutant mice have widespread expression of an optimized form of reverse tetracycline-controlled transactivator (rtTA-M2) protein. This R26-M2rtTA strain may be useful for doxycycline-inducible studies which utilize rtTA/tet-O (tet-on/TRE) models. | ||
| 005491 | B6.Cg-Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Repository- Live |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 012358 | B6.Cg-Pvalbtm1.1(cre)Aibs/J | Repository- Live |
| Mice heterozygous for the Pvalb-2A-Cre allele are viable and fertile, with a viral 2A oligopeptide that mediates ribosomal skipping and a Cre recombinase gene inserted immediately downstream of the parvalbumin translational STOP codon. As such, Pvalb-2A-Cre mice have both endogenous gene and Cre recombinase expression directed to Pvalb-expressing cells by the endogenous promoter/enhancer elements of the parvalbumin locus. When Pvalb-2A-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Pvalb-expressing cells in the offspring. Specifically, the donating investigator reports cre activity in scattered interneuron populations in the cortex and hippocampus, as well as neuronal populations in other brain regions, resembling the Pvalb expression pattern. Additional reporter gene expression is seen in cortical layer 5 neurons, which are unlikely to be interneurons. ..... For more information please see the full phenotype on the strain data sheet | ||
| 012359 | B6.Cg-Pvalbtm1.1(tTA2)Hze/J | Repository- Live |
| Mice homozygous for the Pvalb-2A-tTA2 allele are viable and fertile, with a viral 2A oligopeptide that mediates ribosomal skipping and a synthetic modified tetracycline-regulated transactivator (tTA2S) gene just downstream of the parvalbumin translational STOP codon. As such, Pvalb-2A-tTA2 mice have both endogenous gene and tTA2 expression directed to Pvalb-expressing cells by the endogenous promoter/enhancer elements of the parvalbumin locus. When Pvalb-2A-tTA2 mice are bred with mice carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in the Pvalb-expressing cells may be conditionally abolished with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. Specifically, the donating investigator reports that Pvalb-2A-tTA2 activates tetO-regulated gene expression in scattered interneuronal populations in the cortex and hippo ..... For more information please see the full phenotype on the strain data sheet | ||
| 006149 | B6.Cg-Tg(ACTA1-cre)79Jme/J | Repository- Live |
| Mice hemizygous for this HSA-Cre79 transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These HSA-Cre79 transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. Cre activity is restricted to adult striated muscle fibers and embryonic striated muscle cells of the somites and heart. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in striated muscle-specific deletion of the flanked genome. Specifically, these HSA-Cre79 (or ACTA1-Cre) transgenic mice were originally used to breed with mice heterozygous for a deletion of exon 7 and a loxP-flanked exon 7 mutation on homologous chromosomes of the Smn1 gene (see Stock No. 006138 or Stock No. 006146). The resulting offspring ( ..... 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 | ||
| 005359 | B6.Cg-Tg(Camk2a-cre)T29-1Stl/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 transgenic mice express the Cre recombinase under the control of the mouse calcium/calmodulin-dependent protein kinase II alpha promoter. Cre recombinase expression is detected in the forebrain, specifically to the CA1 pyramidal cell layer in the hippocampus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination occurs in the pyramidal cell layer. | ||
| 007004 | B6.Cg-Tg(Camk2a-tTA)1Mmay/DboJ | Repository- Live |
| Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable and fertile. When hemizygotes are mated to a second strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene can be blocked by administration of the tetracycline analog, doxycycline (dox). These mice are a "Tet-Off" tool that allow the inducible expression of genes in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease (when used in conjunction with Stock No. 005706, Stock No. 007049, Stock No. 007051, Stock No. 007052), Parkinson's ..... For more information please see the full phenotype on the strain data sheet | ||
| 014545 | B6.Cg-Tg(Chat-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the ChAT-mhChR2-YFP BAC transgene (or ChAT-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to cholinergic neuronal populations by the mouse choline acetyltransferase (Chat or ChAT) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 008538 | B6.Cg-Tg(Cspg4-cre/Esr1*)BAkik/J | Repository- Live |
| Mice hemizygous for the NG2CreERTM BAC transgene are viable and fertile, with the mouse NG2 (Cspg4) promoter/enhancer directing expression of a tamoxifen-inducible Cre recombinase (CreERTM). This CreERTM fusion protein is estrogen insensitive, and is only active when it binds the estrogen analog 4-hydroxytamoxifen (OHT) or tamoxifen.
When these NG2CreERTM BAC transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination is expected to result in deletion of the floxed sequences in the Cre recombinase-expressing tissues of the offspring. No background cre activity is reported in the absence of tamoxifen. Following tamoxifen administration, the majority of Cre recombinase activity is reported in NG2-expressing glia (polydendrocytes, oligodendrocyte progenitor cells). The donating investigator specifically reports that tamoxifen-induced Cre recombinase activity is observed throu ..... For more information please see the full phenotype on the strain data sheet | ||
| 016204 | B6.Cg-Tg(Drd1a-tdTomato)6Calak/J | Repository- Live |
| These mutant mice harbor a transgenic BAC containing the mouse dopamine receptor D1A (Drd1a) promoter directing expression of a modified DsRed fluorescent protein, tdTomato. These Drd1a-tdTomato mice (founder line 6) express tdTomato in striatonigral neurons in a more accurate and specific manner than seen in previous founder lines. Hemizygous mice are viable, fertile and normal in size. These mice may be useful for specific visualization of striatonigral projection neurons and for studying dopamine-sensitive behaviors. | ||
| 014095 | B6.Cg-Tg(GFAP-Ccl2)JE95Rmra/J | Repository- Live |
| Mice homozygous for the huGFAP-MCP-1 transgene are viable and fertile, with expression of mouse monocyte chemoattractant protein-1 (MCP-1 or Ccl2) directed primarily to astrocytes of the CNS by the human glial fibrillary acidic protein (GFAP) promoter. Transgene-directed mRNA and protein expression is observed in CNS lysates and astrocyte cultures, as well as in peripheral nerve (such as sciatic; because GFAP is expressed by nonmyelinating Schwann cells). Mice derived from the high-expressing founder line 95 (also called huGFAP-MCP-1hi tg+, huGFAP-CCL2hi tg+, or JE-95 mice) overexpress CCL2 in an astroglial activation-dependent manner. Levels of CCL2 expression in the CNS of huGFAP-CCL2hi tg+ mice were comparable with those observed in CNS tissues from mice with experimental autoimmune encephalomyelitis (EAE). With chronic overexpression of CCL2, aged huGFAP-CCL2hi tg+ mice develop D ..... For more information please see the full phenotype on the strain data sheet | ||
| 005964 | B6.Cg-Tg(GFAP-tTA)110Pop/J | Repository- Live |
| Mice hemizygous for the transgene are viable fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express a tetracycline-controlled transactivator protein (tTA) driven by the human glial fibrillary acidic protein (GFAP) promoter. When these mice are mated to a second transgenic strain that carries a target gene under the regulation of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in astrocytes in the bitransgenic offspring can be induced by withdrawal of the tetracycline analog, doxycycline. Doxycycline may be administered in the animals' water supply. This strain represents an effective tool for generating bitrangenic animals that may be useful to study inducible gene expression in the astrocytes of the central nervous system. | ||
| 007673 | B6.Cg-Tg(Gad1-EGFP)3Gfng/J | Repository- Live |
| Mice hemizygous for this GAD67-GFP transgene are viable and fertile. In the hippocampus, GAD67-GFP (line 3) mice selectively express enhanced green fluorescent protein (EGFP) in newborn dentate granule cells. At two weeks of age, EGFP is expressed in large numbers of dentate granule cells, and the number of EGFP-positive cells diminishes with age in a pattern consistent with the postnatal development of dentate granule cells/age-related reduction in adult neurogenesis in the dentate gyrus. The EGFP expression in newborn dentate granule cells begins within the first week of cell division and disappears as newborn neurons mature (about 4 weeks postmitotic), and EGFP positive dentate granule cells also express the newborn neuron markers PSA-NCAM and doublecortin. The bright labeling of newborn neurons with EGFP makes it possible to visualize the details of dendrites, which reach the outer edge of the molecular layer, and
their axon terminals (mossy fiber boutons) in the CA3 region. In ad ..... For more information please see the full phenotype on the strain data sheet | ||
| 005698 | B6.Cg-Tg(Gfap-TK)7.1Mvs/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, normal in size, and do not display any behavioral abnormalities. Transgenic males are infertile. Proliferating cells that express the herpes simplex virus thymidine kinase (HSV-TK) transgene will metabolize ganciclovir (GCV) to toxic nucleotide analogues and undergo cell death. Transgene-derived HSV-TK is present exclusively in cells expressing endogenous Gfap. This coexpression occurs in brain astrocytes and adult neural stem cells, enteric glia, hepatic stellate cells, and unknown cells in heart, lung, kidney, adrenal, and spleen. Chronic GCV treatment for 21 days depletes GFAP-positive adult neural stem cells from forebrain proliferative zones. GCV treatment eliminated growth of primary multipotent neurospheres cultured from the germinal zones of postnatal and adult, but not early embryonic, transgenic mice. Notably, the same treatment prevented growth of secondary multipotent neurospheres from all three developmental stag ..... For more information please see the full phenotype on the strain data sheet | ||
| 007897 | B6.Cg-Tg(Gt(ROSA)26Sor-EGFP)I1Able/J | Repository- Live |
| Mice hemizygous for this ROSA26-EGFP BAC transgene are viable and fertile, with widespread EGFP expression in all organs and tissues analyzed. In addition, stable and uniform EGFP expression is observed in differentiated progeny of transplanted hematopoietic stem cells (HSC) isolated from ROSA26-EGFP mice. These ROSA26-EGFP BAC transgenic mice may be useful for fluorescent labeling of cells and tissues both in vivo and in vitro, are suitable for use in histological preparations, and are appropriate as a source of fluorescently labeled donor cell populations (such as tracking hematopoietic cell fate in transplant recipients).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as publis ..... | ||
| 005029 | B6.Cg-Tg(Hlxb9-GFP)1Tmj/J | Repository- Live |
| These transgenic mice express Green Fluorescent Protein (GFP) under the direction of the mouse Mnx1 (also called Hlxb9) promoter. Mice homozygous for the transgenic insert are viable, fertile, do not display any gross behavioral abnormalities, but are smaller in size than wildtype littermates. Homozygous pups born to homozygous females have a high mortality rate. Transgenic mice display distinct expression of GFP in dendrites, axons and soma of spinal motor neurons, allowing identification, isolation and purification of spinal motor neurons by FACS. GFP expression mimics endogenous HLXB9 expression pattern. Fluorescence is detected in axons, dendrites and processes of spinal motor neurons at embryonic day 9.5 to postnatal day 10 aged mice. This mutant mouse strain represents a model that may be useful for purification and in vivo tracking of spinal motor neurons. | ||
| 007742 | B6.Cg-Tg(Myh11-cre,-EGFP)2Mik/J | Repository- Live |
| Mice hemizygous for the smMHC/Cre/eGFP transgene (smMHCCre/eGFP) are viable and fertile, with the smooth muscle myosin heavy chain (smMHC or Myh11) promoter directing bicistronic Cre and EGFP protein expression to smooth muscle cells during development as well as in the adult mouse. Hemizygotes from founder line SMCG2 (SM2Cre/GFP) display intense EGFP fluorescence restricted to vascular and nonvascular smooth muscle, with strong concordance between cre expression and EGFP fluorescence (verifying the use of fluorescence as a marker for conditional gene recombination). When bred with mice containing a loxP-flanked sequence of interest, the resulting offspring can have Cre-mediated recombination of the flanked sequence in smooth muscle. Homozygotes are viable and fertile, with smaller litter sizes and a higher incidence of perinatal mortality. These smMHC/Cre/eGFP transgenic mice may be useful in studies utilizing "Cre-lox" technology or fluoresc ..... For more information please see the full phenotype on the strain data sheet | ||
| 003771 | B6.Cg-Tg(Nes-cre)1Kln/J | Repository- Live |
| These transgenic mice express Cre recombinase under the control of the rat nestin promoter and enhancer. Mice that are hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Initial studies utilizing a reporter strain carrying a beta galactosidase transgene whose expression is dependent on Cre-mediated recombination indicate that cre is primarily expressed in the central and peripheral nervous system with a few isolated kidney and heart cells also expressing activity. The donating investigator indicates that Cre recombinase activity is present in nervous tissue by embryonic day 11. The transgene insertion location is on Chromosome 12, as determined by FISH analysis, view pdf.
View cre expression characterization. | ||
| 007902 | B6.Cg-Tg(RP23-268L19-EGFP)2Mik/J | Repository- Live |
| Mice hemizygous for the ChAT(BAC)-eGFP (ChATBAC-eGFP) transgene are viable and fertile, with the endogenous choline acetyltransferase (ChAT) transcriptional regulatory elements (cholinergic gene locus) directing enhanced green fluorescent protein (EGFP) protein expression during development as well as in the adult mouse. As such, EGFP is expressed in central and peripheral cholinergic neurons, including cell bodies and processes of the somatic motor, somatic sensory, and parasympathetic nervous system in gastrointestinal, respiratory, urogenital, cardiovascular, and other peripheral organ systems and neuromuscular junctions. These ChAT(BAC)-eGFP transgenic mice allow fluorescent visualization of cholinergic elements of the central and peripheral nervous system and may be useful for studying cholinergic neurotransmission and neuromuscular coupling. | ||
| 005999 | B6.Cg-Tg(SBE/TK-luc)7Twc/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express luciferase in response to activation of the Smad2/3-dependent signaling pathway. Cultured primary astrocytes isolated from transgenic mice exhibited luciferase activity when stimulated with TGF-beta. Higher treatment levels of activin and nodal elicited similar luciferase activity. Lipopolysaccharide (LPS) challenge results in strong bioluminescence emissions from the intestinal region and brain. Mechanical injury to the neocortex results in an increase of bioluminescence in 2 hours, which peaks at 4 hours and returns to baseline approximately 48 hours after the injury. Biochemical assays for luciferase activity correlated with noninvasive bioluminescence imaging analysis. The strain was backcrossed to the albino C57BL/6J-Tyrc-2J/J strain for 2 generations to facilitate bioluminescence imaging. ..... For more information please see the full phenotype on the strain data sheet | ||
| 003966 | B6.Cg-Tg(Syn1-cre)671Jxm/J | Repository- Live |
| These transgenic mice express Cre recombinase under the direction of a synapsin promoter. Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Recombinase activity is detected in neuronal cells by embryonic day 12.5. | ||
| 007901 | B6.Cg-Tg(Thy1-Brainbow1.0)HLich/J | Repository- Live |
| These Thy1-Brainbow 1.0 (line H) transgenic mice are viable and fertile. The mice possess multiple fluorescent protein sequences uniquely flanked with pairs of incompatible Lox sites alternated to create mutually exclusive recombination events; allowing stochastic expression of multiple fluorescent proteins from a single transgene. Prior to Cre-mediated recombination, the fluorescent protein immediately adjacent to the promoter, tdimer2(12) (RFP), is expressed in peripheral and central neurons. When bred to Cre recombinase expressing mice, the resulting offspring can have one of three expression outcomes for each transgene in each cell of the cre expressing tissue(s): tdimer2(12) (RFP) (no recombination), mYFP, or mCerulean (CFP). A palmitoylation sequence tethers the mYFP and mCerulean (CFP) to the membrane, allowing clear labeling of axonal processes, while cytoplasmic tdimer2(12) (RFP) better labeled neuronal cell bodies and dendrites. Integration of tandem transgen ..... For more information please see the full phenotype on the strain data sheet | ||
| 007911 | B6.Cg-Tg(Thy1-Brainbow1.1)MLich/J | Repository- Live |
| These Thy1-Brainbow 1.1 (line M) transgenic mice are viable and fertile. The mice possess multiple fluorescent protein sequences uniquely flanked with pairs of incompatible Lox sites alternated to create mutually exclusive recombination events; allowing stochastic expression of multiple fluorescent proteins from a single transgene. Although the fluorescent protein immediately adjacent to the promoter, Kusabira-Orange (kOFP), was designed to be expressed prior to Cre-mediated recombination, basal kOFP expression is not observed in mouse tissues. When bred to Cre recombinase expressing mice, however, the resulting offspring can have one of three expression outcomes for each transgene in each cell of the cre expressing tissue(s): mCerulean (CFP), mYFP, or mCherry (RFP). The resulting fluorescent protein expression is observed in astrocytes of all areas of the brain and spinal cord, as well as dentate gyrus granule cells. A palmitoylation sequence tethers the mCherry (RFP), ..... For more information please see the full phenotype on the strain data sheet | ||
| 007921 | B6.Cg-Tg(Thy1-Brainbow2.1)RLich/J | Repository- Live |
| These Thy1-Brainbow 2.1 (line R) transgenic mice are viable and fertile. The mice possess two invertible DNA segments (four fluorescent protein sequences in total) uniquely positioned in tandem and flanked with LoxP sites to generate a larger number of recombination outcomes; allowing stochastic expression of multiple fluorescent proteins from a single transgene. Although the fluorescent protein immediately adjacent to the promoter, hrGFPII (with nuclear localization signal), was designed to be expressed prior to Cre-mediated recombination, basal hrGFPII expression may not be observed in mouse tissues. When bred to Cre recombinase expressing mice, however, the resulting offspring can have one of three different inversions for each transgene in each cell of the cre expressing tissue(s). In addition, two excision events may reduce the construct to one of two single invertible DNA segments which can continue to invert as long as cre is present. These different recomb ..... For more information please see the full phenotype on the strain data sheet | ||
| 003710 | B6.Cg-Tg(Thy1-CFP)23Jrs/J | Repository- Live |
| These mice express a spectral variant of GFP (cyan-CFP) at high levels in motor and sensory neurons, as well as subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. No expression is detectable in nonneural cells. This line provides a strong and specific vital marker for axons; fluorescence is also stable to mild aldehyde fixation. Expression is strong from a mid-gestational stage into adulthood. Availability of multiple spectral variants is useful for double-labeling applications, or breeding to other YFP/GFP lines. | ||
| 014131 | B6.Cg-Tg(Thy1-CFP)IJrs/GfngJ | Repository- Live |
| These founder line I transgenic mice express Cyan Fluorescent Protein gene under the control of the mouse Thy1, thymus cell antigen 1, theta, promoter. Fluorescence is detected in all motor axons, all retinal ganglion cells, dorsal root ganglion, neurons in cortical layers 2 through 6, and all of the cerebellar mossy fibers. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 007940 | B6.Cg-Tg(Thy1-CFP/COX8A)C1Lich/J | Repository- Live |
| These transgenic mice express Cyan Fluorescent Protein (CFP) under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations including retinal cells and in all motor axons. Coronal brain sections reveal a fluorescence pattern showing somatosensory cortex barrel morphology. Neuronal, mitochondrial and neuromuscular junction morphology appears normal in transgenic mice. Axonal mitochondrial density is similar to wildtype. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of mitochondrial transport.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different fro ..... | ||
| 007967 | B6.Cg-Tg(Thy1-CFP/COX8A)S2Lich/J | Repository- Live |
| These transgenic mice express Cyan Fluorescent Protein (CFP) under the control of the mouse thymus cell antigen 1, theta, Thy1, promoter. CFP is specifically localized to the mitochondria by a human cytochrome c oxidase, subunit 8A (ubiquitous), targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations including retinal ganglion cells, bipolar cells, amacrine cell and photoreceptors. Neuronal, mitochondrial and neuromuscular junction morphology appears normal in transgenic mice. Axonal mitochondrial density is similar to wildtype. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of mitochondrial transport in adult motor neurons.
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 chara ..... | ||
| 007612 | B6.Cg-Tg(Thy1-COP4/EYFP)18Gfng/J | Repository- Live |
| These Thy1-ChR2-YFP founder line 18 transgenic mice express the light-activated ion channel, Channelrhodopsin-2 (from the green alga Chlamydomonas reinhardtii), fused to Yellow Fluorescent Protein (ChR2-YFP) under the control of the mouse thymus cell antigen 1 (Thy1) promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of the transgenic ChR2-YFP fusion protein is detected in layer 5 cortical neurons, CA1 and CA3 pyramidal neurons of the hippocampus, cerebellar mossy fibers, neurons in the thalamus, midbrain and brainstem, and the olfactory bulb mitral cells. Neurons expressing the transgene are morphologically and physiologically comparable to non-mutant neurons. This mutant mouse strain may be useful for ex vivo and in vivo neural circuitry mapping studies using light stimulation. The ChR2-YFP fusion protein is composed of a Chlamydomonas reinhardtii-derived ..... | ||
| 007615 | B6.Cg-Tg(Thy1-COP4/EYFP)9Gfng/J | Repository- Live |
| These Thy1-ChR2-YFP founder line 9 transgenic mice express the light-activated ion channel, Channelrhodopsin-2 (from the green alga Chlamydomonas reinhardtii), fused to Yellow Fluorescent Protein (ChR2-YFP) under the control of the mouse thymus cell antigen 1 (Thy1) promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Expression of the transgenic ChR2-YFP fusion protein is detected throughout the brain, including in the cortex, hippocampus, thalamus, midbrain, brainstem, cerebellar mossy fibers and retinal ganglion cells. Neurons expressing the transgene are morphologically and physiologically comparable to non-mutant neurons. This mutant mouse strain may be useful for ex vivo and in vivo neural circuitry mapping studies using light stimulation.
The ChR2-YFP fusion protein is composed of a Chlamydomonas reinhardtii-derived channelrhodopsin-2 (ChR2) fused in-frame with an enh ..... | ||
| 007919 | B6.Cg-Tg(Thy1-EGFP)OJrs/GfngJ | Repository- Live |
| Mice hemizygous for the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). Thy1-GFP mice derived from founder line O express EGFP in subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. High (>80&) EGFP expression is observed in motor axons and cerebellar mossy fibers. Low (<10%) EGFP expression is observed in retinal ganglion cells and lumbar dorsal root ganglion. Sparse EGFP-labeling is also observed in neurons from multiple cortical layers. These Thy1-GFP line O transgenic mice may be useful for fluorescent labeling of neural tissues; especially motor axons and cerebellar mossy fibers, as well as intense, yet sparse, labeling of a variety of cortical neurons.
This strain is one of many from the same transgene ..... | ||
| 003709 | B6.Cg-Tg(Thy1-YFP)16Jrs/J | Repository- Live |
| These mice express spectral variants of GFP (yellow-YFP) at high levels in motor and sensory neurons, as well as in subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. No expression is detectable in nonneural cells. The transgenic insert used to make this strain is identical to that used in the construction of Stock No. 003782. This line provides a strong and specific vital marker for axons; fluorescence is also stable to mild aldehyde fixation. Expression is strong from a mid-gestational stage into adulthood. Availability of multiple spectral variants is useful for double-labeling applications, or breeding to other CFP/GFP lines. | ||
| 003782 | B6.Cg-Tg(Thy1-YFP)HJrs/J | Repository- Live |
| These mice express spectral variants of GFP (yellow-YFP) at high levels in motor and sensory neurons, as well as subsets of central neurons. Axons are brightly fluorescent all the way to the terminals. No expression is detectable in nonneural cells. The transgenic insert used to make this strain is identical to that used in the construction of strain 003709. The primary difference between these two strains is the specific neuron subsets which express YFP. In this strain, a few motor axons are labeled in muscle tissue, allowing determination of branching pattern and definition of which muscle fibers are innervated by a single motor axon. Approximately 10-30% of sensory neurons are labeled in dorsal root ganglia. Layer 5 pyramidal cells are selectively labeled in cerebral cortex. Pyramidal neurons are selectively labeled in the hippocampus. Approximately 10-30% of retinal ganglion cells are exclusively labeled in the retina. Many (but not all) mossy fibers are strongly labeled in cerebel ..... For more information please see the full phenotype on the strain data sheet | ||
| 007606 | B6.Cg-Tg(Thy1-cre/ERT2,-EYFP)AGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 promoter is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line A mice express the transgene in small subsets of motor neurons and dorsal root ganglion neurons.
..... For more information please see the full phenotype on the strain data sheet | ||
| 009614 | B6.Cg-Tg(Wfs1-cre/ERT2)2Aibs/J | Repository- Live |
| Hemizygous Wfs1-Tg2-CreERT2 mice are viable and fertile. As the Cre-ERT2 fusion gene is under control of the Wfs1 promoter/enhancer regions within the BAC transgene, cre activity is directed to cortex, hippocampus, and cerebellum only following tamoxifen administration. The donating investigators report that Cre recombinase expression for this Wfs1-Tg2-CreERT2 line is more restricted than the Wfs1-Tg3-CreERT2 line (Stock No. Stock No. 009103). The donating investigators may not have assessed expression in tissues other than brain. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only ga ..... For more information please see the full phenotype on the strain data sheet | ||
| 008468 | B6.Cg-Tg(tetO-DTA)1Gfi/J | Repository- Live |
| These tet-DTA transgenic mice express diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue diphtheria toxin A expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. These tet-DTA mice may be useful in generating bi-transgenic mutant mice for the reversible, inducible deletion of specific groups of cells.
For example, when bred to a strain expressing tTA in cardiac myocytes (see Stock No. 003170 for example), this mutant mouse strain may be useful in studies of human cardiomyopathies. When bred to a strain expressing tTA in pancreatic beta cells (see Stock N ..... | ||
| 006417 | B6.FVB-Tg(Npy-hrGFP)1Lowl/J | Repository- Live |
| Hemizygous mice are viable and fertile. These mice express humanized Renilla Green Fluorescent Protein (hrGFP, Stratagene) under control of the mouse neuropeptide Y (Npy) promoter. As such, UV light-exposed transgenic brain tissues show GFP fluorescence patterns consistent with the (Npy) gene. The donating investigator reports that the hrGFP expressed from this transgene is more stable and resistant to signal fading compared to other GFP’s. These transgenic mice may be useful for studies of neurobiology, energy metabolism, obesity, seizures, and epilepsy. | ||
| 010714 | B6.FVB-Tg(Pomc-cre)1Stl/J | Repository- Live |
| In this strain, the mouse pro-opiomelanocortin-alpha (Pomc) promoter drives expression of cre in the central nervous system, primarily the hippocampus. Cre expression is strongest and most restricted to the granule cells of the dentate gyrus subregion. Weaker, scattered expression can also be detected in other regions including the arcuate nucleus of the hypothalamus and the habenular nucleus. When crossed with a strain carrying a loxP-flanked genomic segment of interest, tissue-specific excision of that segment may be achieved. | ||
| 016262 | B6;129-Gt(ROSA)26Sortm1(Foxo1/GFP)Jke/J | Repository- Live |
| The FOXO1/GFP allele contains a loxP-flanked transcriptional STOP cassette (PGK-Neo-polyA) upstream of a forkhead box O1 (Foxo1)-green fluorescent protein (GFP) fusion protein. Homozygotes are viable and fertile. In the absence of Cre, reporter gene expression is prevented by the STOP sequence. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s), resulting in FOXO1/GFP expression in Cre-recombinase-expressing cells. FOXO1 is a component of the phosphoinositide 3-kinase (PI3K)-AKT pathway, and shuttles between the nucleus and the cytoplasm upon activation/inhibition by AKT. The PI3K-AKT signaling pathway is activated after administration of insulin and leptin. Exclusion of FoxO1 from the nucleus upon AKT phosphorylation allows visualization of activated/inactivated AKT by monitoring sub-cellular localization of the FOXO1-GFP fusion protein. These mice may be useful for ..... For more information please see the full phenotype on the strain data sheet | ||
| 008475 | B6;129-Nlgn3tm1Sud/J | Repository- Live |
| These mice carry an R451C mutation in exon 7 of the gene. mRNA is detected by real-time PCR analysis of brain from homozygous animals. Mutant mice exhibit enhancements in inhibitory synaptic transmission as well as spacial learning and memory, but show deficits in social interaction. This mutant mouse strain may be useful in studies of the pathophysiology of autism. Exon 7 is additionally flanked by loxP sites. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical abnormalities. | ||
| 012587 | B6;129-Ubbtm3Nat/J | Repository- Live |
| 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 presynaptic structures. | ||
| 008069 | B6;129P2-Pvalbtm1(cre)Arbr/J | Repository- Live |
| This strain expresses Cre recombinase from the endogenous Pvalb, parvalbumin, locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs in more than 90% of neurons that express parvalbumin, such as interneurons in the brain and proprioceptive afferent sensory neurons in the dorsal root ganglia. This mutant mouse strain represents a model that may be useful in studies of neuronal differentiation. | ||
| 014541 | B6;129S-Nos1tm1.1(cre/ERT2)Zjh/J | Repository- Live |
| The nNOS-CreER-KI (or nNOS-CreERT2-KI) knock-in allele was designed to both abolish neuronal nitric oxide synthase 1 (Nos1) gene function and express CreERT2 fusion protein from the Nos1 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when nNOS-CreER-KI mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Nos1-expressing cells of the offspring.
Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The donating investigator reports that the phenotype of nNOS-CreER-KI homozygous mice has not been assessed. However, nNOS-CreER-KI homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (abnormal neuron differentiation, increased ..... | ||
| 014605 | B6;129S-Tg(CMV-BBS1)6Vcs/J | Repository- Live |
| The CMV-BBS1 transgene contains a simian cytomegalovirus (sCMV) IE94 promoter driving expression of the open reading frame of the human Bardet-Biedl syndrome 1 (BBS1) gene, tagged with a 5' 3xFLAG tag and 4xMyc tag. Homozygous mice are viable and fertile. BBS is a pleiotropic disorder characterized by retinal and photoreceptor degeneration, obesity, polydactyly, renal abnormalities, hypogenitalism and cognitive impairment. BBS is associated with an increased incidence of hypertension, diabetes mellitus and heart defects. These mice are phenotypically normal and express the transgene in the eye and testes. | ||
| 006414 | B6;129S4-Mc4rtm1Lowl/J | Repository- Live |
| The mice have a loxp-flanked transcriptional blocking (loxTB) sequence that prevents normal endogenous gene transcription and translation from the endogenous locus. As such, homozygous mice are devoid of functional mRNA in all tested regions of the brain. Homozygous mice exhibit severe early-onset obesity, accompanied by hyperphagia, increased snout-anus length and hyperinsulinemia. The function of this disrupted allele can be restored by the enzymatic activity of Cre-recombinase. These mutant mice may be useful in studies of neurobiology, obesity, diabetes, hunger/appetite, and fat and energy metabolism.
When bred to a strain expressing Cre recombinase in the hypothalamus see Stock No. 006395 for example), this mutant mouse strain exhibits as intermediate phenotype in comparison to homozygous null mice. | ||
| 006410 | B6;129S6-Chattm1(cre)Lowl/J | Repository- Live |
| Homozygous mice maintained at The Jackson Laboratory are viable and fertile. An "IRES-Cre" sequence is inserted downstream of the stop codon such that cre expression is controlled by the endogenous Chat gene promoter. Chat gene expression, however, is unaffected. Cre recombinase activity is reported in all cholinergic neurons. These mice may be useful for "Cre-lox" technology applications in neurobiology, including studies of motor function, learning and memory, Alzheimer's disease, and Down syndrome, and in obesity and diabetes research.
View cre expression characterization. | ||
| 012362 | B6;129S6-Tg(Camk2a-cre/ERT2)1Aibs/J | Repository- Live |
| Mice hemizygous for the Camk2a-CreERT2 transgene are viable and fertile, with expression of CreERT2 fusion protein (CreERT2 fusion protein) directed to neural populations by the mouse calcium/calmodulin-dependent protein kinase II alpha promoter region. Cre-ERT2 fusion gene activity is inducible; observed at high levels following tamoxifen administration. When Camk2a-CreERT2 transgenic mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Camk2a-expressing cells of the double mutant offspring. Specifically, the donating investigator reports that the Camk2a-CreERT2 transgene directs reporter gene expression in sparse populations of neurons in the cortex, hippocampus, striatum, and other structures in the absence of tamoxifen. Following tamoxifen administration, reporter gene expression is turned on in widespread populations of neurons in the same regions ..... For more information please see the full phenotype on the strain data sheet | ||
| 009613 | B6;C3-Tg(Scnn1a-cre)3Aibs/J | Repository- Live |
| Hemizygous Scnn1a-Tg3-Cre mice are viable and fertile, with cre expression directed to cortex, thalamus, midbrain, and cerebellum by the Scnn1a promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Scnn1a-Tg3-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, thalamus, midbrain, and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Scnn1a-Tg3-Cre images). | ||
| 009103 | B6;C3-Tg(Wfs1-cre/ERT2)3Aibs/J | Repository- Live |
| Hemizygous Wfs1-Tg3-CreERT2 mice are viable and fertile. As the Cre-ERT2 fusion gene is under control of the Wfs1 promoter/enhancer regions within the BAC transgene, cre activity is directed to cortex, hippocampus, striatum, thalamus and cerebellum only following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 014650 | B6;C3-Tg(tetO-TARDBP*)4Vle/J | Repository- Live |
| These transgenic mice express the mutant human TARDBP, TAR DNA binding protein, hTDP-43-deltaNLS, with a defective nuclear localization signal, under the direction of the tetO, tetracycline operator promoter. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. It is not known if homozygotes are viable. When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of the hTDP-43-deltaNLS protein may be regulated with tetracycline or its analog doxycycline (DOX) in the double mutant offspring. When mated to Camk2a-tTA mice which express tTA in forebrain neurons (See for example: Stock No. 003010; Stock No. 007004; Stock No. 010712), the resulting bitransgenic mice ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 003010 | B6;CBA-Tg(Camk2a-tTA)1Mmay/J | Repository- Live |
| Transgenic mice expressing the tetracycline-controlled transactivator protein (tTA) under regulatory control of the forebrain-specific calcium-calmodulin-dependent kinase II (Camk2a) promoter are viable, fertile, and display no overt phenotypic defects. Transgene expression can be blocked by the administration of the tetracycline analog doxycycline (dox) to the mice. Mating these transgenic mice to a second transgenic strain carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE; tetO) allows dox-inducible expression of the target gene specifically in forebrain neurons, and may be useful in studying brain disorders such as Alzheimer's disease (when used in conjunction with Stock No. 005706, Stock No. 007049, Stock No. 007051, Stock No. 00 ..... For more information please see the full phenotype on the strain data sheet | ||
| 007910 | B6;CBA-Tg(Thy1-Brainbow1.0)LLich/J | Repository- Live |
| These Thy1-Brainbow 1.0 (line L) transgenic mice are viable and fertile. The mice possess multiple fluorescent protein sequences uniquely flanked with pairs of incompatible Lox sites alternated to create mutually exclusive recombination events; allowing stochastic expression of multiple fluorescent proteins from a single transgene. Prior to Cre-mediated recombination, the fluorescent protein immediately adjacent to the promoter, dTomato (RFP), is expressed in peripheral and central neurons. When bred to Cre recombinase expressing mice, the resulting offspring can have one of three expression outcomes for each transgene in each cell of the cre expressing tissue(s): dTomato (RFP) (no recombination), mCerulean (CFP), or mYFP. Integration of tandem transgene copies yields combinatorial fluorescent protein expression in each cell, and thus many possible cell colors, providing a way to distinguish adjacent neurons and visualize other cellular interactions. Of note, the singl ..... For more information please see the full phenotype on the strain data sheet | ||
| 011070 | B6;CBA-Tg(Thy1-EGFP)SJrs/NdivJ | Repository- Live |
| Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). These thy1-GFP-S mice (derived from founder line S) have EGFP expression in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Thy1-GFP-S mice show EGFP labeling in the superficial layers of the neocortex, including most/all interneuron subtypes, with pyramidal/interneuron ratios of approximately 4:1 that match the distribution in the non-labeled population. While this is similar to Thy1-GFPM mice (Stock No. 007788), the labeling distribution for line S is different from line M. In addition, less than 10% of cerebellum mossy fibers show EGFP labeling and no EGFP expressio ..... 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 | ||
| 014160 | B6;DBA-Tg(S100b-EGFP/cre/ERT2)22Amc/J | Repository- Live |
| These transgenic mice express the eGFPCreERT2 (Enhanced Green Fluorescent Protein and cre/ESR1) fusion gene under the direction of the mouse S100b, S100 protein, beta polypeptide, neural, promoter. Transgene expression is detected in chondrocytes in developing bone and in neural cells in the dorsal root ganglia (DRG). GFP fluorescence is not detectable by fluorescent microscope examination of whole embryos, bones or neural tube sagittal slices from embryos aged 15.5dpc. Tamoxifen induced Cre recombinase activity is detected in a subset of the GFP immunoreactive-positive cells in bone and to a lesser extent in the dorsal root ganglia. GFP immunoreactive-positive cells co-localize with S100b immunoreactive-positive cells in bone and DRG. Other possible sites of expression have not been characterized. Mice that are hemizygous for the transgene are viable, fertile, normal in size and do not display physical or behavioral abnormalities. This strain was transfe ..... For more information please see the full phenotype on the strain data sheet | ||
| 009159 | B6;FVB-Tg(Cnp-EGFP/Rpl10a)JD368Htz/J | Repository- Live |
| These BAC TRAP transgenic mice express the EGFP-L10a fusion gene, EGFP/Rpl10a, under the control of the mouse Cnp (2',3'-cyclic nucleotide 3' phosphodiesterase) promoter. The transgene expression pattern corresponds to endogenous Cnp expression. Green fluorescent protein is detected in mature oligodendrocytes. Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Transgenic male mice are infertile. Attempts at cryopreserving sperm from male transgenic mice have failed. This mutant mouse strain may be useful in affinity purification of polysomal mRNAs (translating ribosome affinity purification or TRAP) from mature oligodendrocytes and tracking mature oligodendrocytes by fluorescence. | ||
| 010576 | B6;SJL-Tg(MMTV-rtTA)4-1Jek/J | Repository- Live |
| The donating investigator claims homozygous mice are viable and fertile. These MMTV-rtTA mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed primarily to the breast epithelia of the mammary ductal system by the mouse mammary tumor virus (MMTV) promoter. The donating investigator also reports some rtTA expression in salivary glands (particularly in the males) as well as prostate glands. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These MMTV-rtTA mice are a Tet-On tool that allows conditional, dox-inducible expression of genes primarily in mammary gland epithelial cells and may be useful in studying the endocrine function of mammary tissues and/or breast cancer (for example). | ||
| 012355 | B6;SJL-Tg(Pvalb-COP4*H134R/EYFP)15Gfng/J | Repository- Live |
| Mice hemizygous for the Prv-mhChR2-YFP BAC transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neuronal populations by the mouse parvalbumin (Pvalb or Prv) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light (450-490 nm) leads to rapid ..... For more information please see the full phenotype on the strain data sheet | ||
| 012348 | B6;SJL-Tg(Thy1-COP3/EYFP)8Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012350 | B6;SJL-Tg(Thy1-COP4*H134R/EYFP)20Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-mhChR2-YFP transgene are viable and fertile with expression of the mhChR2::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 (optimized with an N-terminal beta2 nictinic acytlcholine receptor signal peptide and C-terminal ER-export and Golgi-export motifs) that harbors a gain-of-function H134R substitution fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-expressing neurons with blue light ..... For more information please see the full phenotype on the strain data sheet | ||
| 012332 | B6;SJL-Tg(Thy1-HOP/EYFP)2Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 2 exhibit high expression of EYFP in layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 2 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammalian systems ..... | ||
| 012334 | B6;SJL-Tg(Thy1-HOP/EYFP)4Gfng/J | Repository- Live |
| Mice hemizygous for the Thy1-eNpHR-YFP transgene are viable and fertile with expression of the eNpHR::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The donating investigator specifically reports that Thy1-eNpHR-YFP mice derived from founder line 4 exhibit high EGFP expression in layer 2/3 and layer 5 pyramidal neurons at cortex, dentate gyrus, thalamus, superior colliculus, inferior culliculus, brainstem, amydagala and cerebellum. These Thy1-eNpHR-YFP line 4 transgenic mice may be useful for rapid control of motor behavior by addition or removal of light, for ex vivo and in vivo studies of neural circuitry/connectivity following illumination, or for fluorescent labeling of neural tissues.
The eNpHR::YFP fusion protein, designed with halorhodopsin from the halophilic bacterium Natronomonas pharaonis (NpHR) fused in-frame with an enhanced yellow fluorescent protein (EYFP), was optimized for expression in mammali ..... | ||
| 007610 | B6;SJL-Tg(Thy1-cre/ERT2,-EYFP)VGfng/J | Repository- Live |
| These transgenic mice ("SLICK" for single-neuron labeling with inducible Cre-mediated knock-out) have a tamoxifen inducible Cre-mediated recombination system and Enhanced Yellow Fluorescent Protein driven by 2 bidirectional copies of the mouse thymus cell antigen 1 promoter. Hemizygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing a loxP site flanked sequence of interest, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted neuron-specific deletions only in neurons where the Thy1 is active. These cells will be evident by the expression of Yellow Fluorescent Protein. Transgenic mice express YFP constitutively in neurons. The Donating Investigator reports that founder line V mice express the transgene sparsely in neurons of the central nervous system.
This strain is one of ..... | ||
| 014555 | B6;SJL-Tg(Tph2-COP4*H134R/EYFP)5Gfng/J | Repository- Live |
| Mice hemizygous for the TpH2-mhChR2-YFP BAC transgene (or TpH2-ChR2-YFP BAC transgene) are viable and fertile, with expression of the mhChR2::YFP fusion protein directed to serotonergic neuronal populations by the mouse tryptophan hydroxylase 2 (Tph2 or TpH2) promoter/enhancer regions on the BAC transgene. The mhChR2::YFP fusion protein is composed of a mammalian codon-optimized Chlamydomonas reinhardtii-derived channelrhodopsin-2 that was modified to harbor a gain-of-function H134R substitution (mhChR2; also called hChR2-H134R) fused in-frame with an enhanced yellow fluorescent protein (EYFP). The mhChR2 is designed to cause larger stationary photocurrents compared to ChR2. The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this mhChR2 functions as a blue light-driven cation channel that depolarizes the cell and causes action potentials. As such, illuminating mhChR2-ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 010577 | B6;SJL-Tg(tetO-Erbb2*)8-4Jek/J | Repository- Live |
| The donating investigator reports that homozygous mice are viable and fertile. These TetRE-ErbB2 (TRE-ErbB2 or TRE-Neu) transgenic mice have expression of an activated form of the rat ErbB2 regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator) and cytomegalovirus minimal promoter. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of the constitutively active ErbB2 protein may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring.
The amino acid mutation within the transmembrane domain of the ErbB2 receptor protein kinase facilitates its oligomerization and activation independent of a ligand; resulting in hyperplasia in tissues where it is expressed.
These TetRE-ErbB2 mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/r ..... For more information please see the full phenotype on the strain data sheet | ||
| 016556 | B6N.129-Ptpn5tm1Pjlo/J | Repository- Live |
| In this STEP KO strain, a neo cassette replaces the catalytic site of the protein tyrosine phosphatase, non-receptor type 5 (Ptpn5) gene, abolishing gene expression. Homozygotes are viable, fertile, and normal in size. Striatal enriched protein phosphatase (STEP) is a neuron-specific tyrosine phosphatase which regulates synaptic plasticity following glutamatergic and dopaminergic input. Expressed mainly in the striatum, hippocampus, amygdala, and cortex of the brain, glutamate-activated STEP controls synaptic plasticity through limiting the duration of ERK 1/2 MAP kinase activity and by endocytosis of glutamate receptors. Activation of ERK1/2 in STEP-expressing regions of the brain is required for memory formation and learning. STEP levels are also shown to be increased in prefrontal cortex of Alzheimer's Disease (AD) models. Homozygous STEP KO mice lack expression of all STEP isoforms, and exhibit enhanced phosphorylation of ERK1/2 in the striatum, hippocampus ..... For more information please see the full phenotype on the strain data sheet | ||
| 008603 | C.129P2(B6)-Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally describe ..... | ||
| 008393 | C3H;101-Dync1h1Swl/PopJ | Repository- Live |
| Mice heterozygous for the radiation-induced Sprawling mutation of the cytoplasmic dynein heavy chain 1 gene (Dync1h1Swl) are viable and fertile (the donating investigator reports that less than 50% of males breed successfully). Heterozygous mice display an early-onset hereditary proprioceptive sensory neuropathy with muscle spindle deficiency. Mice are distinguishable around one week after birth by the presence of hindlimb flexion during tail suspension, and around three to four weeks of age develop a typical unsteady gait characterized by jerky and wobbly locomotion. At rest, the hindlimbs are splayed and flexed forward and hindpaws are incapable of gripping structures. Defective proprioception is suggested as proprioceptive sensory neurons are severely compromised in the lumbar dorsal root ganglia of newborns and the H reflex is defective despite normal motor nerve function in the hindlimbs. Homozygous mice die in utero before embryonic day (E)8.5, indicating ..... For more information please see the full phenotype on the strain data sheet | ||
| 014096 | C57BL/6-Ces1ctm1.1Loc/J | Repository- Live |
| These Es1-/- knockout mice lack exon 5 of the carboxylesterase 1C (Ces1c or Es1) gene, abolishing gene function. Mice that are homozygous for this allele are viable, fertile, and normal in size. Carboxylesterases are expressed in the liver and are found in many tissues including the intestine, lung, and in the plasma of mice, but not in the plasma of humans. To mimic the lack of ES1 in human plasma and the resulting increase in susceptibility to nerve agents and to drugs that are hydrolyzed by ES1, these mice have had plasma ES1 activity eliminated. ES1 acts as an organophosphorus (OP) bioscavenger which reduces the level of OP reaching biologically relevant targets and protects against lethal toxicity from nerve agents. Es1-/- mice have normal acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and paraoxonase plasma activity, with normal levels of carboxylesterase activity in other tissues, including the brain, lungs, liver, ..... For more information please see the full phenotype on the strain data sheet | ||
| 009062 | C57BL/6-Magel2tm1Stw/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 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 | ||
| 010712 | C57BL/6-Tg(Camk2a-tTA)1Stl/J | Repository- Live |
| When these transgenic mice are crossed with a tissue or cell-specific cre strain to remove a floxed stop cassette, tetracycline-controlled transactivator (tTA) is expressed in hippocampal CA3 and the dentate gyrus under the control of the calcium/calmodulin-dependent protein kinase II alpha (Camk2a) promoter. When further mated to a transgenic strain that carries a gene of interest driven by a tetracycline-responsive promoter element (TRE; tetO), expression of that gene can be conditionally regulated by the presence or absence of doxycycline in the drinking water. Expression in tTA/tetO animals can be reversibly inhibited by the presence of doxycycline or induced by withdrawal of the tetracycline analog. | ||
| 011086 | C57BL/6-Tg(Cck-cre)CKres/J | Repository- Live |
| A minimal Cck (cholecystokinin) promoter drives expression of Cre in this transgenic strain. These mice express Cre at high levels in the brain cortex in a pattern that is qualitatively similar to that of the wildtype Cck gene. There is virtually no expression in subcortical regions. Although a component of the transgene, DsRed2 is not expressed. This strain may be useful for various psychiatric and neuroscience studies of this neuropeptide promoter. | ||
| 010713 | C57BL/6-Tg(tetO-GFP/tetX)5696Stl/J | Repository- Live |
| These transgenic mice express tetanus toxin (tetX) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator), and may be useful in generating bi-transgenic mutant mice for the reversible, inducible inhibition of synaptic transmission. Although GFP is fused to tetX, fluorescence may not be detectable. | ||
| 016181 | C57BL/6-Tg(tetO-Nr1d1)1Schb/J | Repository- Live |
| These transgenic mice express hemagglutinin-tagged Nr1d1 (nuclear receptor subfamily 1, group D, member 1) cDNA under the control of a tetracycline-responsive element (TRE; tetO)/minimal cytomegalovirus (CMV) promoter. When hemizygotes are bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled tranactivator protein (tTA) under the regulation of tissue-specific promoters, transgene expression can be conditionally regulated with doxycycline. | ||
| 009655 | C57BL/6J-Tg(Dcx-DsRed)14Qlu/J | Repository- Live |
| These transgenic mice express red fluorescent protein variant (DsRed-Express) under the direction of the mouse doublecortin promoter. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Fluorescence is first detected at embryonic day 11.5. By embryonic day 13.5 fluorescence is restricted to the CNS and mimics the endogenous doublecortin expression pattern. This mutant mouse strain may be useful in studies of neural development and visualization of developing neurons. | ||
| 008661 | C57BL/6J-Tg(Nkx2-1-cre)2Sand/J | Repository- Live |
| Mice homozygous for the Nkx2.1Cre (or BAC-Nkx2.1-Cre) transgene are viable and fertile, with cre expression directed to major subgroups of brain interneuron progenitors, developing lung, thyroid, and pituitary by the Nkx2.1 promoter/enhancer regions within the BAC transgene. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. For example, when bred with beta-galactosidase reporter mice, the first detectable Cre recombinase expression in double mutant offspring is observed on embryonic day (E)10.5 in the basal telencephalon. These Nkx2.1Cre (or BAC-Nkx2.1-Cre) transgenic mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain progenitors (including future major interneurons in telencephalon and hypothalamus cells), as well as developing lung, thyroid, and pituitary. | ||
| 009593 | C57BL/6J-Tg(Pomc-EGFP)1Low/J | Repository- Live |
| Mice hemizygous for this POMC-EGFP transgene are viable and fertile, with EGFP expression directed to POMC-expressing neurons by the mouse Pomc (pro-opiomelanocortin-alpha) promoter/enhancer regions. The donating investigator reports that transcripts from the transgene encode EGFP but do not express any POMC prohormone or peptides. Direct EGFP fluorescence is observed in the arcuate nucleus of the hypothalamus (ARC), in melanotrophs/corticotrophs of the pituitary gland, and (unlike other POMC promoter-driven fluorescent mice) in a subpopulation of newly born granule neurons of the dentate gyrus of the hippocampus. EGFP expression is also observed in the nucleus of the solitary tract of the medulla. EGFP expression is downregulated as neurons mature and migrate deeper into the granule cell layer. These POMC-EGFP mice may be useful in studying neuronal signaling pathways, energy metabolism, leptin activity, obesity, seizures, depression, and epilepsy. | ||
| 008239 | C57BL/6J-Tg(Th-SNCA*A30P*A53T)39Eric/J | Repository- Live |
| These hm2α-SYN-39 mice express a doubly-mutant form of human alpha-synuclein (hα-SYN) containing the A30P and A53T human mutations associated with autosomal dominant Parkinson's disease, under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of hm2α-SYN-39 mice is more severe than that of the control strain (hwα-SYN-5, see Stock No. > ..... For more information please see the full phenotype on the strain data sheet | ||
| 000667 | C57BR/cdJ | Repository- Live |
| C57BR/cdJ mice develop early-onset hearing loss that is moderate at seven weeks of age, is severe by 20 weeks and progresses with increasing age (Henry 1982; Zheng et al. 1999). The loss is greatest in the higher frequency range; at seven weeks, Henry reported 50% of the mice showed no 64 kHz auditory brainstem response (ABR), and by 100 days both the 2 kHz and 32 kHz responses were absent. Both labs found this strain to be least vulnerable to loss of the16 kHz response, which persisted through 200 days but was lost before 300 days of age (Henry 1982). C57BR/cdJ did not exhibit aberrant ABR wave patterns, suggesting that the hearing loss results from defects of the peripheral, rather than central auditory system (Zheng et al. 1999). F1 hybrid progeny from matings with the good-hearing strain CAST/Ei exhibited good hearing even at advanced ages, indicating that the allele(s) responsible for hearing loss in C57BR/cdJ are recessive. An allelism test between C57BR/cdJ and NOD ..... For more information please see the full phenotype on the strain data sheet | ||
| 007677 | CB6-Tg(Gad1-EGFP)G42Zjh/J | Repository- Live |
| Mice hemizygous for this GAD67-GFP transgene are viable and fertile. GAD67-GFP (line G42) mice selectively express enhanced green fluorescent protein (EGFP) in the calcium-binding protein parvalbumin (Pv)-expressing subclass of basket interneurons (soma, dendrites, and axons) and also in putative presynaptic boutons. Transgene expression (EGFP expression) is published as early as postnatal day 0 (P0) with high expression levels throughout postnatal development. EGFP expression remains restricted to ~50% of Pv-expressing interneurons in adulthood. The donating investigator additionally reports transgene expression as early as embryonic day 14 (E14). EGFP expression is not reported in other interneuron classes positive for somatostatin (SOM), cholecystokinin (CCK), calretinin (CR), and VIP. These GAD67-GFP (line G42) mice may be useful for fluorescent labeling of the Pv-expressing subset of GABAergic neurons, allowing reliable and efficient characterization of perisomatic innervation ..... For more information please see the full phenotype on the strain data sheet | ||
| 007075 | CByJ.B6-Tg(CAG-EGFP)1Osb/J | Repository- Live |
| This transgenic mouse line with an "enhanced" GFP (EGFP) cDNA under the control of a chicken beta-actin promoter and cytomegalovirus enhancer makes all of the tissues, with the exception of erythrocytes and hair, appear green under excitation light. Note that mice homozygous for this transgene die within the first two weeks following birth.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. Of note, it has been the experience at The Jackson Laboratory that Stock No. 006567 (C57BL/6-Tg(CAG-EGFP)131Osb/LeySopJ) demonstrates the highest proportion of GFP expr ..... | ||
| 013585 | FVB-Tg(Cdh5-tTA)D5Lbjn/J | Repository- Live |
| These transgenic mice express tetracycline regulated transactivator under the direction of the mouse Cdh5, cadherin 5, promoter. When these VE-Cadherin-tTA mice are bred with mice carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of that gene in blood vessel endothelial cells may be conditionally inactivated with administration of the tetracycline in the double mutant offspring. Tetracycline was used by the Donating Investigator in the original publication Proc Natl Acad Sci 2005;102:128-33. When crossed with a strain carrying a tetracycline-responsive promoter driven lacZ transgene, beta-galactosidase is expression is observed in VEGFR-2, CD31 expressing cells in the blood vessels of bi-transgenic day 13.5 aged embryos. Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 004600 | FVB-Tg(GFAP-cre)25Mes/J | Repository- Live |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Mice that are homozygous for the transgene are not viable. This transgenic mouse strain expresses Cre recombinase under the control of the human glial fibrillary acidic protein promoter (GFAP). When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination occurs primarily in the central nervous system, affecting astrocytes, oligodendroglia, ependyma and some neurons. Expression activity is also present in periportal cells of the liver. Developmental onset of transgene expression occurs in the dorsal and medial regions of the telencephalon by embryonic day 13.5. In adult cerebellum, only astrocytes are immunoreactive for GFAP or Cre recombinase. This mutant mouse strain represents an effective tool for generating central ner ..... For more information please see the full phenotype on the strain data sheet | ||
| 003718 | FVB-Tg(GadGFP)45704Swn/J | Repository- Live |
| Mice homozygous for the TgN(GadGFP)45704Swn transgene express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse Gad1 (GAD67) gene promoter. Homozygous mice exhibit no apparent physical or behavioral defects. Transgene expression occurs in a specific subpopulation of hippocampal and cortical GABAergic interneurons that express somatostatin. This subset of interneurons has been shown to be prone to injury during epilepsy, ischemia, and Alzheimer's disease. These transgenic mice are useful for the morphological identification and study of these interneurons in both living and fixed brain tissue. Of note, this strain is one of many fluorescent GABAergic neuron strains, each with unique labeling characteristics (see Stock No. 006334 and Stock No. 006340). | ||
| 006364 | FVB-Tg(Nr5a1-cre)2Lowl/J | Repository- Live |
| Mice hemizygous for the "Sf1-Cre" transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgene expression mimics the mRNA pattern of Nr5a1; with Cre activity observed in steroidogenic factor-1 (SF1)-positive neurons in the ventromedial hypothalamic nucleus (VMH) as well as pituitary, gonad, and adrenal tissue. Expression is also noted in the cerebral cortex and in a few scattered cells in the caudal brainstem of mice derived from line 2 (but not line 7). If bred with mice containing a loxP-flanked sequence of interest, tissue-specific deletion of that genome results in the offspring. Specifically, these cre-expressing mice may be useful in studies involving the hypothalamus, such as body weight homeostasis, obesity, leptin metabolism, or as a reporter strain for SF1-transcription factor activity. | ||
| 006421 | FVB-Tg(Pomc1-hrGFP)1Lowl/J | Repository- Live |
| Hemizygous mice are viable and express humanized Renilla Green Fluorescent Protein (hrGFP, Stratagene) under control of the mouse pro-opiomelanocortin-alpha (Pomc1) promoter. As such, UV light-exposed transgenic brain tissues show GFP fluorescence patterns consistent with the endogenous Pomc1 gene, specifically POMC expressing neurons. The donating investigator reports that hrGFP is more stable and resistant to signal fading compared to other GFP's. The donating investigator reports that transgenic males have smaller seminal vesicles, and breeding transgenic males results in infrequent and very small (<2 pups) litter sizes. When non-transgenic males are crossed with transgenic females, fertility is normal. These POMC-GFP transgenic mice may be useful for studies of neurobiology, energy metabolism, obesity, seizures, and epilepsy. | ||
| 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 ..... | ||
| 003257 | FVB/N-Tg(GFAPGFP)14Mes/J | Repository- Live |
| Transgenic mice overexpress Green Fluorescent Protein under the control of the astrocyte-specific glial fibrillary acidic protein promoter. Bright fluorescence is observed in the cell bodies and processes of unfixed or fixed astrocyte preparations throughout the CNS of hemizygous mice. In addition retinal Mullers cells expressed the GFP transgene in response to degeneration of neighboring photoreceptors. These mice provide a method to follow changes in astrocyte morphology during development or disease processes. | ||
| 009610 | FVB/N-Tg(LRRK2)1Cjli/J | Repository- Live |
| Mice hemizygous for the BAC LRRK2 transgene are viable and fertile, with expression of a wild-type human leucine-rich repeat kinase 2 (LRRK2) gene directed by its endogenous promoter/enhancer regions on the BAC transgene. These BAC LRRK2 mice (also called WT-OX mice) "overexpress" the wildtype human LRRK2 protein in cortex, cerebellum, striatum and ventral midbrain at an approximately five- to ten-fold greater level than endogenous mouse Lrrk2, and are a control strain for the BAC LRRK2R1441G Parkinson's disease strain (Stock No. 009604). Contrary to the hypokinetic motor deficit of the BAC LRRK2R1441G Parkinson's disease mice, WT-OX mice exhibit slightly increased motor activities compared to nontransgenic wild-type controls. | ||
| 009609 | FVB/N-Tg(LRRK2*G2019S)1Cjli/J | Repository- Live |
| Mice hemizygous for the BAC LRRK2 (G2019S) transgene are viable and fertile, with expression of a mutant form of human leucine-rich repeat kinase 2 (LRRK2*G2019S) associated with autosomal dominant, late-onset Parkinson's disease directed by the endogenous LRRK2 promoter/enhancer regions on the BAC transgene. The phenotype of these LRRK2*G2019S mice is not yet characterized. These mice represent an in vivo model for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the dominant toxic effects of mutant LRRK2*G2019S expression. | ||
| 009604 | FVB/N-Tg(LRRK2*R1441G)135Cjli/J | Repository- Live |
| Mice hemizygous for the BAC LRRK2R1441G transgene are viable and fertile, with expression of a mutant form of human leucine-rich repeat kinase 2 (LRRK2*R1441G) associated with autosomal dominant, late-onset Parkinson's disease directed by the endogenous LRRK2 promoter/enhancer regions on the BAC transgene. LRRK2R1441G mice from founder line RP135 express the mutant protein in cortex, cerebellum, striatum and ventral midbrain at an approximately five- to ten-fold greater level than endogenous mouse Lrrk2. LRRK2R1441G mice exhibit multiple late-onset and progressive characteristics of Parkinson's disease; including hypokinetic motor deficits (reversible with administration of levodopa or apomorphine [a direct-acting dopamine agonist]), progressive dopaminergic neuron dysfunction and degeneration, axon injury pathology, and hyperphosphorylated tau. These LRRK2R1441G mice recapitulate the motor behavioral, neurochemical, and histopa ..... For more information please see the full phenotype on the strain data sheet | ||
| 009090 | FVB/NJ-Tg(Slc6a3-PARK2*Q311X)AXwy/J | Repository- Live |
| Hemizygous Parkin-Q311X(A) mice are viable and fertile, with expression of a FLAG-tagged, C-terminal truncated human parkin-Q311X mutation associated with Turkish early-onset Parkinson's disease directed to dopaminergic neurons of the substantia nigra pars compacta (SNc) and ventral tegmentum area (VTA) by the mouse Slc6a3 promoter/enhancer sequences. Parkin-Q311X(A) mice (derived from founder line A) have expression of the FLAG-tagged parkin-Q311X protein in dopaminergic neurons at a level that is approximately equivalent to or just below that expected from a heterozygous endogenous parkin allele. Parkin-Q311X(A) mice exhibit multiple late-onset and progressive hypokinetic motor deficits, progressive dopaminergic neuron dysfunction and degeneration, and age-dependent accumulation of proteinase K-resistant endogenous alpha-synuclein. Compared to founder line D, Parkin-Q311X(A) mice have a higher transgene copy number that results in more robust and earlier onset of hypokinetic m ..... For more information please see the full phenotype on the strain data sheet | ||
| 010710 | FVB;129S6-Sncatm1Nbm Tg(SNCA)1Nbm/J | Repository- Live |
| These PAC-Tg(SNCAWT);Snca-/- mice are viable and fertile, harboring a Snca knockout allele and a transgene encoding the human α-synuclein. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by human α-synuclein from the two total insertions of the PAC-Tg(SNCAWT). While brain RNA expression of SNCAWT is more than 50-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAWT are ~100-fold greater than normal endogenous mouse α-synuclein. PAC-Tg(SNCAWT);Snca-/- mice do not show any enteric nervous system abnormalities or widespread α-synuclein aggregation in brain or colon. No detectable motor behavior impairments, autonomic abnormalities, olfactory dysfunction, dopaminergic deficits, Lewy body inclusions or neurodegeneration are ..... For more information please see the full phenotype on the strain data sheet | ||
| 010788 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A30P)1Nbm Tg(SNCA*A30P)2Nbm/J | Repository- Live |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA30P);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A30P-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A30P from the PAC-Tg(SNCAA30P). Because PAC-Tg(SNCAA30P) line 1 inserted on the X chromosome and line 2 inserted on a somatic chromosome, homozygous females have four total insertions and homozygous males have three total insertions. While brain RNA expression of SNCAA30P is more than 10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA30P are ~80-fold greater than normal endogenous mouse α-synuclein. ..... For more information please see the full phenotype on the strain data sheet | ||
| 010799 | FVB;129S6-Sncatm1Nbm Tg(SNCA*A53T)1Nbm Tg(SNCA*A53T)2Nbm/J | Repository- Live |
| These double transgenic homozygous mice (dbl-PAC-Tg(SNCAA53T);Snca-/- mice) are viable and fertile, harboring a Snca knockout allele and two independently inserted transgenes encoding the human A53T-mutant α-synuclein associated with autosomal dominant Parkinson's disease. As homozygotes, expression of endogenous mouse α-synuclein is abolished and replaced by α-synuclein*A53T from the four total insertions of the PAC-Tg(SNCAA53T). While brain RNA expression of SNCAA53T is ~10-fold greater compared to normal endogenous mouse α-synuclein, protein levels are only 1 to 1.5-fold greater. In colon however, both RNA and protein expression of SNCAA53T are ~80-fold greater than normal endogenous mouse α-synuclein. By three months of age, dbl-PAC-Tg(SNCAA53T);Snca-/- mice show robust abnormalities in enteric nervous system function (impaired colonic motility [males only] and prolonge ..... For more information please see the full phenotype on the strain data sheet | ||
| 012882 | STOCK Ascl1tm1.1(Cre/ERT2)Jejo/J | Repository- Live |
| In Ascl1-CreERT2 mice, the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced by a CreERT2 fusion protein. Cre activity is induced following tamoxifen administration. As such, when Ascl1-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Ascl1-expressing cells of the offspring. The creERT2 fusion protein is expressed in all Ascl1 expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout central nervous system (CNS) and peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for this allele are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distin ..... For more information please see the full phenotype on the strain data sheet | ||
| 012881 | STOCK Ascl1tm1Reed/J | Repository- Live |
| In this strain the entire coding region of the endogenous mouse achaete-scute complex homolog 1 (Ascl1 or Mash1) gene is replaced with a nuclear localized green fluorescent protein (GFP) gene, abolishing gene function. GFP, driven by the Ascl1 promoter sequence, is expressed in all Ascl1-expressing neural progenitor cells in the embryo and the adult brain, including subsets of neurons throughout the central nervous system (CNS) and the peripheral nervous system (PNS), and in neuroendocrine cells in lung and kidney. Homozygotes die within hours of birth due to CNS and PNS disruptions in neural development. Mice heterozygous for the targeted mutation are viable, fertile, and normal in size. These mice may be useful for studying the lineage of distinct cell populations, neuronal turnover, and neuronal replacement upon traumatic injury. | ||
| 008882 | STOCK Bcl2tm1Irt/J | Repository- Live |
| Mice homozygous for this Bcl2flox conditional allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 2, as well as a loxP site downstream of exon 2 of the Bcl2 (B-cell leukemia/lymphoma 2) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 2 deleted, or both the neo selection cassette and exon 2 deleted. The two latter genotypes result in loss of Bcl2 protein expression and are reported to confer the null phenotype. These Bcl2flox mutant mice may be useful in generating conditional mutations for studying apoptosis, mitochondrial permeability, cell survival signaling, cancer, neurological disorders, and immunity.
For example, when crossed to a strain expressing Cre recombinase in myeloid cell lineages (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 012706 | STOCK Ccktm1.1(cre)Zjh/J | Repository- Live |
| The Cck-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the cholecystokinin locus (Cck). As such, cre expression is directed by the endogenous Cck promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cck-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Cck-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Cck expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in cholecystokinin positive neurons (interneurons) of the cortex. Characterization of cre expression in tissues other than brain is not ..... | ||
| 010910 | STOCK Corttm1(cre)Zjh/J | Repository- Live |
| The Cst-T2A-Cre (Cort-T2A-Cre) allele harbors a a T2A oligopeptide that mediates ribosomal skipping (foot-and-mouth disease virus 2A from the insect Thosea asigna virus) and Cre recombinase in the 3' UTR of the cortistatin locus (Cort). As such, cre expression is directed by the endogenous Cort promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Cst-T2A-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Cort-expressing cells (CST positive neurons) of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Cort expression pattern with highly efficient recombination). They report Cre recombinase activity is observed in so ..... | ||
| 013170 | STOCK Dclk1tm1.2Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 of the Dclk1 (doublecortin-like kinase 1) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing mouse, this strain is useful in eliminating tissue-specific expression of DCX-domain containing isoforms of this gene. This strain may be useful in studies of neuronal migration. | ||
| 013172 | STOCK Dclk2tm1Jgg/J | Repository- Live |
| These mice possess loxP sites on either side of exon 2 of the Dclk2 (doublecortin-like kinase 2) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful in studies of neurodevelopment and epilepsy. | ||
| 005992 | STOCK Efna2tm1Jgf Efna5tm1Ddmo/J | Repository- Live |
| Mice homozygous for both targeted mutations are viable, fertile, and normal in size. While the donating investigator reports that 10-20% of females homozygous at both loci neglect their litters, no such neglect is reported in the colonies at The Jackson Laboratory (Aug 2009). Double homozygous mice have no endogenous protein expression in inferior colliculus (IC) or superior colliculus (SC), and thus lack the concentration gradient created by the endogenous proteins across the midbrain in wildtype mice. Temporal and nasal retinal axon termination is severely altered: multiple ectopic aborizations in the SC indicate abnormalities in both anteroposterior and dorsoventral topography. Following surgical ablation of portions of the midbrain (including IC and SC), cross-modal innervation by retinal neurons is greater in double homozygous mutants compared to wildtype. Mice heterozygous at both loci are reported to have greater reproductive performance compared to double homozygous mice. Furth ..... For more information please see the full phenotype on the strain data sheet | ||
| 015831 | STOCK Erc2tm1.2Sud/J | Repository- Live |
| A 5'UTR exon and the first coding exon of the Erc2 (ELKS/RAB6-interacting/CAST family member 2; ELKS2, CAST1) gene are flanked by loxP sites in these targeted mutant mice. An in-frame tetracysteine tag is located in exon 1. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Normal expression of the targeted gene is demonstrated by the floxed allele.
Widespread cre excision of the floxed exons blocks expression (see Stock No. 008391). | ||
| 010702 | STOCK Gad2tm1(cre/ERT2)Zjh/J | Repository- Live |
| The Gad2-CreERT2 knock-in allele both abolishes Gad2 gene function and expresses a CreERT2 fusion protein (creERT2 fusion protein) from the Gad2 promoter/enhancer elements. Heterozygous mice are viable and fertile with no reported abnormalities. Homozygous mice are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit increased seizure activity (although no early death is reported). Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Gad2-CreERT2 mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Gad2-expressing cells of the offspring. The donating investigator reports tamoxifen-inducible Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Gad2 expression pattern with highly efficient inducibility). ..... | ||
| 010802 | STOCK Gad2tm2(cre)Zjh/J | Repository- Live |
| The Gad2-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the Gad2 (glutamic acid decarboxylase 2) locus. As such, cre expression is directed by the endogenous Gad2 promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Gad2-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Gad2-expressing cells (GAD2 positive neurons) of the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Gad2 expression pattern with highly efficient recombination). The donating investigator did not examine cre expression in tissues other than brain. For characterization information, see image ..... | ||
| 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. | ||
| 008873 | STOCK Gli3tm1Alj/J | Repository- Live |
| Mice homozygous for this Gli3flox conditional allele are viable and fertile, with loxP sites flanking exon 8 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have exon 8 deleted in the cre-expressing tissue(s). This results in a frameshift mutation upstream of the DNA-binding domain following splicing of mRNA from exon 7 to 9 and is reported to confer the null phenotype. These Gli3flox mutant mice may be useful in generating conditional mutations for studying Hedgehog/Sonic Hedgehog signaling in the development of many organs (such as central nervous system and limb patterning), as well as the role of Gli3 in adult organs.
When bred to a strain expressing Cre recombinase in the nervous system (see Stock No. 003771 for example), this mutant mouse strain may be useful in studies of mid/hind brain development. When bred to a str ..... | ||
| 013731 | STOCK Gt(ROSA)26Sortm1(CAG-Brainbow2.1)Cle/J | Repository- Live |
| Mice homozygous for the R26R-Confetti conditional allele are viable and fertile, with a CAG promoter, loxP site, and STOP cassette preventing transcription of the downstream Brainbow 2.1 sequences. The Brainbow 2.1 region contains two loxP-flanked dimers, each uniquely positioned in head-to-tail tandem. One dimer has nuclear-localized green fluorescent protein (hrGFPII) and a reverse-oriented cytoplasmic yellow fluorescent protein (mYFP). The other dimer has cytoplasmic red fluorescent protein (tdimer2(12)) and a reverse-oriented membrane-tethered cyan fluorescent protein (mCerulean). The Brainbow2.1 region may be written as loxP-STOP-loxP-GFP-PFY-Pxol-loxP-RFP-PFC-Pxol to show the transcriptional direction of each part. When bred to mice that express Cre recombinase, the resulting offspring may have a recombination event that stochastically places one of the four fluorescent proteins into position directly downstream of the CAG promote ..... For more information please see the full phenotype on the strain data sheet | ||
| 008600 | STOCK Gt(ROSA)26Sortm1(tTA)Roos/J | Repository- Live |
| Mice heterozygous for the ROSA:LNL:tTA conditional mutation of the Gt(ROSA)26Sor locus are viable and fertile, with a loxP-flanked STOP cassette preventing transcription of a downstream optimized/modified tetracycline-controlled transactivator protein ("mtTA"). Applying both Cre-lox and Tet-Off technologies, these ROSA:LNL:tTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracycline-responsive promoter element (TRE; also called tet-operator or tetO)-driven gene of interest can be both directed to the cell types defined by the chosen Cre recombinase expression, as well as turned off by the addition of tetracycline (or its analog doxycycline (dox)). | ||
| 012266 | STOCK Gt(ROSA)26Sortm5(ACTB-tTA)Luo/J | Repository- Live |
| Mice homozygous for this ROSA26-ZtTA (or ZtTA) conditional allele are viable and fertile, although the donating investigator reports that heterozygous mice are more healthy and fertile than homozygous mice. This ROSA26-ZtTA (or ZtTA) conditional allele is designed with a loxP-flanked β-geo transcriptional STOP cassette preventing transcription of the downstream tetracycline-controlled transactivator protein (tTA). When bred to mice that express Cre recombinase, offspring will have the STOP cassette deleted and subsequent expression of the tTA in the cre-expressing cells. The donating investigator reports that the CMV enhancer/chicken beta-actin core promoter (pCA) allows stronger and persistent expression of the downstream tTA (especially in adult cells) compared to the endogenous Gt(ROSA)26Sor locus alone. Applying both Cre-lox and Tet-Off technologies, these ZtTA mutant mice may be useful to generate compound mutant mice in which expression of a tetracyclin ..... For more information please see the full phenotype on the strain data sheet | ||
| 004779 | STOCK Mapttm1(EGFP)Klt/J | Repository- Live |
| Mice that are homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A knock-in of the EGFP coding sequence into the first exon disrupts expression of the Mapt gene and produces a cytoplasmic EGFP fused to the first 31 amino acids. No gene product (isoform proteins) is detected in whole brain lysates by Western blot analysis. EGFP signal is detected beginning at 9.0 days post coitum in the trigeminal ganglion and by 10.75 days post coitum fluorescent signal is detected throughout the developing central nervous system. EGFP expression persists to adult and closely patterns the expression of neuron specific beta-tubulin III, as detected by the TuJ1 antibody. The expression of cytoplasmic EGFP in the central nervous system of this mutant allows for non-invasive visualization of elongating nerve axons. | ||
| 015832 | STOCK Rims1tm3Sud/J | Repository- Live |
| 015833 | STOCK Rims2tm1.1Sud/J | Repository- Live |
| These mice possess loxP sites on either side of exon 26 in the Rims2 (regulating synaptic membrane exocytosis 2) gene. An in-frame ECFP-tetracysteine tag is fused to the floxed exon, enabling immunofluorescent detection. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the α, β, and γ isoforms of the gene. | ||
| 008212 | STOCK Smn1tm1Msd Tg(Prnp-SMN)92Ahmb Tg(SMN2)89Ahmb/J | Repository- Live |
| 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 | ||
| 013044 | STOCK Ssttm2.1(cre)Zjh/J | Repository- Live |
| The Sst-IRES-Cre (or SOM-IRES-Cre) allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the somatostatin locus (Sst). As such, cre expression is directed by the endogenous Sst promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Sst-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Sst-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient; largely recapitulating the endogenous somatostatin expression pattern with efficient recombination. They report Cre recombinase activity is observed in somatostatin positive neurons (including dendritic inhibitory interneurons such as Martinotti cells and Oriens-Lacunosum-Molecular ..... | ||
| 015836 | STOCK Syt12tm1.1Sud/J | Repository- Live |
| Exon 4 of this Syt12 (synaptotagmin XII) targeted mutation strain is flanked by loxP sites and carries a serine to alanine mutation at residue 97 (S97A). Serine 97 is a protein kinase A (PKA) phosphorylation site and the point mutation abolishes the increase of spontaneous neurotransmitter release by Syt12 overexpression in primary cortical culture. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. Floxed mice express the targeted gene at levels comparable to wild type, as demonstrated by Western blot of whole brain. | ||
| 013158 | STOCK Utrntm1Ked/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 (protein) is detected by Western blot analysis of kidney, lung and brain tissues. Levels of transcript are significantly reduced, as detected by RNase protection assay. Neuromuscular junctions from homozygotes lack extrasynaptic nerve sprouts, exhibit reduced postsynaptic membrane folding and fewer (approximately 40% reduction) acetylcholine receptors. The amplitude of miniature endplate currents (in extensor digitorum longus muscle) is reduced by 20%. Homozygotes exhibit abnormal Schwann cell compartments and reduced internodal length.
When bred with mice carrying the Dmdmdx allele (see Stock No. 001801) the resulting double mutant mice exhibit a more severe phenotype than single Dmdmdx mutants: earlier onset ..... | ||
| 010908 | STOCK Viptm1(cre)Zjh/J | Repository- Live |
| The Vip-IRES-Cre allele harbors an internal ribosome entry site and Cre recombinase in the 3' UTR of the vasoactive intestinal polypeptide locus (Vip). As such, cre expression is directed by the endogenous Vip promoter/enhancer elements. The donating investigator reports that homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When Vip-IRES-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the Vip-expressing cells in the offspring.
The donating investigator reports Cre recombinase activity is specific and efficient (largely recapitulates the endogenous Vip expression pattern with highly efficient recombination). They report Cre recombinase activity in some GABAergic interneurons, and did not examine cre expression in the intestine or tissues other than brain. | ||
| 012691 | STOCK Et(icre/ERT2)14374Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), some minor Cre recombinase activity is observed without tamoxifen in these mice.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
many cells in hippocampus (including dentate gyrus projections), with very sparse coverage in all oth ..... For more information please see the full phenotype on the strain data sheet | ||
| 012692 | STOCK Et(icre/ERT2)14602Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration).
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in most areas of the brain, with more cells in hippocampus (perhaps more staining in CA2 & CA3 regions; dentate gyrus projections are stained more than cell bodies). No Cre ..... For more information please see the full phenotype on the strain data sheet | ||
| 012693 | STOCK Et(icre/ERT2)14624Rdav/J | Repository- Live |
| Mice hemizygous for this enhancer trap lentiviral transgene are viable and fertile, with expression of an iCreERT2 fusion gene (an optimized variant of Cre recombinase [iCre; improved with mammalian codon usage, removed putative cryptic splice sites, altered stop codon, and reduced CpG content to limit the chances of epigenetic silencing in mammals] fused to Cre-ERT2 [a G400V/M543A/L544A triple mutation of the human estrogen receptor ligand binding domain]) under control of the promoter/enhancer regions surrounding the site where the enhancer trap lentiviral transgene randomly inserted. While Cre-ERT2 fusion gene activity is designed to be inducible (observed following tamoxifen administration), some minor Cre recombinase activity is observed without tamoxifen in these mice.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
scattered cells in cortex, hippocampus, with more cells in the CA3 region, midbrain, and granule cell l ..... For more information please see the full phenotype on the strain data sheet | ||
| 013749 | STOCK Tg(ACTB-EGFP,-tdTomato)11Luo/J | Repository- Live |
| Homozygous MADM-11GT mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11GT allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the MYC-tagged C-terminal portion of a red fluorescent protein (tdTomato) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11GT mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11TG mice harboring a reciprocal mutation at the same locus (see Stock No. 013751). The resulting GT/TG offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygou ..... For more information please see the full phenotype on the strain data sheet | ||
| 014092 | STOCK Tg(ACTB-tTA2,-MAPT/lacZ)1Luo/J | Repository- Live |
| Homozygous CAG-stop-tTA2 transgenic mice are viable and fertile. CAG-stop-tTA2 transgenic mice harbor the ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene; designed with a loxP-flanked transcriptional STOP cassette preventing transcription of the downstream modified tetracycline-regulated transactivator (tTA2). The ii-CAG-stop-tTA2-IRES-tau-lacZ-ii transgene is flanked by two copies of the chicken β-globin HS4 insulator on each side to preserve expression fidelity (see additional information below). When bred to mice that express a tamoxifen-inducible Cre recombinase (CreERT2), administration of tamoxifen to the double mutant offspring allows the CreERT2 fusion protein to enter the nucleus of the cre-expressing cells; this deletes the STOP cassette and results in expression of tTA2. The donating investigator reports that tau-lacZ fusion protein expression in the tamoxifen-treated double mutant offspring is faint. Of note, the donating investigator h ..... For more information please see the full phenotype on the strain data sheet | ||
| 013751 | STOCK Tg(ACTB-tdTomato,-EGFP)11Luo/J | Repository- Live |
| Homozygous MADM-11TG mice are viable and fertile with no gross behavioral or observable abnormalities. The MADM-11TG allele has the CMV enhancer/chicken beta-actin core promoter, the N-terminal portion of a red fluorescent protein (tdTomato), a beta-globin intronic sequence containing an frt site and a loxP-flanked neomycin resistance gene, and the C-terminal portion of a mutant enhanced green fluorescent protein (mut4-EGFP) all inserted into the Hipp11 locus on chromosome 11 (cytoband A1 at ~3cM between the Eif4enif1 and Drg1 loci). These MADM-11TG mutants are designed for MADM (mosaic analysis with double markers), and must be crossed to MADM-11GT mice harboring a reciprocal mutation at the same locus (see Stock No. 013749). The resulting TG/GT offspring have one copy of each reciprocal mutation on homologous chromosomes ("trans-heterozygous"), and mu ..... For more information please see the full phenotype on the strain data sheet | ||
| 007684 | STOCK Tg(Atoh1-cre/Esr1*)14Fsh/J | Repository- Live |
| Mice hemizygous for this Math1-CreERT2 transgene are viable and fertile. Under control of the Math1 (Atoh1) enhancer, tamoxifen-inducible cre activity is observed in neural progenitors of the cerebellar rhombic lip, dorsal hindbrain and spinal cord, as well as in inner-ear primordia (with a limited amount of ectopic expression in the primordium of the hippocampus but not the cortex). The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone ma ..... For more information please see the full phenotype on the strain data sheet | ||
| 013753 | STOCK Tg(CAG-KikGR)33Hadj/J | Repository- Live |
| CAG::KikGR33 transgenic mice express a Kikume Green-Red (KikGR) photoconvertible fluorescent protein under the control of a CMV enhancer/chicken beta-actin promoter (CAGGS) promoter. Mice homozygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. KikGR, engineered from Favia favus coral, changes color from green to red upon activation in embryos, adult mice, and embryonic stem (ES) cells. At basal state, green fluorescence is seen in all cells. A single cell or group of cells at basal state, exposed to 405 nm wavelength light, undergo photo conversion and fluoresce red. Since KikGR is developmentally neutral and non-toxic, the movement of these fluorescent cells, and their progeny, can be imaged during embryonic development. Mice from founder line 33 exhibits widespread expression of KikGR, while mice from founder line 75 (Stock No. ..... For more information please see the full phenotype on the strain data sheet | ||
| 009615 | STOCK Tg(Cartpt-cre)1Aibs/J | Repository- Live |
| Hemizygous Cart-Tg1-Cre mice are viable and fertile, with cre expression directed to cortex, hippocampus, and cerebellum by the Cartpt promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Cart-Tg1-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, hippocampus, and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Cart-Tg1-Cre images). | ||
| 008241 | STOCK Tg(Cspg4-DsRed.T1)1Akik/J | Repository- Live |
| Mice hemizygous for the NG2DsRedBAC transgene are viable and fertile, expressing an optimized red fluorescent protein variant (DsRed.T1) under the control of the mouse NG2 (Cspg4) promoter/enhancer. DsRed.T1 fluorescence is detected in NG2 cells (oligodendrocyte progenitor cells) throughout the postnatal central nervous system, including the gray and white matter of the brain, cerebellum and spinal cord, and vascular mural cells; but not in mature oligodendrocytes, astrocytes, resting microglia, or neurons. DsRed.T1 fluorescence intensity is highest in cell bodies and can also be detected in distal processes, suggesting that tetrameric DsRed.T1 remains soluble and is not toxic to cells. In addition, DsRed.T1 fluorescence may be readily detected without using anti-DsRed antibodies and is suitable for identifying NG2 cells in live slices or for purifying NG2 cells via FACS. These NG2DsRedBAC transgenic mice may be useful for fluorescent labeling of NG2 cells (oligodendrocyte p ..... For more information please see the full phenotype on the strain data sheet | ||
| 005938 | STOCK Tg(Eno2-cre)39Jme/J | Repository- Live |
| Mice hemizygous for this NSE39-Cre transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These NSE39-Cre mice harbor a transgenic insert consisting of the cre recombinase gene under the control of the promoter region of the rat neuron specific enolase (NSE or Eno2) gene. As such, Cre recombinase activity is directed to neurons with expression in many tissue types. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome.
Specifically, these NSE39-Cre transgenic mice may also be useful in studies of spinal muscular atrophy (SMA) along with mice harboring a conditional (floxed) Smn1 gene (see Stock No. 006138 or Stock No. 006146).
Additional SMA strains expressing cre in striated muscle are av ..... For more information please see the full phenotype on the strain data sheet | ||
| 008755 | STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J | Repository- Live |
| This strain was generated by breeding Stock No. 008168 and Stock No. 008250 together at The Jackson Laboratory. The resulting double transgenic colony was established as Stock No. 008755. The Ins2-rtTA (or RIP7-rtTA) transgene expresses the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat insulin 2 (Ins2) promoter. The tet-DTA (or tetO-DTA) (transgene expresses diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. Mice harboring both of these transgenes has doxycycline-inducible expression of DTA in pancreatic beta cells; i.e. addition of the tetracycline analogue doxycycline (dox) results in ablation of pancreatic beta cells. | ||
| 012462 | STOCK Tg(Nr5a1-cre)7Lowl/J | Repository- Live |
| These transgenic mice express Cre recombinase under the direction of the mouse Nr5a1, nuclear receptor subfamily 5, group A, member 1, promoter. The Cre recombinase activity pattern mimics the endogenous gene expression (mRNA) pattern. Cre mediated recombination is detected in steroidogenic factor-1 (SF1)-positive neurons in the ventromedial hypothalamic nucleus (VMH) as well as pituitary, gonad, and adrenal tissue. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator has not attempted to make the strain homozygous. When crossed with a strain containing loxP site flanked sequence, Cre-mediated recombination results in tissue-specific deletion of the flanked sequence in the offspring. | ||
| 012586 | STOCK Tg(Slc1a3-cre/ERT)1Nat/J | Repository- Live |
| This BAC transgenic line expresses CreERT under the control of the Slc1a3 (solute carrier family 1 (glial high affinity glutamate transporter); GLAST) promoter. When crossed with a strain containing a loxP site flanked sequence, the offspring are useful for generating tamoxifen-induced, Cre-mediated targeted glia and neural progenitor cell-specific deletions. Injection of 4-hydroxytamoxifen leads to recombination specifically in Muller glia in the retina, in astrocytes of the brain, and in neural progenitors, including those that give rise to hippocampal neurons and olfactory neurons in the rostral migratory stream. This strain is a useful tool in studies of neurodevelopment. | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Repository- Live |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 007788 | STOCK Tg(Thy1-EGFP)MJrs/J | Repository- Live |
| Mice harboring the Thy1-GFP transgene are viable and fertile with enhanced green fluorescent protein (EGFP) expression under the control of a modified Thy1 promoter region (containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells). Homozygous or hemizygous Thy1-GFPM mice (derived from founder line M) express EGFP in sparse subsets of neurons within specific populations; providing a bright, vital Golgi-like stain. Less than 10% of all motor axons, retinal ganglion cells, lumbar dorsal root ganglion, and cortex express EGFP. These Thy1-GFPM transgenic mice may be useful in neurobiological studies for fluorescent labeling of neural tissues, especially for mossy fibers in the cerebellum and intense, yet sparse, labeling of a variety of neuronal subsets.
This strain is one of many from the donating investigator with specific/differential fluorescent protein expression in neural tissues (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 012708 | STOCK Tg(Thy1-cre/ERT2,-EYFP)HGfng/PyngJ | Repository- Live |
| The "single-neuron labeling inducible Cre-mediated knockout" (SLICK) transgene is designed with two separate copies of the modified mouse Thy1 promoter region (each containing the sequences required for neuronal expression but lacking the sequences required for expression in non-neural cells) driving expression of a CreERT2 fusion protein and an enhanced yellow fluorescent protein (EYFP). Mice harboring the SLICK transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. mRNA coexpression of both CreERT2 and YFP is highly correlated. YFP expression is directed primarily to projection neurons with variations in the extent and brightness of labeling observed in different founder lines (see below). CreERT2 fusion gene activity is inducible; observed at high levels following tamoxifen administration (see below). When SLICK transgenic mice are bred with mice containing loxP-flanked seque ..... For more information please see the full phenotype on the strain data sheet | ||
| 008199 | STOCK Tg(dlx6a-cre)1Mekk/J | Repository- Live |
| Homozygous Dlx5/6-Cre transgenic mice are viable and fertile. Expression of Cre recombinase (Cre) is directed to differentiating and migrating forebrain GABAergic neurons during embryonic development by the I56i and I56ii enhancers from the zebrafish dlx5a/dlx6a intergenic region (with the 5' promoter region of zebrafish dlx6a in place to increase the activity of the intergenic enhancers rather than direct tissue-specific expression). When Dlx5/6-Cre transgenic mice are bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequence in the offspring in the offspring. These Dlx5/6-Cre transgenic mice may be useful in generating specific deletions of floxed alleles in GABAergic forebrain neurons. | ||
| 012345 | STOCK Tg(tetO-tdTomato,-Syp/EGFP*)1.1Luo/J | Repository- Live |
| Hemizygous TRE-Bi-SG-T line 1.1 transgenic mice are viable and fertile, with no reported phenotypic abnormalities. The TRE-Bi-SG-T transgene has Myc-tagged tdTomato and full-length mouse synaptophysin/mut4EGFP fusion protein (Syp-GFP) expression under the control of the bi-directional tet-responsive promoter (tetO or TRE). When bred with another mouse expressing tetracycline-controlled transactivator protein (tTA) or reverse tetracycline-controlled transactivator protein (rtTA), tdTomato and Syp-GFP fusion protein expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. In tTA(-dox) or rtTA(+dox)-expressing cells, tdTomato expression is directed to the entire cell, while GFP expression is directed to the synapse/synaptic vesicle. The donating investigator reports that direct GFP fluorescence and direct tdTomato fluorescence may be visualized in these mice when tTA is present/dox is absent. In addition, the three Myc epi ..... For more information please see the full phenotype on the strain data sheet | ||
| 003833 | B6.Cg-Tg(Eno2-Ighmpb2)17Cx Ighmbp2nmd-2J/Cx | Research Strain |
| Mice hemizygous for the transgene are viable and fertile. RT-PCR analysis indicates that transgene expression is limited to the central nervous system including forebrain, cerebellum and spinal cord. The presence of the transgene rescues the neuromuscular degeneration exhibited by nmd-2J mice. These mice have no obvious phenotype. This strain is useful for studies involving the role of Ighmpb2 in motor neuron disease. | ||
| 000516 | C57BLKS-Rpl24Bst/J | Research Strain |
| Belly spot and tail (Rpl24Bst) is a semidominant, homozygous in utero lethal mutation. Adult heterozygotes are viable and fertile although a reduced birth rate for heterozygotes has been reported. This may reflect incomplete penetrance, or, more likely, prenatal mortality. The Rpl24Bst mutation has variable expressivity and the heterozygous phenotypic traits include shortened and kinked tail, white feet and belly spot, malocclusion, smaller body size, exencephaly, abnormalities of the spine, ocular defects, and polydactyly. Polydactyly is found predominantly in the right rear paw, occasionally in the left front paw and rarely in the left rear or right front paws. Approximately 50-60% of the heterozygotes have a reduction in pupillary light reflex in one or both eyes due to an underlying optic nerve atrophy. Ontological studies showed a delay in the developmental fusion of the optic fissure, a disruption of the retinal layers by embryonic day 1 ..... For more information please see the full phenotype on the strain data sheet | ||
| 002484 | 129-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 003518 | 129/Sv-L1camtm1Sor/J | Cryopreserved - Ready for recovery |
| The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 008715 | 129S-Ywhaetm1Awb/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. Most homozygotes die at birth, less than 1% of homozygotes survive to adulthood. Survivors remain smaller in size than wildtype controls. No gene product (protein) is detected by immunoblot analysis of brain tissue from homozygotes. Homozygotes exhibit hippocampal defects with thinning of the cortex, hippocampal pyramidal cell layer disorganization and neuronal migration abnormalities. Heterozygotes exhibit less severe hippocampal defects. Mutants have increased apoptosis in the brain. This mutant mouse strain may be useful in studies of Miller-Dieker Lissencephaly Syndrome and neuronal migration during brain development. | ||
| 008077 | 129S1/Sv-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 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). | ||
| 012400 | 129S6.129X1(B6)-Syt4tm1Hrh/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 (mRNA) is detected by Northern blot analysis of total brain RNA. Homozygotes exhibit impaired locomotor coordination (reduced performance on accelerating rotarod), diminished contextual fear conditioning, impaired social transmission of food preference, enhanced long-term potentiation (LTP) and hyperactivity. Anxiety-like behavior and depression-like behavior is decreased in homozygous animals. Posterior pituitary nerve terminals isolated from homozygotes exhibit lower Ca2+ current density than wildtype controls, decreased exocytosis and accelerated endocytosis with high Ca2+ entry, and increased exocytosis with low Ca2+ entry. Hippocampal neurons isolated from homozygotes display increased rate of synpatic vesicle exocytosis from presynaptic terminals. Inner hair cells from homozygotes have abnormal exocytotic Ca2+ ..... For more information please see the full phenotype on the strain data sheet | ||
| 009580 | B6(129S4)-Et(cre/ERT2)1382Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)1382Rdav images). The C ..... | ||
| 009583 | B6(129S4)-Et(cre/ERT2)1957Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)1957Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 009584 | B6(129S4)-Et(cre/ERT2)2007Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)2007Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 009574 | B6(129S4)-Et(cre/ERT2)21Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)21Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre reco ..... | ||
| 009578 | B6(129S4)-Et(cre/ERT2)398Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)398Rdav images). The Cre-E ..... | ||
| 009573 | B6(129S4)-Et(cre/ERT2)4Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)4Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recomb ..... | ||
| 010688 | B6(129S4)-Et(cre/ERT2)6691Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)6691Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010691 | B6(129S4)-Et(cre/ERT2)7149Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)7149Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre reco ..... | ||
| 010692 | B6(129S4)-Et(cre/ERT2)7381Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OH ..... | ||
| 010693 | B6(129S4)-Et(cre/ERT2)8120Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)8120Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 010694 | B6(129S4)-Et(cre/ERT2)8131Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)8131Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre re ..... | ||
| 009579 | B6(129S4)-Et(cre/ERT2)837Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)837Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre reco ..... | ||
| 010695 | B6(129S4)-Et(cre/ERT2)9699Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration (although some cre activity is reported prior to tamoxifen administration). The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)9699Rdav images). The Cre- ..... | ||
| 009587 | B6(129S4)-Et(icre)1402Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of a codon-improved Cre recombinase (iCre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. The donating investigator reports Cre recombinase activity in brain tissues (but may not have assessed expression in other tissues). When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. For characterization information, see images at the Allen Institute for Brain Science website (Et(icre)1402Rdav images). | ||
| 009588 | B6(129S4)-Et(icre)1470Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of a codon-improved Cre recombinase (iCre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. The donating investigator reports Cre recombinase activity in brain tissues (but may not have assessed expression in other tissues). When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. For characterization information, see images at the Allen Institute for Brain Science website (Et(icre)1470Rdav images). | ||
| 009589 | B6(129S4)-Et(icre)1555Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of a codon-improved Cre recombinase (iCre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. The donating investigator reports Cre recombinase activity in brain tissues (but may not have assessed expression in other tissues). When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. For characterization information, see images at the Allen Institute for Brain Science website (Et(icre)1555Rdav images). | ||
| 009586 | B6(129S4)-Et(icre)754Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of a codon-improved Cre recombinase (iCre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. The donating investigator reports Cre recombinase activity in brain tissues (but may not have assessed expression in other tissues). When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(icre)754Rdav images). | ||
| 010697 | B6(129S4)-Et(icre/ERT2)10727Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the iCre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Codon-improved Cre recombinase (iCre) activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
The iCre-ERT2 fusion protein (iCre-ERT2) consists of a codon-improved Cre recombinase [iCre] fused to a triple mutant form of the human estrogen receptor; which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic ..... | ||
| 008149 | B6(Cg)-Snord116tm1.1Uta/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Snord116del (1-loxP or knockout) allele are viable and fertile. As the Snord116 gene cluster is imprinted and expressed only from the paternal allele, mice with paternal inheritance of the deletion lack expression of the targeted Snord116 small nucleolar RNAs (snoRNAs) gene cluster in brain tissues. Similarly, paternal transmission of the mutant allele is required to obtain the mutant phenotype in offspring. Affected heterozygotes (paternal deleted/maternal wildtype) recapitulate a subset of Prader-Willi syndrome (PWS) characteristics, including early-onset postnatal growth retardation, delayed sexual maturation, increased anxiety, motor learning deficit and hyperphagia (but not obesity). Other reported abnormalities include altered metabolic fuel usage, prolonged meal time, and increased levels of circulating ghrelin. These Snord116del mice may be useful in studying growth and feeding regulation, mechanisms of obesity, and pa ..... For more information please see the full phenotype on the strain data sheet | ||
| 009592 | B6.129(Cg)-Kcnn2tm1.1Jpad/J | Cryopreserved - Ready for recovery |
| Homozygous SK2-delta (SK2-null) mice are viable but subfertile (homozygous males exhibit poor reproductive success and homozygous females are nurturing but produce small, infrequent litters). No RNA or protein expression from the targeted allele is observed in brain tissues, and no EGFP expression is reported. Homozygous mice are smaller than wild-type until approximately 5 weeks of age. SK2-deficient mice exhibit whole body tremor beginning around 10 days of age, with ataxia and impaired righting reflex when placed on their back at young ages. Homozygotes also have inner ear abnormalities (impaired exocytotic response of immature inner hair cells and impaired function/long-term survival of olivocochlear fibers and efferent synapses on cochlear outer hair cells). These SK2-delta mice may be useful in studying the role of small-conductance calcium-activated potassium (SK) channels in after-hyperpolarization and action potentials of neuronal, inner ear (cochlea), and urinary bladder tiss ..... For more information please see the full phenotype on the strain data sheet | ||
| 006874 | B6.129-Gabra4tm1.2Geh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this GABAA-R alpha4F allele are viable and fertile. These mutant mice have loxP sites flanking exon 3 of the targeted gene. When bred to Cre-recombinase expressing mice, offspring will have a deletion of exon 3 in the cre expressing tissue(s). These "floxed" mice may be useful in neurological studies including behavior and neurotransmitter function. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. 006874), Gabra6 (Stock No. 002710), Gabrb3 (Stock No. 002711), Gabrd (Stock No. ..... | ||
| 007747 | B6.129-Kcnab1tm1Sva/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Kvβ1.1 targeted allele are viable and fertile. Brain tissue from homozygotes shows no mRNA or protein expression from the targeted allele. Homozygous loss of Kvβ1.1 results in a reduced K+ current inactivation in hippocampal CA1 pyramidal neurons. Homozygous mice have enhanced neuronal excitability that can facilitate long-term potentiation (LTP) induction and improve learning and memory in aged mice (but not in a N7/8 C57BL/6 backcrossed background). Impaired learning in water maze tests and social transmission of food preference tasks is also observed. On a mixed B6;129 genetic background, homozygotes exhibit a prominent reduction in frequency-dependent spike broadening and slow afterhyperpolarization (sAHP) (this phenotype is less prominent on the N7/8 backcrossed C57BL/6 genetic background). These Kvβ1.1 mutant mice may be useful for neurological studies including hippocampal long-term potentiation, spatial learning, and voltage-gated potassi ..... For more information please see the full phenotype on the strain data sheet | ||
| 009591 | B6.129-Kcnn1tm1.2Jpad/J | Cryopreserved - Ready for recovery |
| Homozygous SK1-flox (delta neo) mice are viable and fertile, with loxP sites flanking the coding sequences of exons 3-5 (and an enhanced green fluorescent protein (EGFP) coding sequence just downstream of the second loxP site) in the Kcnn1 (also called SK1) locus. The donating investigator reports that homozygotes exhibit no overt phenotype and that the SK1-flox (delta neo) allele may confer a null phenotype even before exposure to Cre recombinase: RT-PCR shows the EGFP sequence disrupts splicing such that no full length transcripts are detected. No EGFP expression is reported. When bred to mice that express Cre recombinase, the SK1 sequences encoding the translation initiation site through transmembrane domain five are deleted in the cre-expressing tissues of the offspring. These SK1-flox (delta neo) mutant mice may be useful in studying the role of small-conductance calcium-activated potassium (SK) channels in after-hyperpolarization and action potentia ..... For more information please see the full phenotype on the strain data sheet | ||
| 008518 | B6.129-Leprtm1Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprS1138 mutant allele (or s/s mice) are viable and partially fertile with a Tyr->Ser replacement at amino acid residue 1138 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-STAT3 transcription factor signaling. The mutant protein, LRbS1138, is expressed normally on the cell surface and mediates other leptin signals normally, but fails to activate STAT3. Similar to homozygous db/db mice (which are devoid of all leptin signaling), homozygous s/s mice display hyperphagia, decreased energy expenditure, and decreased thyroid function resulting in profound obesity and dramatically increased serum leptin levels compared to wild-type. Unlike db/db mice, however, s/s mice are fertile and long bodied, have improved glucose tolerance (less hyperglycemic), are not protected from intimal hyperplasia following vessel injury, and do not exhibit elevated hypothalamic ex ..... For more information please see the full phenotype on the strain data sheet | ||
| 008385 | B6.129-Leprtm2Mgmj/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LeprLeu985 mutant allele (or l/l mice) are viable and fertile with a Tyr->Leu replacement at amino acid residue 985 of the leptin receptor long form (LRb)-specific exon 18b. The mutation specifically disrupts LRb-SHP2 and LRb-SOCS3 transcription factor signaling. The mutant protein, LRbL985, is expressed normally and mediates other leptin signals normally, but fails to recruit SHP2 or SOCS3. Homozygous male and female mice are neuroendocrinologically normal, but homozygous females may exhibit decreased feeding, body weight, adipocity, circulating leptin, circulating insulin, expression of orexigenic neuropeptides, protection from high-fat diet-induced obesity, and increased leptin sensitivity depending upon diet and genetic background. Homozygous LeprLeu985 mutant mice may be useful for studying the influence of LRb-SHP2 and LRb-SOCS3 signaling in the physiological and metabolic function of leptin; specifically b ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 005697 | B6.129-Otx1tm4(cre)Asim/J | Cryopreserved - Ready for recovery |
| This strain expresses Cre recombinase from the targeted locus. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygotes have a perinatal lethal phenotype. Expression of the Cre recombinase gene (mRNA) under the control of the endogenous gene promoter, is detected in the lateral midbrain of embryonic day 10.5 aged embryos and in the presumptive alar-basal plate boundary of embryonic day 12.5 aged embryos, closely mimicking the endogenous gene expression pattern. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in tissue-specific deletion of the target. Recombination is first detected at embryonic day 8.7. This strain represents an effective tool for generating tissue specific-targeted mutants that would be useful to study developmentally critical gene function in the brain. | ||
| 010559 | B6.129-Pou4f2tm2.1Nat/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of the Pou4f2 (POU domain, class 4, transcription factor 2) coding region followed by an alkaline phosphatase (AP) reporter. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a cre recombinase-expressing strain, the offspring express AP in the retina, several brain nuclei, dorsal root ganglia, trigeminal ganglion, and other cells/tissues. | ||
| 010560 | B6.129-Pou4f3tm1.1Nat/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of the Pou4f3 (POU domain, class 4, transcription factor 3) coding region followed by an alkaline phosphatase (AP) reporter. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a cre recombinase-expressing strain, the offspring express AP in the retina, dorsal root ganglia, and other cells/tissues. | ||
| 008201 | B6.129-Sepp1tm1Rfb/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this targeted mutation are viable and fertile. No RNA or selenoprotein P (Se-P) protein expression from the targeted gene is observed in plasma. Homozygous (Sepp1-deficient) mice are viable with altered selenium metabolism rendering them intolerant of low dietary selenium intake and resulting in significantly shortened life span. Homozygotes have lower brain selenium concentrations and develop progressive neurological dysfunction (impaired movement and coordination); the progression of which is preventable (but not reversible) with dietary selenium supplement. Homozygous females are fertile but have difficulty producing and raising pups. Homozygous males have sharply reduced fertility due to flagellar structural defects ("kinked sperm") which, unlike the neurological phenotype, are not prevented with dietary selenium supplement. Sepp1-deficient mice, supplemented with dietary selenium and infected with an African Trypanosomiasis parasite, exhibit increased ..... For more information please see the full phenotype on the strain data sheet | ||
| 006146 | B6.129-Smn1tm1Jme/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this SMNF7 floxed allele are viable and fertile and do not display any gross physical or behavioral abnormalities. Mutant mice exhibit no transcript splicing defects. Cre-mediated recombination of the loxP-flanked sequences results in deletion of exon 7 of the targeted gene. As mutations of this exon are implicated in 95% of all human spinal muscular atrophy (SMA), these mice may be useful in studying SMA or other neuromuscular degenerative diseases.
When crossed to a strain expressing Cre recombinase in neurons (see Stock No. 005938, Stock No. 006297, and Stock No. 006663), this mutant mouse strain may be useful as a model of SMA. When crossed to a strain expressing Cre recombinase in striated muscle fibers (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 002463 | B6.129S-Itga4tm1Hyn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Itga4tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4. | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock ..... | ||
| 007923 | B6.129S1-Nf1tm1Cbr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted allele (Nf123a-/-) lack the alternatively spliced exon 23a (which modifies the GTPase-activating protein (GAP) domain of Nf1), and are viable and fertile. Protein and mRNA isolated from homozygous brain tissue shows normal type I (exon 1-21 containing) neurofibromin isoform but absence of the alternatively spliced, exon 23a-containing type II neurofibromin isoform (which has a greater affinity for Ras but lower GAP activity than the type I isoform). Homozygotes have no reported increase in tumor predisposition, but show specific learning impairments in contextual discrimination, spatial learning, and coordination. These Nf123a-/- mutant mice may be useful for neurological studies of Neurofibromatosis Type I, growth, differentiation, and learning and memory. | ||
| 009602 | B6.129S4(Cg)-Kcnn2tm2Jpad/J | Cryopreserved - Ready for recovery |
| The SK2T mutant allele has a tetracycline-based genetic switch inserted into the 5' UTR of the targeted gene, just upstream of the translation initiation site. This genetic switch harbors both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator). The donating investigator reports that long term administration of tetracycline (or its analog doxycycline (dox)) does not block transcription of the downstream Kcnn2 locus. The donating investigator also reports that homozygous mice are viable but do not thrive without dox treatment. SK2-tTA heterozygotes (SK2T) exhibit approximately ten-fold overexpression of SK2 protein before dox treatment. In the absence of dox, homozygous mice exhibit enhanced SK channel-mediated restriction of glutamatergic activity in CA1 neurons, attenuated hippocampal synaptic plasticity, impaired spatial learning ..... For more information please see the full phenotype on the strain data sheet | ||
| 006490 | B6.129S4-Abcb7tm1Mdf/J | Cryopreserved - Ready for recovery |
| Homozygous mice are viable and fertile with no reported neurological or hematological abnormalities. These mutant mice have loxP sites flanking exons 9 and 10 of the endogenous gene. When bred to Cre recombinase expressing mice, exons 9 and 10 are deleted in the offspring dependent on the tissue specificity of the Cre recombinase expressing parent. The donating investigator reports that the null allele is not transmissible due to an effect on the extraembryonic tissues. This mutant may be useful in studying cytosolic Fe-S cluster assembly and metabolism, Friedreich ataxia, anemia, and hematopoiesis.
When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatocyte iron metabolism.
When bred to a strain expressing Cre recombinase in epiblast derived cells (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 010960 | B6.129S4-Grk5tm2Rjl/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 7 and 8 of Grk5 (G protein-coupled receptor kinase 5). Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene, exons 7 and 8 of the targeted gene are deleted in the cre-expressing tissues in the offspring mice. The floxed allele appears to be fully functional and expresses normal levels of GRK5 protein. | ||
| 010962 | B6.129S4-Grk6tm1Mca/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 3-9 of Grk6 (G protein-coupled receptor kinase 6). Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene, exons 3-9 of the targeted gene are deleted in the cre-expressing tissues in the offspring mice. The floxed allele appears to be fully functional and expresses normal levels of GRK6 protein. | ||
| 009603 | B6.129S4-Kcnn3tm1Jpad/J | Cryopreserved - Ready for recovery |
| The SK3T mutant allele has a tetracycline-based genetic switch inserted into the 5' UTR of the targeted gene, just upstream of the translation initiation site. This genetic switch harbors both the tetracycline-controlled transactivator protein (tTA) as well as the tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator); allowing transcription of the downstream Kcnn3 locus to be blocked by administration of tetracycline (or its analog doxycycline (dox)). SK3-tTA homozygotes (SK3T/T) exhibit approximately three-fold overexpression of SK3 before dox treatment, and SK3 expression is effectively eliminated by addition of dox. Heterozygous mice exhibit similar expression from both their wild-type and SK3T mutant allele before dox treatment, and no SK3 expression from the mutant allele during dox treatment. In the absence of dox, homozygous mice exhibit abnormal respiratory responses to hypoxia. Homozygous ..... For more information please see the full phenotype on the strain data sheet | ||
| 003823 | B6.129S4-Ttpatm1Far/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous null for the Ttpa gene are viable, normal in size and do not display any gross physical abnormalities. The Ttpa protein product is required for the maintenance of proper alpha-tocopherol levels, the major form of vitamin E in plasma and tissues. The absence of Ttpa protein product in homozygous-null animals results in a corresponding 95% reduction in alpha-tocopherol. Low levels of alpha-tocopherol render female mice infertile, a condition that can be addressed with vitamin E supplements. Male fertility is unimpaired. These mice provide a viable model for studying vitamin E deficiency. | ||
| 006469 | B6.129S4-Tg(PSEN1H163R)G9Btla/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this "H163R mutant PSEN1 YAC" transgene are viable and fertile, while the donating investigator reports that homozygous mice are non-viable. Semi-quantitative RT-PCR of multiple tissues shows expression of H163R mutant human PSEN1 at levels comparable to that of wildtype mouse PSEN1 (50–70%). In contrast to other PSEN1 transgenic models, tissues from this strain express alternatively spliced human PSEN1 transcripts encoding PSEN1 protein (with or without the tetrapeptide VRSQ) and accumulated an 18-kDa PSEN1 C-terminal fragment as shown by western blots, thus expressing a wide spectrum of different human PSEN1 mRNAs and proteins. When crossed to other FAD transgenic strains (for example Stock No. 005300), this transgene is associated with elevated levels of the 42 amino acid form of amyloid-beta (1–42) in both brain and plasma. These mice may be useful in studying neurological disorders such as Familial Alzheimer’s Disease and Down syndrome. | ||
| 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 | ||
| 002741 | B6.129S7-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| 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 | 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. | ||
| 004366 | B6.129X1-Brs3tm1Jfb/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation are viable, normal in size at birth and do not display any gross physical or behavioral abnormalities. This targeted mutation is X-linked; males bearing the targeted allele display a mutant phenotype. At 15 to 16 weeks of age male mice heterozygous for the mutant allele display increased body weight as compared to wildtype littermates. This mutant mouse strain represents a model that may be useful in studies related to energy metabolism and obesity. | ||
| 003479 | B6.C3-Tg(Fos-luc)1Rnd/J | Cryopreserved - Ready for recovery |
| C57BL/6-TgN(c-fosLuc)1Rnd mice are viable and fertile. They carry a firefly luciferase reporter gene driven by the c-fos promoter. The luciferase transgene is expressed constitutively in all tissues of these mice, at the lowest levels in kidney, liver, lung, spleen, heart and various areas of the brain, and at the highest levels in skin and testis. Activation of the c-fos promoter in response to a wide range of stimuli results in increased luciferase expression. C57BL/6-TgN(c-fosLuc)1Rnd mice provide a unique system to monitor c-fos promoter activity in living tissue explant or dispersed cell cultures. | ||
| 012360 | B6.Cg-Erbb4tm1.1(cre/ERT2)Aibs/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Erbb4-2A-CreERT2 allele are viable and fertile, with a viral 2A oligopeptide that mediates ribosomal skipping and a CreERT2 fusion protein (CreERT2 fusion protein) inserted immediately downstream of the translational STOP codon of the Erbb4 locus (v-erb-a erythroblastic leukemia viral oncogene homolog 4 (avian)). As such, Erbb4-2A-CreERT2 mice have both endogenous gene and CreERT2 fusion protein expression directed to Erbb4-expressing cells. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. When Erbb4-2A-CreERT2 mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Erbb4-expressing cells of the double mutant offspring. Specifically, the donating investigator reports that following tamoxifen induction, Erbb4-2A-CreERT2 directs reporter gene expression in scattered interneuron s ..... For more information please see the full phenotype on the strain data sheet | ||
| 007942 | B6.Cg-Isl2tm1Arbr/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Isl2DTA targeted mutation are viable and fertile. These mice have the diphtheria toxin (DTA) gene inserted into the Isl2 (insulin related protein 2 (islet 2)) locus. Expression of DTA in Isl2-expressing cells is blocked by an upstream loxP-flanked STOP sequence. When bred to Cre recombinase-expressing mice, the STOP sequence is deleted in tissues where Cre is present, permitting DTA expression and subsequent cell ablation.
When bred to a strain expressing Cre recombinase in motor neurons (see Stock No. 006600 for example), this mutant mouse strain may be useful in neurodevelopmental studies. These Isl2DTA mutant mice are available on a STOCK genetic background (Stock No. 007603), as well as a C57BL/6J-backcrossed background (Stock No. 007942 ..... | ||
| 009346 | B6.Cg-Lrrk2tm1.1Shn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LRRK2 R1441C knockin allele (R1441C KI) are viable and fertile. The expression of the R1441C mutant form of leucine-rich repeat kinase 2 (Lrrk2) is associated with Parkinson's disease. Homozygous LRRK2 R1441C KI mice appear grossly normal and exhibit no spontaneous dopaminergic neurodegeneration or alterations in steady-state levels of striatal dopamine up to two years of age. Homozygous mice have significantly impaired dopaminergic transmission and impaired dopamine D2 receptor-mediated function. Specifically, homozygotes show reduced psychostimulant (amphetamine)-induced locomotor activity and reduced sensitivity to D2 receptor agonist (quinpirole)-induced locomotor inhibition. Also, nigral neurons from homozygous acute horizontal midbrain slices exhibit decreased sensitivity to inhibition of firing induced by dopamine, quinpirole, and amphetamine. Chromaffin cells cultured from homozygous mice also show compromised potassium-stimulated exocytotic catec ..... For more information please see the full phenotype on the strain data sheet | ||
| 006865 | B6.Cg-Magtm1Rod/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile. The endogenous protein had previously been thought to be necessary for myelin formation. However in the homozygous mutant the degree of myelination and its compaction are normal. Finer motor coordination abilities are significantly affected in the homozygous mutant and they exhibit a subtle intention tremor. The organization of the periaxonal region is partially impaired with the periaxonal cytoplasmic collar frequently missing in optic nerve, cervical spinal cord, and ventral roots. Later in life, beginning at 6 months, oligodendrocytes degenerate. This strain may serve as a model for some aspects of multiple sclerosis. MAG also tranduces a signal to axons. Therefore, axons in the MAG-deficient mice are smaller in calliber due to the aberrant phosphorylation of neurofilaments. MAG has also been shown to be an inhibitor of nerve regeneration. MAG-deficient mice congenic on a C57BL/6 background may exhibit substantially ..... For more information please see the full phenotype on the strain data sheet | ||
| 007575 | B6.Cg-Tg(CAG-Ngb,-EGFP)1Dgrn/J | Cryopreserved - Ready for recovery |
| These transgenic mice express mouse neuroglobin and Enhanced Green Fluorescent Protein under the direction of the chicken beta actin promoter coupled with the cytomegalovirus (CMV) distal enhancer. Western blot analysis detects increased NGB protein in heart brain of homozygotes. Transgenic mice have NGB-overexpressing neurons, astrocytes and endothelial cells in the cerebral cortex. The donating investigator reports that fluorescence is detected in all tissues. Experimentally induced ischemia in transgenic mice results in cerebral infarct volume reduction of approximately 30% and myocardial infarct volume reduction of approximately 25% when compared to wild-type. Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of cerebral (CNS) and myocardial ischemia and stroke. In an attempt to offer alleles on well-characterized or multiple genetic ..... | ||
| 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. | ||
| 006663 | B6.Cg-Tg(Eno2-cre)39Jme/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this NSE39-Cre transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These NSE39-Cre mice harbor a transgenic insert consisting of the cre recombinase gene under the control of the promoter region of the rat neuron specific enolase (NSE or Eno2) gene. As such, Cre recombinase activity is directed to neurons with expression in many tissue types. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome.
Specifically, these NSE39-Cre transgenic mice may also be useful in studies of spinal muscular atrophy (SMA) along with mice harboring a conditional (floxed) Smn1 gene (see Stock No. 006138 or Stock No. 006146).
Additional SMA strains expressing cre in striated muscle are av ..... For more information please see the full phenotype on the strain data sheet | ||
| 003767 | B6.Cg-Tg(Eno2tTA)5021Nes/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the tetracycline-controlled activator protein (tTA) under the control of a rat neuron-specific enolase (Eno2) promoter. Although the Eno2 promoter has been shown to direct high levels of expression in brain tissue in general, this strain selectively expresses tTA at high levels in the striatum and cerebellum. When B6.Cg-Tg(Eno2tTA)5021Nes/J transgenic mice are mated to a second transgenic strain carrying a gene of interest under the regulation of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring may be induced in the tTA-expressing tissues by the withdrawal of the tetracycline analog, doxycycline (dox). For example, when these transgenic mice are bred with Stock No. 003762, a transgenic strain that expresses a Fosb variant under the direction of a TRE, the resulting bitransgenic offspring can be induced to express h ..... For more information please see the full phenotype on the strain data sheet | ||
| 003763 | B6.Cg-Tg(Eno2tTA)5030Nes/J | Cryopreserved - Ready for recovery |
| These transgenic mice express the tetracycline-controlled activator protein (tTA) under the control of a rat neuron-specific enolase (Eno2) promoter. Although the Eno2 promoter has been shown to direct high levels of expression in brain tissue in general, this strain selectively expresses tTA at high levels in the striatum and to a lesser extent in the cerebral cortex and hippocampus. When these transgenic mice are mated to a second transgenic strain carrying a gene of interest under the regulation of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring may be induced in the tTA-expressing tissues by the withdrawl of the tetracycline analog, doxycycline (dox). For example, when these transgenic mice are bred with Stock No. 003762, a transgenic strain that expresses a Fosb variant under the direction of a TRE, the resulting bitransgenic offspring ca ..... For more information please see the full phenotype on the strain data sheet | ||
| 006851 | B6.Cg-Tg(Per1-luc)025Jt/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the "mPer1-Luc" transgene are viable and fertile, with luciferase (luc) expression driven by the mouse Per1 promoter and 5'-UTR elements. Expression of luc RNA is highly specific to the suprachiasmatic nuclei (SCN) with a clear circadian rhythm that correlates with endogenous Per1. Slice cultures taken from hemizygous mice maintain a circadian rhythm of luminescence for at least 5 days after culturing. A prolonged (6 hour) light pulse treatment during the subjective night rapidly induces both mPer1-luc and endogenous mRNA expression; while the endogenous mRNA level decreased to baseline during the 6 hour period, the mPer1-luc mRNA levels remain higher. These mPer1-luc transgenc mice may be useful in studying circadian rhythms and as a real-time reporter of Per1 expression.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from ..... | ||
| 007180 | B6.Cg-Tg(Prnp-ITM2B/APP695*40)1Emcg/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this BRI-Abeta40 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; with highest expression in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. The BRI-Abeta40 fusion protein takes advantage of the BRI protein that is normally cleaved by furin or a furin-like protease near the COOH-terminus (releasing a soluble 23 amino acid peptide in the wildtype BRI protein). As Abeta1-40 is fused to the C terminus of the BRI protein at the furin cleavage site, cleavage releases Abeta into the lumen or extracellular space, resulting in efficient secretion of Abeta1-40. Therefore, these mice specifically express the Abeta1-40 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to the BRI-Abeta42 strain (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 007182 | B6.Cg-Tg(Prnp-ITM2B/APP695*42)A12Emcg/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this BRI-Abeta42 transgene are viable and fertile with a normal lifespan and no obvious behavioral abnormalities. Transgenic BRI-Abeta42 mRNA is expressed in a pattern characteristic of the mouse prion protein promoter; with highest expression in the cerebellar granule cells and hippocampus, followed by the cortex, pons, thalamus, and midbrain. The BRI-Abeta42 fusion protein takes advantage of the BRI protein that is normally cleaved by furin or a furin-like protease near the COOH-terminus (releasing a soluble 23 amino acid peptide in the wild-type BRI protein). As Abeta1-42 is fused to the C terminus of the BRI protein at the furin-like cleavage site, cleavage releases Abeta into the lumen or extracellular space, resulting in efficient secretion of Abeta1-42. Therefore, these mice specifically express the Abeta1-42 isoform in the absence of human amyloid beta protein precursor (APP) overexpression. In contrast to the BRI-Abeta40 strain (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 007894 | B6.Cg-Tg(Rgs4-EGFP)4Lvt/J | Cryopreserved - Ready for recovery |
| Hemizygous RGS4 BAC transgenic mice are viable and fertile. As the RGS4 BAC transgene has an IRES2-eGFP construct inserted into the 3' UTR of the regulator of G-protein signaling 4 (Rgs4) locus, transgenic RGS4 transcripts and EGFP protein expression is observed in a pattern consistent with endogenous Rgs4. While the transgene is designed to co-express EGFP and RGS4, over-expression of RGS4 is not reported to result in unfaithful reporting of endogenous RGS4 expression. Under the control of the RGS4 promoter/enhancer elements, transgene expression reports dynamic developmental, regional, and cellular specific expression in developing and mature cerebral cortex neurons across all cortical domains, as well as developing and mature subcortical regions (telencephalon, diencephalon, and brainstem). While immunostaining against the transgenic product ("RGS4-GFP") allows detailed cellular resolution of neuronal cell bodies and processes, the subcellular localization of EGFP cann ..... For more information please see the full phenotype on the strain data sheet | ||
| 008284 | B6.Cg-Tg(Scg2-tTA)1Jt/J | Cryopreserved - Ready for recovery |
| Homozygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These mice express tetracycline-controlled transactivator protein (tTA) under the control of a mouse secretogranin II promoter. When these mice are mated to a second transgenic strain that carries a gene of interest driven by a tetracycline-responsive promoter element (TRE; tetO), expression of that gene can be conditionally regulated by the presence or absence of doxycycline in the drinking water. Expression in the suprachiasmatic nucleus and brain of bitransgenic animals can be reversibly inhibited by the presence of doxycycline or induced by withdrawal of the tetracycline analog. | ||
| 008750 | B6.Cg-Tg(Th-Oprm1)4Jtw/J | Cryopreserved - Ready for recovery |
| These FLAGMOR transgenic mice express the mouse Oprm1, opioid receptor, mu 1, with an amino-terminal FLAG epitope (FLAG-tagged), under the direction of the rat Th, tyrosine hydroxylase, promoter. Expression of the transgene (fluorescent immunohistochemical staining of the FLAG epitope) is detected in the plasma membrane of locus coeruleus neurons, and other catecholamine neurons in the olfactory bulb, arcuate nucleus, substantia nigra, and ventral tegmental area. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygotes may develop a hydrocephaly phenotype. This mutant mouse strain may be useful to label catecholamine neurons and in studies of opioid receptor signaling and G-protein coupled receptor trafficking. | ||
| 005630 | B6.Cg-Tg(Thy1-EYFP)15Jrs/J | Cryopreserved - Ready for recovery |
| These transgenic mice conditionally express Enhanced Yellow Fluorescent Protein (EYFP) under the direction of the mouse thymus cell antigen 1, theta, promoter. Expression of the EYFP gene is blocked by a loxP-flanked STOP fragment placed between the promoter and EYFP gene. Cre-mediated excision of the STOP cassette results in expression of EYFP in motor neurons. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. For example, when crossed to a strain with widespread expression of Cre recombinase (see Stock No. 003376), this mutant mouse strain may be useful in studies of synaptic function. | ||
| 005627 | B6.Cg-Tg(Thy1-YFP/Syp)10Jrs/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a fusion gene consisting of synaptophysin and Yellow Fluorescent Protein (EYFP) under the direction of the mouse thymus cell antigen 1, theta promoter. Expression of EYFP is detected in vestibular and pontine neurons by birth to 2 days of age. Fluorescent signal is punctuate in the mossy fibers of cerebellar granule layer. The donating investigator reports high levels of fluorescence is detected in synaptic vesicles of neuromuscular junctions. Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of synapse formation at nerve terminals. | ||
| 009344 | B6.Cg-Tg(tetO-Ifng)184Pop/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These TRE/IFN-γ transgenic mice have expression of mouse interferon-gamma (IFN-γ) regulated by the tetracycline-responsive promoter (tetO [also called tetracycline-responsive element (TRE or tet-operator)] fused to the human cytomegalovirus minimal promoter). When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), expression of IFN-γ may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. Because interferon-gamma (IFN-γ) is a pleiotropic cytokine secreted by activated T-lymphocytes and natural killer cells, these line 184 TRE/IFN-γ mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/reversible) expression of IFN-γ for studying antiviral responses, immune surveillance, inhibiting cellular prol ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 008210 | B6.D1-Pde10atm1Pfi/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the phosphodiesterase 10A (PDE10A) targeted mutation are viable and fertile with no gross abnormalities, although breeding homozygotes together produces reduced liter sizes. The targeted gene generates a truncated transcript. A small amount of functionally inactive protein is detected in striatum, cortex and cerebellum. Homozygous mice on the C57BL/6N genetic background (PDE10AC57) exhibit multiple behavioral abnormalities; decreased locomotor activity when placed in a novel environment, delayed acquisition of conditioned avoidance response, blunted response to the NMDA receptor antagonist MK-801 (but not PCP), altered locomotor responses to both amphetamine and methamphetamine, and increased striatal dopamine utilization. These PDE10AC57 mutant mice may be useful in neurobiological studies including metabolic inactivation of intracellular signal transduction pathways by cyclic phosphodiesterases (PDEs), regulation of information processing by ..... For more information please see the full phenotype on the strain data sheet | ||
| 013097 | B6;129-Dlg1tm1Rlh/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of an exon encoding portions of both the PDZ1 and PDZ2 domains of the Dlg1 (discs, large homolog 1 (Drosophila); SAP97) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene.
Widespread deletion of expression leads to neonatal lethality due to failure of maxillar bone fusion. If deletion is specific to motor neurons (Stock No. 006600), neurite extension is suppressed. This strain may be useful for further characterizaton of the targeted gene's synaptic function. | ||
| 011080 | B6;129-Ednrbtm1.1Nat/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites flanking portions of exon 2 and intron 2 of the Ednrb (endothelin receptor type B) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. This strain may be useful for studying the variety of functions associated with this gene ranging from coat color to cell signaling, digestive and immune phenotypes.
When crossed with a Sox2-cre transgenic strain, mice homozygous for the resulting allele lack Ednrb expression and have a phenotype identical to mice with the spotted lethal (s-l, piebald lethal) allele. | ||
| 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. | ||
| 003137 | B6;129-Gabrg2tm1Geh/J | Cryopreserved - Ready for recovery |
| The gamma subunit of the gamma aminobutyric acid type A receptor is essential for bestowing both normal single channel conductance and sensitivity to benzoidiazepines. Alternate RNA splicing produces two alternative forms of the gamma2 subunit from Gabrg2. The two forms, gamma2L and gamma2S are expressed in different brain regions. This strain is a knockout of the gamma2L form. Mice homozygous for this exon deletion are viable and superficially indistinguishable from wild type mice. Behaviorally, gamma2L knockout mice show increased levels of anxiety in the elevated plus maze relative to controls and also longer sleep time than control mice in response to midazolam and zolpidem. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) receptor mutations are available from this donating investigator (Dr. Gregg Homanics, University of Pittsburgh), including Gabra1 (Stock No. 004318), Gabra4 (Stock No. ..... | ||
| 008883 | B6;129-Gt(ROSA)26Sortm1(SNCA*A53T)Djmo/TmdJ | Cryopreserved - Ready for recovery |
| Homozygous ROSA26-Syn-A53T mice are viable and fertile, with the familial Parkinson's disease-associated A53T missense mutant form of human alpha-synuclein (human A53T α-Syn or SYNA53T) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human A53T α-Syn is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human A53T α-Syn protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human A53T α-Syn expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn-A53T mice allow inducible expression of a human mutation associated with familial Parkinson's disease and may be useful for studying the progressive dopaminergic neurodegeneration of Parkinson's dise ..... For more information please see the full phenotype on the strain data sheet | ||
| 008889 | B6;129-Gt(ROSA)26Sortm2(SNCA*119)Djmo/TmdJ | Cryopreserved - Ready for recovery |
| Homozygous ROSA26-Syn119 mice are viable and fertile, with the familial Parkinson's disease-associated Syn119 C-terminal truncation of human alpha-synuclein (human α-Syn119 or SynCT119) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human α-Syn119 is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human α-Syn119 protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human α-Syn119 expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn119 mice allow inducible expression of a human mutation associated with familial Parkinson's disease and may be useful for studying the progressive dopaminergic neurodegeneration of Parkinson's disease and ..... For more information please see the full phenotype on the strain data sheet | ||
| 008886 | B6;129-Gt(ROSA)26Sortm3(SNCA*E46K)Djmo/TmdJ | Cryopreserved - Ready for recovery |
| Homozygous ROSA26-Syn-E46K mice are viable and fertile, with the E46K missense mutant form of human alpha-synuclein (human E46K α-Syn or SYNE46K; associated with familial Parkinson's disease, dementia, and visual hallucinations) inserted into the Gt(ROSA)26Sor (ROSA26) locus. Widespread expression of human E46K α-Syn is blocked by an upstream loxP-flanked STOP sequence (in the absence of Cre recombinase, no human E46K α-Syn protein is observed in brain regions). When bred to cre expressing mice, the STOP sequence is deleted in the tissues of offspring where Cre recombinase is present; resulting in human E46K α-Syn expression. In particular, Stock No. 008601 B6.Cg-Tg(Th-cre)1Tmd/J may be useful for this application. These ROSA26-Syn-E46K mice allow inducible expression of a human mutation associated with familial Parkinson's disease, dementia, and visual hallucinations and may be usefu ..... For more information please see the full phenotype on the strain data sheet | ||
| 009347 | B6;129-Lrrk2tm1.1Shn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the LRRK2 R1441C knockin (R1441C KI) allele are viable and fertile, with expression of the R1441C mutant form of leucine-rich repeat kinase 2 (Lrrk2) associated with Parkinson's disease. Homozygous LRRK2 R1441C KI mice appear grossly normal and exhibit no spontaneous dopaminergic neurodegeneration or alterations in steady-state levels of striatal dopamine up to two years of age. Homozygous mice have significantly impaired dopaminergic transmission and impaired dopamine D2 receptor-mediated function. Specifically, homozygotes show reduced psychostimulant (amphetamine)-induced locomotor activity and reduced sensitivity to D2 receptor agonist (quinpirole)-induced locomotor inhibition. Also, nigral neurons from homozygous acute horizontal midbrain slices exhibit decreased sensitivity to inhibition of firing induced by dopamine, quinpirole, and amphetamine. Chromaffin cells cultured from homozygous mice also show compromised potassium-stimulated exocytotic catecho ..... For more information please see the full phenotype on the strain data sheet | ||
| 010558 | B6;129-Pou4f1tm2.1Nat/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of the Pou4f1 (POU domain, class 4, transcription factor 1) coding region followed by an alkaline phosphatase (AP) reporter. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a cre recombinase-expressing strain, the offspring express AP in the retina, several brain nuclei, dorsal root ganglia, trigeminal ganglion, and other cells/tissues. AP enzyme activity can be clearly detected histochemically. | ||
| 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. | ||
| 008532 | B6;129-Thtm1(cre/Esr1)Nat/J | Cryopreserved - Ready for recovery |
| This creER knock-in line can be used to produce target gene recombination specifically in dopaminergic neurons following 4-hydroxytamoxifen treatment. Heterozygotes and homozygotes are normal in size and viability. | ||
| 010590 | B6;129-Ubbtm1Nat/J | Cryopreserved - Ready for recovery |
| A targeted insertion placed 2 kb 5' of the ubiquitin b (Ubb) gene provides 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, synaptic vesicle protein 2B (SV2B), GFP, 3xHA (hemagglutinin) 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 (SV2B, GFP, 3xHA epitope) labels presynaptic structures.
This reporter can be activated by cre recombinase in any cell in the body at any ..... For more information please see the full phenotype on the strain data sheet | ||
| 008678 | B6;129-Ubbtm1Rrk/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function. Direct visualization of GFP fluorescence is observed in ovaries, testes, hypothalamus (arcuate nucleus) and cerebral cortex. Homozygotes have no Ubb mRNA observed in the various tissues tested, and are viable but sterile due to failure of germ cells to progress through meiotic prophase I and hypogonadism. Homozygotes also exhibit a complex metabolic phenotype initially characterized by dysfunction of neurons within the central nervous system accompanied by retarded perinatal growth that progresses to adult-onset obesity linked to selective hypothalamic neurodegeneration. Homozygotes also develop adult-onset hyperleptinemia (but normal levels of circulating glucose and insulin) as a consequence of increased fat content. These Ubb-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet | ||
| 010745 | B6;129P2-Aviltm1(ALPP)Fawa/J | Cryopreserved - Ready for recovery |
| A human placental alkaline phosphatase (ALPP) gene was used to disrupt the mouse advillin(Avil) locus. Approximately 50% of mice that are homozygous for the targeted mutation die before E10.5, however, the remaining homozygotes are viable, fertile, and normal in size and do not display any gross physical or behavioral abnormalities. Alkaline phosphatase staining of heterozygote sections allows visualization of peripheral sensory neurons. Trigeminal sensory neurons cultured from homozygotes display a reduction in regenerative axon growth. Following whisker cauterization in homozygotes, trigeminal central projections exhibit a reduced plasticity. This mutant mouse strain may be useful in the visualization of sensory neurons and axon projections as well as in the study of axon remodeling and regrowth. | ||
| 008333 | B6;129P2-Dldtm1Ptl/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the Dld (dihydrolipoamide dehydrogenase or E3 component) targeted mutation are viable and fertile. Heterozygous mice exhibit approximately half of wild-type enzymatic activity levels for E3 and all affected mitochondrial multienzyme complexes. Heterozygotes (on a C57BL/6;129P2 genetic background) exhibit increased vulnerability to treatments with MPTP (dopaminergic neurotoxin used to induce Parkinson's disease-like lesions), malonate (inhibitor of cellular respiration used to mimic Huntington's disease features), and 3-NP (mitochondrial toxin used to mimic Huntington's disease features). Homozygous mice exhibit normal development and metabolism during the preimplantation period, explained by the persistence of E3 enzyme from the oocyte. Homozygotes exhibit developmental delays shortly after implantation (7.5 to 8.5 days postcoitum (dpc)) and cease development within the subsequent two days. These Dld mutant mice may be useful to study early murine em ..... For more information please see the full phenotype on the strain data sheet | ||
| 006717 | B6;129P2-Olfr124tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Mice carrying the Olfr124tm1Mom allele have tau-linked green fluorescent protein co-expressed with the OLFR124 protein. OLFR124 expressing olfactory sensory neurons are found densely packed in the septal organ and at a much lower density in the main olfactory epithelium, and have been found to respond to a notably wide array of compounds. | ||
| 006720 | B6;129P2-Olfr124tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons with the Olfr124 locus actively transcribed can be identified as expressing red fluorescent protein, even though no OLFR124 protein is expressed. The density of these cells in the septal organ is 14 times lower than OLFR124 expressing cells in mice with an intact Olfr124 locus tagged with an IRES-tauGFP. Of the OLFR124 deficient neurons, only 18% in the septal organ and only 14% in the main olfactory epithelium responded to all 5 odorants that stimulate 100% of OLFR124 expressing olfactory sensory neurons. This indicates that OLFR124 is responsible for the unusually broad response profile of the olfactory sensory neurons that express it. | ||
| 006712 | B6;129P2-Olfr545tm1Mom/MomJ | Cryopreserved - Ready for recovery |
| The Olfr545tm1Mom allele has a fully intact coding sequence with a tauGFP tag permitting bicistronic expression of the endogenous gene and the green fluorescent protein tag. The olfactory sensory neurons that express this tagged allele typically project to a single dorsal-medial and a single anterior-lateral glomerulus per olfactory bulb, and, when co-expressed with Tg(P-taulacZ)8Mom expression is found not to overlap. | ||
| 006713 | B6;129P2-Olfr545tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that select to express Olfr545 are labeled with tauRFP | ||
| 006716 | B6;129P2-Olfr545tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| With the coding sequence of class I olfactory receptor Olfr545 excised and replaced with venusYFP, this strain allows assessment of the role of a specific olfactory receptor in olfactory sensory neuron development. Mice carrying this allele display a normal pattern of labeled axons projecting diffusely to a large subset of glomeruli in the dorsal-medial and anterior-medial olfactory bulb, but also an abnormal finding of labeled axons innervating glomeruli at the caudal margins of the olfactory bulb. Co-staining for five dorsal class I olfactory receptors shows 3.8% co-expressing class I olfactory receptor genes and the disrupted Olfr545tm4Mom allele, while co-staining for five dorsal class II olfactory receptors shows no co-expression with the disrupted Olfr545tm4Mom allele. | ||
| 004946 | B6;129P2-Omptm2(spH)Mom/J | Cryopreserved - Ready for recovery |
| These mutant mice express synapto-pHluorin (spH) from the endogenous locus encoding the olfactory marker protein (OMP) as a result of a targeted knockin mutation that replaces the OMP coding region with that of spH. The OMP locus directs expression of spH at high levels and exclusively in mature sensory neurons of the main olfactory epithelium (OSNs) and the vomeronasal epithelium. SpH is a pH-sensitive variant of the green fluorescent protein (ecliptic pHluorin) fused to the mouse synaptic vesicle-associated protein (VAMP2). The protein is localized preferentially in synaptic vesicles, but is also present on the plasma membrane of OSN axons and nerve terminals. The fluorescent domain of spH is exposed to the acidic lumen of synaptic vesicles where it is ~ 20 fold less fluorescent than at neutral pH. Upon synaptic release, the lumen of the synaptic vesicles becomes continuous with the extracellular space resulting in an increase in pH that causes a rapid increase in fluorescence. In mu ..... For more information please see the full phenotype on the strain data sheet | ||
| 006726 | B6;129P2-Vmn2r81tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| Olfactory sensory neurons that express the vomeronasal receptor Vmn2r81 also 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. | ||
| 008686 | B6;129P2-Vmn2r81tm4Mom/MomJ | Cryopreserved - Ready for recovery |
| This mutant is valuable in characterizing the development of vomeronasal sensory neurons and the vomeronasal organ. While the axons of vomeronasal sensory neurons bearing the wild-type Vmn2r81 coalesce into glomeruli at several sites in the posterior accessory olfactory bulb, those of Vmn2r81tm4Mom homozygotes instead spread out diffusely over the posterior accessory olfactory bulb and a few extend into the anterior olfactory bulb. Distinct from normal vomeronasal sensory neurons at 3 weeks of age, 25% of those expressing lacZ, indicative of active transcription at the Vmn2r81 locus, also co-express transcript for another family ABD V2R gene. 68% of wild-type Vmn2r81-expressing neurons co-express Vmn2r2 but rarely co-express Vmn2r1. However, 9.5% of lacZ-bearing neurons also co-express Vmn2r1 and only 8.1% co-express Vmn2r2. 93% of wild-type Vmn2r81-expressing neurons co-express Omp, a marker of matu ..... For more information please see the full phenotype on the strain data sheet | ||
| 010539 | B6;129S-Fgf17tm1Dor/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. No gene product (mRNA) is detected by in situ hybridization analysis of midbrain-hindbrain from homozygous embryos. Significant portions of the inferior colliculus and the vermis cerebellum are absent in homozygotes (2 days of age and adult). The remaining midbrain and cerebellum have normal morphology although the size of the vermis cerebellum is approximately 82% of the wildtype control. The size of the rostal-most lobe of the vermis is 1/3 of the wildtype control. The fissure separating lobe III (most rostal lobe) and lobe IV does not form completely, resulting in partially fused lobes. The dorsal frontal cortex is reduced in size with a rostral shift of sensory cortical areas. Homozygotes exhibit impaired social interaction behavior. Homozygous pups vocalize less than wildtype controls when separated from mothers. Homozygous adult male ..... For more information please see the full phenotype on the strain data sheet | ||
| 003177 | B6;129S2-Gm2atm1Rlp/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Gm2atm1Rlp targeted mutation demonstrate neuronal storage of GM2 ganglioside in restricted regions of the brain (piriform, entorhinal cortex, amygdala, and hypothalmic nuclei) reminiscent of the asymptomatic Tay-Sachs model (B6;129S4-Hexatm1Rlp/J Stock No. 002367) mice. They also display abnormal storage in the cerebellum and exhibit defects in balance and coordination. Mice homozygous for the Gm2atm1Rlp targeted mutation serve as a model of the human genetic disease known as the AB Variant of GM2-gangliosidosis or GM2 activator deviciency (OMIM#272750). | ||
| 009576 | B6;129S4-Et(cre/ERT2)278Rdav/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of the Cre-ERT2 fusion gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Cre recombinase activity is observed in brain tissues following tamoxifen administration. The donating investigators may not have assessed expression in tissues other than brain. When these enhancer trap transgenic mice are bred with mice containing a loxP-flanked sequence of interest, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring.
For characterization information, see images at the Allen Institute for Brain Science website (Et(cre/ERT2)278Rdav images). The Cre-ERT2 fusion protein (Cre-ERT2) consists of Cre reco ..... | ||
| 003524 | B6;129S6-Lrp8tm1Her/J | Cryopreserved - Ready for recovery |
| Mutant mice have a targeted mutation of the apolipoprotein E receptor Lrp8 (also called Apoer2). Homozygotes are viable with no gross morphological abnormalities. Homozygous males have reduced fertility, while females are not affected. Using C-terminal specific antibodies, no endogenous protein is detected in the brains of homozygotes. Homozygous mice have a smaller and less foliated cerebellum with various hippocampus defects in granule cell positioning, cortical neuron migration, granule cell laminar organization, commissural fiber distribution, CA1 microtubule-associated protein 2 (MAP-2) distribution, and long term potentiation (LTP). Mutant mice show contextual fear conditioning deficits. These mice may be useful in studies of brain development, neuronal cytoarchitecture, Reelin signaling pathways, NMDA receptor activity, lipoprotein receptors, synaptic plasticity and learning, schizophrenia, and neurodegenerative disorders such as Alzheimer's disease. | ||
| 002317 | B6;129S7-Alpltm1Sor/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 003120 | B6;129S7-L1camtm1Sor/J | Cryopreserved - Ready for recovery |
| The L1 gene is localized to the X chromosome. As a result, hemizygous males are affected and the mutation has to be propagated through females. Male mice hemizygous for the L1camtm1Sor targeted mutation have defects in the guidance of axons of the corticospinal tract. A substantial proportion of axons do not take their normal crossed course to the dorsal column at the pyramidal decussation. There is also a varying, but reduced number of corticospinal axons in the dorsal columns of the spinal cord. | ||
| 009616 | B6;C3-Tg(A930038C07Rik-cre)4Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous A930038C07Rik-Tg4-Cre mice are viable and fertile, with Cre recombinase expression directed to to cortex, striatum, and cerebellum by the epidermacan (A930038C07Rik) promoter/enhancer regions within the BAC transgene. When A930038C07Rik-Tg4-Cre mice are bred with mice containing loxP-flanked sequences, Cre-mediated recombination will result in deletion of the floxed sequences in the epidermacan-expressing cells of the double mutant offspring. The donating investigators may not have assessed expression in tissues other than brain. The phenotype of homozygous mice has not yet been characterized (July 2009).
For characterization information, see images at the Allen Institute for Brain Science website (A930038C07Rik-Tg4-Cre images). | ||
| 008844 | B6;C3-Tg(Ctgf-cre)2Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous Ctgf-Tg2-Cre mice are viable and fertile, with cre expression directed to cortex and hippocampus by the Ctgf promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Ctgf-Tg2-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex and hippocampus).
For characterization information, see images at the Allen Institute for Brain Science website (Ctgf-Tg2-Cre images). | ||
| 008839 | B6;C3-Tg(Cyp39a1-cre)1Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous Cyp39a1-Tg1-Cre mice are viable and fertile, with cre expression directed to cortex, hippocampus, striatum, olfactory bulb and cerebellum by the Cyp39a1 promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Cyp39a1-Tg1-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, hippocampus, striatum, olfactory bulb and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Cyp39a1-Tg1-Cre images). | ||
| 009117 | B6;C3-Tg(Cyp39a1-cre)7Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous Cyp39a1-Tg7-Cre mice are viable and fertile, with cre expression directed to cortex, hippocampus and cerebellum by the Cyp39a1 promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Cyp39a1-Tg7-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, hippocampus and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Cyp39a1-Tg7-Cre images). | ||
| 008848 | B6;C3-Tg(Mybpc1-cre)2Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous 8030451F13Rik-Tg2-Cre mice (also called Mybpc1-Cre mice) are viable and fertile, with cre expression directed to scattered populations within the cortex and hippocampus by the Mybpc1 (8030451F13Rik) promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These 8030451F13Rik-Tg2-Cre (Mybpc1-Cre) mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in the cortex of the brain and hippocampus.
For characterization information, see images at the Allen Institute for Brain Science website (Mybpc1-Cre images). | ||
| 009111 | B6;C3-Tg(Scnn1a-cre)1Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous Scnn1a-Tg1-Cre mice are viable and fertile, with cre expression directed to cortex, striatum, hippocampus and cerebellum by the Scnn1a promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Scnn1a-Tg1-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, striatum, hippocampus and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Scnn1a-Tg1-Cre images). | ||
| 009112 | B6;C3-Tg(Scnn1a-cre)2Aibs/J | Cryopreserved - Ready for recovery |
| Hemizygous Scnn1a-Tg2-Cre mice are viable and fertile, with cre expression directed to cortex, thalamus, midbrain and cerebellum by the Scnn1a promoter/enhancer regions within the BAC transgene. The donating investigators may not have assessed expression in tissues other than brain. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in the offspring. These Scnn1a-Tg2-Cre mice may be useful for generating conditional mutations for studying gain or loss of function and/or fate mapping in subgroups of brain tissues (including cortex, thalamus, midbrain and cerebellum).
For characterization information, see images at the Allen Institute for Brain Science website (Scnn1a-Tg2-Cre images). | ||
| 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 | ||
| 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. | ||
| 012812 | B6;D2-Tg(Eno2-MFN2*R94Q)L51Ugfm/J | Cryopreserved - Ready for recovery |
| MitoCharc1 transgenic mice have the neuron specific rat enolase (Eno2) promoter directing expression of a mutated human Mitofusin 2 (MNF2) gene in neurons. Hemizygous mice are viable, fertile, and normal in size. MitoCharc1 contains the amino acid mutation R94Q (Arginine to Glutamine) to mimic the most common mutation found in human Charcot-Marie-Tooth disease type2A (CMT2A). These mice exhibit symptoms of CMT2A including locomotor impairment, and a shift in the size of myelinated axons correlating with an increase in mitochondria in these axons at 5 months of age. These mice may be useful for studying the neurophysiology of human CMT2A disease. | ||
| 005621 | B6;D2-Tg(S100B-EGFP)1Wjt/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. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the human S100 calcium-binding protein, beta (neural) promoter. Fluorescence is detected in Schwann cells of the sternomastoid, soleus, extensor digitorum longus, triangularis sterni and diaphragm muscles, some astrocytes, Bergmann glia and a few muscle macrophages. EGFP expression is detected at birth. This mutant mouse strain may be useful in studies of vital imaging of neuronal and glial cells, and neuromuscular junctions. | ||
| 005620 | B6;D2-Tg(S100B-EYFP)1Wjt/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. These transgenic mice express Enhanced Yellow Fluorescent Protein (EYFP) under the direction of the human S100 calcium-binding protein, beta (neural) promoter. Fluorescence is detected in Schwann cells, motor axons, microglia, a subset of Bergmann glia and some muscle macrophages. Strong fluorescent signal is detected in the Schwann cells of sternomastoid, extensor digitorum longus, triangularis sterni and diaphragm muscles and in the motor axons of the triangularis sterni. EYFP expression is detected at birth in glial cells and at postnatal day 7 in motor axons. This mutant mouse strain may be useful in studies of vital imaging of neuronal and glial cells. | ||
| 004690 | B6;FVB-Tg(Pcp2-EGFP)2Yuza/J | Cryopreserved - Ready for recovery |
| These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse Purkinje cell protein 2 promoter. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Transgenic mice display distinct expression of EGFP in dendrites, axons and soma of Purkinje cells, allowing identification, isolation and purification of Purkinje cells by FACS. EGFP expression mimics endogenous Purkinje cell protein 2 expression pattern. Fluorescence is detectable at embryonic day 17 in Purkinje cells and also occurs in retinal bipolar cells. Low levels of fluorescence are seen in olfactory periglomerular cells, interpeduncular nucleus and superior colliculus neurons. This mutant mouse strain represents a model that may be useful for purification and in vivo tracking of Purkinje cells. | ||
| 010574 | B6;SJL-Tg(Gh1-rtTA)4-3Jek/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These GH-rtTA transgenic mice have expression of the reverse tetracycline-controlled transactivator (rtTA) protein directed to GH1-producing cells (pituitary somatotropes) by the rat growth hormone (Gh1) promoter. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in GH1-producing cells may be induced with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These GH-rtTA transgenic mice are a Tet-On tool that allows conditional, dox-inducible expression of genes in GH1-producing cells/tissues (such as pituitary somatotropes) and may be useful for studying pituitary hormone secretion and proliferation. | ||
| 006043 | B6;SJL-Tg(Oxt/EGFP)AI03Wsy/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. This transgene expresses an enhanced green fluorescent protein (EGFP) fused to the end of the neurophysin at the C-terminus of the oxytocin pre-prohormone. The transgene is selectively expressed in oxytocin-magnocellular neurons of the paraventricular and supraoptic nuclei of the hypothalamus. The fusion protein is faithfully trafficked to secretory granules and transported to neurosecretory terminals in the neurohypophysis, where the EGFP fluorescence undergoes depolarization-induced calcium-dependent secretion. Immunohistochemical detection of EGFP in individual oxytocin-magnocellular neurons is suggested as intrinsic fluorescence is low. However, the endogenous fluorescence in the neural lobes is sufficiently intense to image secretory events in individual oxytocin nerve terminals (neurosecretosomes) isolated from the posterior pituitary. These mice may be useful in studies of hormone biology, pharmaco ..... For more information please see the full phenotype on the strain data sheet | ||
| 010573 | B6;SJL-Tg(Prl-tTA)6-5Jek/J | Cryopreserved - Ready for recovery |
| The donating investigator claims homozygous mice are viable and fertile. These Prl-tTA transgenic mice have expression of the tetracycline-controlled transactivator (tTA) protein directed to PRL-producing cells (pituitary lactotropes/mammotropes) by the rat prolactin (Prl) promoter. The donating investigator also reports some expression in testis. When mated to a mutant strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE, TetRE or tetO), expression of the target gene in the PRL-producing cells may be conditionally abolished with administration of the tetracycline analog doxycycline (dox) in the double mutant offspring. These Prl-tTA transgenic mice are a Tet-Off tool that allows dox-conditional expression of genes in PRL-producing cells/tissues (such as pituitary lactotropes/mammotropes) and may be useful for studying pituitary hormone secretion and proliferation. | ||
| 012341 | B6;SJL-Tg(Thy1-COP3/EYFP)1Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 012344 | B6;SJL-Tg(Thy1-COP3/EYFP)4Gfng/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the Thy1-VChR1-YFP transgene are viable and fertile with expression of the VChR1::YFP fusion protein directed to neural cells by the modified murine Thy1 promoter region. The VChR1::YFP fusion protein is composed of a synthetic, mammalian codon-optimized, red-shifted channelrhodopsin-1 derived from Volvox carteri (VChR1) fused in-frame with an enhanced yellow fluorescent protein (EYFP). Compared with ChR2, VChR1 has a markedly (~70 nm) red-shifted action spectrum with a maximum at ~535 nm (green light). The bacterial opsins are retinal-binding proteins that provide light-dependent ion transport and sensory functions to a family of halophilic bacteria; and this VChR1 functions as a green light-driven cation channel that depolarizes the cell and causes action potentials. As such, illumination of VChR1-expressing neurons leads to rapid and reversible photostimulation of action potential firing/neural activity in these cells. The donating investigator spec ..... For more information please see the full phenotype on the strain data sheet | ||
| 010575 | B6;SJL-Tg(tetO-Egfr*)2-9Jek/J | Cryopreserved - Ready for recovery |
| The donating investigator reports that homozygous mice are viable and fertile. These TetRE-EGFR-tr (TRE-EGFR-tr) transgenic mice express a dominant negative, cytoplasmic tyrosine kinase domain-deleted mutant form of epidermal growth factor receptor (EGFR-tr) regulated by the tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator) and cytomegalovirus minimal promoter. When mated to a mutant strain expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue EGFR-tr expression may be regulated with the tetracycline analog doxycycline (dox) in the double mutant offspring. EGFR-tr expression disrupts subsequent activation of signal transduction pathways that are involved in regulating cellular proliferation, differentiation, and survival. These TetRE-EGFR-tr mice may be bred to generate bi-transgenic mutant mice with conditional (inducible/reversible) expressi ..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 001311 | BALB/cWtEiJ | Cryopreserved - Ready for recovery |
| Experimental allergic encephalitis (EAE) is an autoimmune disease of the nervous system induced by sensitization of experimental animals with homogenates of whole brain and/or spinal cord tissue, myelin, or myelin components. Many of the clinical and histologic aspects of EAE are similar to those of multiple sclerosis (MS), making EAE a useful MS model (Alvord et al., 1984). Mice of different sublines of the BALB/c inbred strain exhibit marked differences in the incidence and severity of EAE induced by immunization with spinal cord homogenate (Hickey et al., 1986) or with myelin proteolipid protein (PLP) (Tuohy et al., 1988). The most severe response to PLP was development in nine of ten BALB/cPt mice of rapid onset, severe clinical disease with limb paralysis accompanied histologically by meningeal and perivascular infiltration by mononuclear and polymorphonuclear lymphocytes, particularly of the spinal cord. At the opposite end of the spectrum, none of ten BALB/ ..... For more information please see the full phenotype on the strain data sheet | ||
| 007662 | C57BL/6-Arctm1Stl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. A destabilized form of GFP (d2EGFP) is expressed under the control of the endogenous Arc promoter which is activated by neuronal stimulation in forebrain regions. The half-life of EGFP expression is shortened to approximately two hours which is comparable to the decay time of ARC protein. Homozygous mice have a reduced orientation specificity in the visual cortex. The loss of Arc mRNA expression in homozygous mice was verified by RT-PCR analysis of brain total RNA preparations. This strain may be useful in studies of cortical functions. | ||
| 006575 | C57BL/6-Camk2atm1Vyb/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this "falpha-CaMKII" allele are viable and fertile with no reported neurological abnormalities. These mutant mice have loxP sites flanking exon 2 of the endogenous gene. When bred to Cre-recombinase expressing mice, exon 2 is deleted in the resulting offspring dependent on the tissue specificity of the promoter of the cre transgene. For example, when crossed with transgenic mice expressing Cre-recombinase in hippocampal CA3 pyramidal cells (see Stock No. 006474), the resulting offspring show altered neurotransmitter release. These "floxed" mice may be useful for neurological studies such as calcium/calmodulin-dependent protein kinase activity. | ||
| 006468 | C57BL/6-Chrm1tm1Stl/J | Cryopreserved - Ready for recovery |
| Homozygotes are viable and fertile with complete absence of the wildtype allele mRNA in forebrain tissues. Mice homozygous for this M1 muscarinic acetylcholine receptor deficiency have elevated dopaminergic transmission in the striatum, significantly increased locomotor activity, increased response to the stimulatory effects of amphetamine. These mutant mice may be useful in neurological studies, including the regulation of dopaminergic transmission by the M1 receptor and M1 dysfunction in psychiatric disorders. | ||
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable and fertile, although the donating investigator reports that hemizygous mice have breeding problems likely resulting from a social anxiety-related phenotype. These "BDNF (line A9)" mice express the rat brain-derived neurotrophic factor (BDNF) primarily in forebrain regions, including the neocortex and hippocampus. Weak transgenic BDNF expression is detected also in cerebellum. Within the primary visual cortex, transgene expression is highest in the superficial layers. Hemizygous mice exhibit accelerated maturation of GABAergic innervation and inhibition, earlier termination of the critical period for ocular dominance plasticity, and accelerated development of visual acuity. These transgenic mice may be useful for studies involving BDNF overexpression and synaptic maturation and plasticity in the visual cortex. | ||
| 010800 | C57BL/6-Tg(Thy1-PTGS2)300Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These moderate overexpressing C57BL/6J COX-2 transgenic line 300 mice have PGE2 levels that are ~10-12-fold greater than non-transgenic controls (compared to ~25-40-fold overexpression in line 303; see Stock No. 010703). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic m ..... For more information please see the full phenotype on the strain data sheet | ||
| 010703 | C57BL/6-Tg(Thy1-PTGS2)303Kand/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (PTGS2 or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. 010800). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhib ..... For more information please see the full phenotype on the strain data sheet | ||
| 005706 | C57BL/6-Tg(tetO-CDK5R1/GFP)337Lht/J | Cryopreserved - Ready for recovery |
| Hemizygous transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. Mice homozygous for this transgene may not be viable. When these transgenic mice are bred with mice expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, expression of the CDK5R1/GFP fusion protein in the appropriate tissue of the bitransgenic offspring can be regulated by doxycycline administration. These mice may be useful in studies of Alzheimer's disease and other neurodegenerative tauopathies, amyotrophic lateral sclerosis (ALS), Niemann Pick Type C (NPC) disease, and Parkinson's disease.
Note: this transgenic strain was designed to breed with Tg(Camk2a-tTA) transgenic mice, (Stock No. 003010), a transgenic strain that expresses tTA in forebrain neurons. The resulting bitransgenic offspring exhibit the hallmark phenotype of Alzheimer's disease; ..... | ||
| 007857 | C57BL/6J-Tg(Eno2-YFP/Cox8a)YRwb/J | Cryopreserved - Ready for recovery |
| These transgenic mice express Yellow Fluorescent Protein (YFP) under the control of the neuron specific rat enolase 2, gamma, Eno2, promoter. YFP is specifically localized to the mitochondria by a mouse cytochrome c oxidase, subunit VIIIa, targeting signal fused to the N-terminus. Fluorescence is detected in many neuronal populations. The donating investigator reports that fluorescence is detected in subcortical structures including the thalamus, basal ganglia, and caudate/putamen; interneurons of the cortex and hippocampus; a subset of retinal ganglion cells; cerebellum mossy fiber rosette terminals of the granule cell layer and spinal cord preganglionic autonomic neurons. It is not known if homozygotes are viable. This mutant mouse strain may be useful in studies of mitochondrial transport and neuronal metabolism. | ||
| 008245 | C57BL/6J-Tg(Th-SNCA)5Eric/J | Cryopreserved - Ready for recovery |
| These hwα-SYN-5 mice express wildtype human alpha-synuclein (hα-SYN) under the control of the rat tyrosine hydroxylase promoter. Expression of hα-SYN is detected in cell bodies, axons, and terminals of the nigrostriatal system (mRNA expression in midbrain, eye, and adrenal gland, with high levels of protein expression in the cell bodies of dopaminergic neurons in the midbrain and striatum). Hemizygous mice exhibit several Parkinson's disease-related characteristics including increased density of the dopamine transporter, impairments of the ubiquitin-proteasome system, and age-related progressive loss of locomotor activity and substantia nigra pars compacta dopaminergic neurons. The Parkinson's disease-related phenotype of these hwα-SYN-5 mice is intermediate between that of the C57BL/6J wild-type controls and the severely affected hm2α-SYN-39 strain (see Stock No. 008239). As such, these h ..... For more information please see the full phenotype on the strain data sheet | ||
| 007898 | CBy.Cg-Tg(Gt(ROSA)26Sor-EGFP)I1Able/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this ROSA26-EGFP BAC transgene are viable and fertile, with widespread EGFP expression in all organs and tissues analyzed. In addition, stable and uniform EGFP expression is observed in differentiated progeny of transplanted hematopoietic stem cells (HSC) isolated from ROSA26-EGFP mice. These ROSA26-EGFP BAC transgenic mice may be useful for fluorescent labeling of cells and tissues both in vivo and in vitro, are suitable for use in histological preparations, and are appropriate as a source of fluorescently labeled donor cell populations (such as tracking hematopoietic cell fate in transplant recipients).
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as publish ..... | ||
| 007578 | CBy.Cg-Tg(HDexon1)61Gpb/J | Cryopreserved - Ready for recovery |
| Mice have been generated that are transgenic for the 5' end of the human HD gene carrying approximately 100 CAG repeat expansions. In this founder line (61Gpb), the transgene is ubiquitously expressed. Transgenic mice exhibit a progressive neurological phenotype that mimics many of the features of HD, including choreiform-like movements, involuntary stereotypic movements, tremor, and epileptic seizures, as well as nonmovement disorder components, including unusual vocalization. They urinate frequently and exhibit loss of body weight and muscle bulk through the course of the disease. Neurologically they develop Neuronal Intranuclear Inclusions (NII) which contain both the huntingtin and ubiquitin proteins. These NII have also been identified in human HD patients. The age of onset of HD symptoms is reported to occur between 15 and 21 weeks for this 61Gpb line. On the BALB/cByJ genetic background, the CAG tract remains somatically stable throughout the life span of the mouse but may contr ..... For more information please see the full phenotype on the strain data sheet | ||
| 009638 | FVB-Tg(GFAP-luc,GAPDH-rluc)172.9Mes/J | Cryopreserved - Ready for recovery |
| These Dual-glo transgenic mice express both firefly luciferase (luc) under the control of the human GFAP (glial fibrillary acidic protein) promoter and Renilla luciferase under the control of the 0.5kb human GAPDH (glyceraldehyde-3-phosphate dehydrogenase) promoter. GFAP-fLuc transgene expression is highest in brain, with lower levels detected in heart and no detectable expression in kidney, muscle, lung and liver. The firefly luciferase protein co-localizes with GFAP in astrocytes after kainic acid induced injury. GAPDH-RLuc transgene expression is highest in brain and heart, with lower levels detected in kidney, muscle, lung and liver. Interindividual variability in firefly luciferase expression is reduced with normalization of the GFAP-fLuc signal to the GAPDH-RLuc signal. Retinal expression of luciferase is increased due to photoreceptor degeneration for mice on the FVB background and the homozygous presence of the retinal degeneration 1, Pde6brd1 ..... 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 | ||
| 005625 | FVB-Tg(Pcp2-tTA)3Horr/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Cerebellar Purkinje cell-specific tTA expression has been confirmed using PCR. Constitutive expression of tTA in Purkinje cells makes this strain suitable for creating bitransgenic mice that can, by withdrawing tetracycline (or its derivative doxycycline), inducibly express a gene of interest in Purkinje cells when the gene of interest is under the direction of a tetracycline-responsive element (TRE; tetO). | ||
| 013156 | FVB-Tg(tetO-CDK5R1*)1Vln/J | Cryopreserved - Ready for recovery |
| These tetO-CDK5R1* mice express a truncated human cyclin-dependent kinase 5, regulatory subunit 1 (CDKR1 or p35) cDNA sequence, also referred to as p25, under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE, TetRE) or tet-operator). The N-terminal truncated isoform of p35 is p25. Unlike p35, which is membrane bound in postmitotic neurons in the brain, p25 is non-tethered and expression is seen in all cellular compartments of neuronal somata and dendrites. Mice that are hemizygous for this transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), CDK5R1 expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. For example, when bred to a strain expressing ..... For more information please see the full phenotype on the strain data sheet | ||
| 008685 | FVB-Tg(tetO-Kdr*)4377.5Rwng/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a truncated mouse Kdr (kinase insert domain protein receptor) gene under the control of a tetracycline-responsive promoter element (TRE or tetO). The truncated gene encodes amino acids 1 through 828, which includes the cytoplasmic tyrosine kinase domain, and has a hemaglutin (HA) tag fused at the C terminus. When bred with a transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), a bitransgenic animal can be produced that has tissue-specific expression of Kdr that can be regulated with the tetracycline analog, doxycycline.
For example, when bred to a strain expressing tTA in liver (see Stock No. 003563) and a targeted mutation of Kdr (see Stock No. 002938) , this mutant mouse strain may be useful in studies of liver organogenesis. ..... | ||
| 006138 | FVB.129(B6)-Smn1tm1Jme/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this SMNF7 floxed allele are viable and fertile and do not display any gross physical or behavioral abnormalities. Mutant mice exhibit no transcript splicing defects. Cre-mediated recombination of the loxP-flanked sequences results in deletion of exon 7 of the targeted gene. As mutations of this exon are implicated in 95% of all human spinal muscular atrophy (SMA), these mice may be useful in studying SMA or other neuromuscular degenerative diseases.
When crossed to a strain expressing Cre recombinase in neurons (ssee Stock No. 005938, Stock No. 006297, and Stock No. 006663), this mutant mouse strain may be useful as a model of SMA. When crossed to a strain expressing Cre recombinase in striated muscle fibers (see Stock No. 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 | ||
| 012563 | FVB.129(Cg)-Slc9a3tm1Ges/J | Cryopreserved - Ready for recovery |
| These mice harbor a targeted mutation of the Na+/H+ exchanger isoform 3 locus (Nhe3 or Slc9a3) that abolishes endogenous gene expression. While no full-length mRNA is detected in kidney or intestine of homozygous mice, a truncated mutant mRNA lacking codons 320-831 (encoding sequences required for Na+/H+ exchange) is observed but expected to impart no dominant negative effects. When maintained as congenic on the FVB/N genetic background, homozygous mice exhibit a high mortality rate beginning just after weaning, with ~30% surviving to adulthood. Homozygous females are fertile, but homozygous males are infertile.
Homozygous (Nhe3-null) mice lack Na+/H+ exchanger isoform 3 function, and exhibit impaired intestinal absorption; resulting in severe diarrhea, altered salt and water homeostasis, and increased luminal fluid throughout the intestinal tract. Nhe3-null mice have increased PCNA-positive cells in the cryp ..... 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). | ||
| 006139 | FVB.Cg-Tg(ACTA1-cre)79Jme/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this HSA-Cre79 transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These HSA-Cre79 transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. Cre activity is restricted to adult striated muscle fibers and embryonic striated muscle cells of the somites and heart. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in striated muscle-specific deletion of the flanked genome. Specifically, these HSA-Cre79 (or ACTA1-Cre) transgenic mice were originally used to breed with mice heterozygous for a deletion of exon 7 and a loxP-flanked exon 7 mutation on homologous chromosomes of the Smn1 gene (see Stock No. 006138 or Stock No. 006146). The resulting offspring ( ..... For more information please see the full phenotype on the strain data sheet | ||
| 006297 | FVB.Cg-Tg(Eno2-cre)39Jme/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this NSE39-Cre transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These NSE39-Cre mice harbor a transgenic insert consisting of the Cre recombinase gene under the control of the promoter region of the rat neuron specific enolase (NSE or Eno2) gene. As such, Cre recombinase activity is directed to neurons with expression in many tissue types. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. Specifically, these NSE39-Cre transgenic mice may also be useful in studies of spinal muscular atrophy (SMA) along with mice harboring a conditional (floxed) Smn1 gene (see Stock No. 006138 or Stock No. 006146).
Additional SMA strains expressing cre in striated muscle are available ..... | ||
| 003315 | FVB/N-Tg(tetORo1-lacZ)3Conk/J | Cryopreserved - Ready for recovery |
| 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 | 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. | ||
| 008607 | STOCK Aspanur7/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this ENU-induced mutation, the neurological 7 (nur7) allele of Aspa (Aspanur7), are viable and fertile, although the donating investigator reports homozygotes are poor breeders. The Aspanur7 mutation encodes a Q193X transition that generates a nonsense codon and results in a predicted 120 amino acid truncation of the protein. While mutant Aspa mRNA expression is reduced by 40% (compared to wildtype), no truncated Aspa protein expression is reported in homozygous oligodendrocytes or brain tissue. Homozygous mice display early-onset spongy degeneration of central nervous system myelin with increased NAA levels similar to that observed in Canavan disease; an Aspa-deficiency-induced fatal childhood autosomal recessive leukodystrophy. Homozygous mice are easily distinguished at 21 days of age by their small body size and a wide-based ataxic gait. Neurological disease progresses with age to tremors and seizures. These Aspa For more information please see the full phenotype on the strain data sheet | ||
| 013073 | STOCK Dnm1tm2.1Pdc/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exons 2-4 of the Dnm1 (dynamin 1) gene. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. A widespread block of expression results in a failure to thrive, defects in neurotransmission and lethality by 2 weeks of age. This strain may be useful in studies of endocytosis. | ||
| 009063 | STOCK Ednrbtm1Nrd/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for this Ednrbflex3 allele are viable and fertile, with a loxP-flanked neo cassette upstream of exon 3, as well as a loxP site downstream of exon 3 of the Ednrb (endothelin receptor type B or ET-B receptor) gene. When bred to mice that express Cre recombinase, the resulting offspring can have one of three resulting genotypes in the cre-expressing tissue(s); only the neo selection cassette deleted, only exon 3 deleted, or both the neo selection cassette and exon 3 deleted. The two latter genotypes are expected to result in a frameshifted transcript that is reported to confer the null phenotype. These mutant mice may be useful in generating conditional mutations for studying the role of Ednrb in development of melanocytes, development of neurons and glia of the enteric nervous system, neural crest-derived cells, mesenchymal-derived smooth muscle cells, vasodilation, mitogen signaling and cancer, and human Hirschsprung's dis ..... For more information please see the full phenotype on the strain data sheet | ||
| 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 | ||
| 007674 | STOCK Esrrbtm1.1Nat/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Nr3b2CKO allele possess loxP sites flanking exon 2 of the targeted gene and are viable and fertile. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have the exon containing the initiator methionine codon and encoding the N-terminal 132 amino acids (including part of the DNA-binding domain) deleted in the cre-expressing tissue(s). Of note, if the conditional Nr3b2CKO is deleted by Cre recombinase in the placenta and embryo, embryonic lethality will result (placental defect). If the conditional Nr3b2CKO is deleted by Cre recombinase only in the embryo, the resulting mice exhibit an inner ear defect (decreased endolymph production) resulting in deafness and defective balance. These Nr3b2CKO mutant mice may be useful in generating conditional mutations to study disorders of hearing and balance, inner ear development (such as endolymph-producing epithelia withi ..... For more information please see the full phenotype on the strain data sheet | ||
| 007749 | STOCK Hap1tm1Xjl/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this Huntingtin Associated Protein (HAP1)-deficient allele have neurodegeneration in areas of the hypothalamus that control feeding behavior, resulting in decreased feeding behavior, dehydration, hypoactivity, and death between two and 15 days after birth. No protein expression from the targeted gene is observed in brain tissue from homozygous mice. Hypothalamus tissue from HAP1-deficient homozygotes exhibit reduced levels of gamma-aminobutyric acid-A (GABAA; a neurotransmitter associated with feeding) and tropomyosin-related kinase A receptor tyrosine kinase (TrkA; a nerve growth factor receptor associated with neurite outgrowth). Heterozygous mice are viable and fertile with no abnormalities in HAP1 expression levels, life span, behavior, and body weight. These huntingtin-associated protein-1 (HAP1) mutant mice may be useful in studying the hypothalamic neurodegeneration and loss of body weight in Huntingon's disease (HD), neurotransmitters, microtubule ..... For more information please see the full phenotype on the strain data sheet | ||
| 004808 | STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted allele and hemizygous for the transgene are viable and fertile. Although no endogenous mouse MAPT is detected, all six isoforms (including both 3R and 4R forms) of human MAPT are expressed. Hyperphosphorylated MAPT is detected in cell bodies and dendrites by three months of age. Paired helical filaments of aggregated insoluble MAPT can be isolated from brain tissue as early as two months of age. These mutant mice may be useful in studies examining the relationship between human MAPT and Alzheimer's disease pathogenesis. | ||
| 010928 | STOCK Mnx1tm1Spf/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites on either side of exon3 of the Mnx1 (motor neuron and pancreas homeobox 1) gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When bred to mice with a cre recombinase gene, exon 3 is deleted in cre-expressing tissues in the offspring. This strain may be useful in studies of neurodevelopment. | ||
| 006702 | STOCK Ntstm1Mom/MomJ | Cryopreserved - Ready for recovery |
| Through bicistronic expression of enhanced green fluorescing protein and neurotensin, this strain permits the visualization of the mitral and tufted cells of the main olfactory bulb thereby permitting developmental analysis in the lateral olfactory tract. | ||
| 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 | ||
| 006570 | STOCK Smn1tm1Msd Tg(Hlxb9-GFP)1Tmj Tg(SMN2)89Ahmb/J | Cryopreserved - Ready for recovery |
Similar to Stock No. 005024, 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). As an addition to Stock No. 005024, this line carries a transgene containing a Green Fluorescent Protein (GFP) under the direction of the mouse Hlxb9 promoter. Transgenic mice display distinct expression of GFP in dendrites, axons and soma of spinal motor neurons, allowing identification, isolation and purification of spinal motor neurons by FACS. GFP expression mimics endogenous HLXB9 expression pattern. Fluorescence is detected in axons, dendrites and processes of spinal motor neurons at embryonic day 9.5 to postnatal day 10 aged mice. This mutant mouse strain represents a model that may be useful for pu ..... | ||
| 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): | ||
| 008779 | STOCK Thtm1Srt/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. A small amount of gene product (protein) is detected by Western blot analysis of heads of homozygotes embryonic day 14.5 in age. Homozygous mice have an embryonic lethal phenotype, begin to die at embryonic day 11.5 and fail to develop past embryonic day 14.5. Homozygous embryos exhibit abnormal heart development with dilated atria, thin atrial walls, ventricular hypoplasia and blood congestion, dying with symptoms of congestive heart failure. Catecholamine containing cells are not detected by glyoxylic acid-induced histofluorescence analysis of embryos. Administration of L-Dopa or +/- isoproterenol to pregnant heterozygous females rescues approximately 90% of the homozygous pups, which then survive up to 3 weeks after birth. Homozygous pups can also be rescued by exposuring the pregnant dam to high oxygen (33-60%). Norepinephrine, ..... For more information please see the full phenotype on the strain data sheet | ||
| 006632 | STOCK Vmn1r49tm2Mom/MomJ | Cryopreserved - Ready for recovery |
| This targeted mutant is valuable in mapping the patterns of axonal projections of vemeronasal sensory neurons. Vomeronasal sensory neurons that express the vomeronasal receptor V1rb2 also co-express the tauGFP fusion protein by virtue of IRES-mediated co-translation. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. The V1rb2 gene is expressed monoallelically, and homozygotes have fluorescence in approximately twice as many vomeronasal sensory neurons as do heterozygotes. | ||
| 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. | ||
| 013754 | STOCK Tg(CAG-KikGR)75Hadj/J | Cryopreserved - Ready for recovery |
| CAG::KikGR75 transgenic mice express a Kikume Green-Red (KikGR) photoconvertible fluorescent protein under the control of a CMV enhancer/chicken beta-actin promoter (CAGGS) promoter. Mice homozygous for the transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. KikGR, engineered from Favia favus coral, changes color from green to red upon activation in embryos, adult mice, and embryonic stem (ES) cells. At basal state, green fluorescence is seen in all cells. A single cell or group of cells, exposed to 405 nm wavelength light, undergo photo conversion and fluoresce red. Since KikGR is developmentally neutral and non-toxic, the movement of these fluorescent cells, and their progeny, can be imaged during embryonic development. Mice from founder line 75 exhibit KikGR expression in a widespread mosaic pattern allowing for analysis of cell morphology and cell behavior dynamics, while mice from founder lin ..... For more information please see the full phenotype on the strain data sheet | ||
| 005105 | STOCK Tg(Chx10-EGFP/cre,-ALPP)2Clc/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The transgene insert contains a fusion product involving Cre recombinase and an Enhanced Green Fluorescent Protein (EGFP) and a fusion product involving an internal ribosome entry site/human placental alkaline phosphatase under the control of the mouse Chx10, C. elegans ceh-10 homeo domain containing homolog promoter. This strain serves as a multifunctional reporter strain. Expression of the Chx10 BAC, as detected by in situ hybridization, mimics the endogenous Chx10 gene expression pattern. Alkaline phosphatase expression is mosaic, but specific to the retina and Muller glial cells. EGFP expression is detected in the outer neuroblastic layer of the retina at embryonic days 14.5, 17.5 and neonates. When crossed to a cre reporter strain, the resulting mice exhibit mosaicism in reporter gene expression. This mutant mouse str ..... For more information please see the full phenotype on the strain data sheet | ||
| 003528 | STOCK Tg(GFAP-TVA)5Hev/J | Cryopreserved - Ready for recovery |
| This strain expresses the avian cell surface receptor(TVA) for subgroup A avian leukosis viruses. The transgene is under the control of an astrocyte-specific promoter derived from the human glial fibrillary acidic protein (GFAP ) gene. The result is to render glial cells specifically susceptible to infection by viral vectors making possible the glia-specific viral transfer of genes. | ||
| 006334 | STOCK Tg(Gad1-EGFP)94Agmo/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse Gad1 (glutamic acid decarboxylase 1 or GAD67) promoter. In the forebrain, EGFP expression is restricted to the somatosensory barrel neocortex, mostly in laminar layers 4 and 5B, to a lesser extent in layers 2/3, 5A and upper 6. EGFP expression is also found in subsets of cerebellar interneurons and in the brainstem. In founder line 94 transgenic mice fluorescence is observed in neocortical neurons with axonal arborizations in layer 4 that have a stuttering firing pattern. Fluorescence levels are low in animals younger than 2 weeks of age. The fluorescently labeled subset of somatostatin-containing (SOM+) interneurons in founder line 94 transgenic mice is distinct from the population of neurons labeled in founder line 98 (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 006340 | STOCK Tg(Gad1-EGFP)98Agmo/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the mouse Gad1 (glutamic acid decarboxylase 1 or GAD67) promoter. In the neocortex, EGFP expression is detected predominantly in layers 5B and 6, and to a lesser extent in layers 2/3. Low levels of fluorescence are detected in small cells with glial morphology. EGFP expression is also observed in area CA1 of the hippocampus, mainly in large interneurons in the oriens-alveus layers. In the neocortex of founder line 98 transgenic mice, fluorescence is observed in infragranular, calbindin immunoreactive interneurons with axonal arborizations in layer 1. In animals younger than two weeks of age, an increased number of EGFP labeled neurons is observed in the supragranular layers, and EGFP expression is also observed in some cells with pyramidal m ..... For more information please see the full phenotype on the strain data sheet | ||
| 007577 | STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J | Cryopreserved - Ready for recovery |
| Transgenic "G117H BChE" mice are viable and fertile. These mice express a mutant form of human butyrylcholinesterase (BCHE or BChE), harboring a single amino acid change at codon 117 (His for Gly), under the control of the ROSA26 promoter. This mutation has the unusual ability to hydrolyze organophosphorus toxicants (OP), as well as acetylcholine and is resistant to inhibition by OP. All tested tissues show G117H BChE enzymatic activity. In the founder mice and immediate offspring, plasma concentrations of the mutant protein are approximately 25% of endogenous wildtype mouse BChe. No reported abnormalities result from BChE overexpression in homozygous mutant mice. Transgenic mice injected with the OP echothiophate are protected from the severe toxicity and lethality observed in wildtype controls. This is the first transgenic mouse strain that expresses human BChE as well as the first mammal with hereditary OP resistance. These G117H BChE transgenic mice may be useful for biodefe ..... For more information please see the full phenotype on the strain data sheet | ||
| 007896 | STOCK Tg(Gt(ROSA)26Sor-EGFP)I1Able/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this ROSA26-EGFP BAC transgene are viable and fertile, with widespread EGFP expression in all organs and tissues analyzed. In addition, stable and uniform EGFP expression is observed in differentiated progeny of transplanted hematopoietic stem cells (HSC) isolated from ROSA26-EGFP mice. These ROSA26-EGFP BAC transgenic mice may be useful for fluorescent labeling of cells and tissues both in vivo and in vitro, are suitable for use in histological preparations, and are appropriate as a source of fluorescently labeled donor cell populations (such as tracking hematopoietic cell fate in transplant recipients). | ||
| 003529 | STOCK Tg(NES-TVA)J12Ech/J | Cryopreserved - Ready for recovery |
| This strain expresses the avian cell surface receptor(TVA) for subgroup A avian leukosis viruses. The transgene is under the control of a glial progenitor-specific promoter derived from the human nestin (NES) gene. The result is to render glial progenitor cells specifically susceptible to infection by viral vectors making possible the glia-specific viral transfer of genes. Please note: Mice recovered from this cryopreserved colony may have retinal degeneration. | ||
| 009102 | STOCK Tg(Nefh-cre)12Kul/J | Cryopreserved - Ready for recovery |
| Mice hemizygous for this mNF-H-cre transgene are viable and fertile, with nuclear localized-Cre recombinase expression directed to neurons, coinciding with late stages of brain development, by the mouse neurofilament-H gene (Nefh) promoter. The cre expression in neurons (but not astrocytes) of the brain and spinal cord is mosaic with highest expression in the cortex and hippocampus. Cre recombinase activity begins around embryonic day (E)16.5-E18.5, with significantly robust activity observed after one week of age. The donating investigator reports that mNFHcre mouse line 12 homozygotes develop a neurological phenotype with seizures and become infertile and moribund. When bred with mice containing a loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the resulting offspring. | ||
| 006207 | STOCK Tg(Pcp2-cre)1Amc/J | Cryopreserved - Ready for recovery |
| Hemizygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Cre activity is observed in parasagittal domains of the cerebellum beginning at embryonic day 17 (E17). At E19, low level expression is observed in the most rostral lobe of cerebellum and expression broadens until all Purkinje cells express the transgene in adult mice. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These transgenic mice may be useful in studies utilizing "Cre-lox" technology, specifically regarding the nervous system, development and patterning of cerebellum, and cerebellar hypotrophy converse of Lhermitte-Duclos. Important Note: These mice also carry a GFP transgene that co-integrated with the Tg(Pcp2-cre)1Amc transgene. As such, GFP expression is reported in the cerebellum. | ||
| 003198 | STOCK Tg(huS100B)5Daoh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this transgene are viable and fertile. They have impaired learning and electrophysiological disturbances in the hippocampus. This strain may serve as a model of the mild learning impairment seen in human beings with Down syndrome (trisomy 21). | ||
| 010815 | STOCK Tg(mI56i-FLPe)39Fsh/J | Cryopreserved - Ready for recovery |
| Hemizygous Dlx5/6-Flpe mice are viable and fertile, with expression of Myc-tagged FLPe recombinase directed to GABAergic neuron populations in the forebrain by the mouse Dlx5/Dlx6 (id6/id5) intergenic enhancer region and β-globin basal promoter. The donating investigator reports that no abnormal phenotype is observed in hemizygous mice. When bred with mice containing an FRT-flanked sequence, FLPe-mediated recombination will result in deletion of the FRT-flanked sequence in forebrain GABAergic populations of the offspring. | ||
| 008790 | STOCK Tg(tetO-DISC1*)1001Plet/J | Cryopreserved - Ready for recovery |
| These transgenic mice express a myc peptide-tagged, mutant (truncated) human DISC1 (disrupted in schizophrenia 1) gene under the control of tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator). The Donating Investigator reports that mice homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. When bred with another transgenic mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) to create a bitransgenic animal, tissue-specific mutant DISC1 transgene expression can be regulated with the tetracycline analog, doxycycline. When bred to a strain expressing rtTA or tTA in brain tissues (see Stock No. 003010, B6;CBA-Tg(Camk2a-tTA)1Mmay/J, for example), this mutant mouse strain may be useful in studies of psychiatric disor ..... For more information please see the full phenotype on the strain data sheet | ||
| 008168 | STOCK Tg(tetO-DTA)1Gfi/J | Cryopreserved - Ready for recovery |
| These tet-DTA transgenic mice express diphtheria toxin A (DTA) under the control of a tetracycline operator (tetO; also called tetracycline-responsive element (TRE) or tet-operator) and a cytomegalovirus minimal promoter. When bred with another mouse expressing reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA), tissue diphtheria toxin A expression can be regulated with the tetracycline analog doxycycline (dox) in the resulting double mutant offspring. These tet-DTA mice may be useful in generating bi-transgenic mutant mice for the reversible, inducible deletion of specific groups of cells. For example, when bred to a strain expressing tTA in cardiac myocytes (see Stock No. 003170 for example), this mutant mouse strain may be useful in studies of human cardiomyopathies. | ||
| 006409 | 129S1.129(Cg)-Tg(APPSw)40Btla/Mmjax | Transferred |
| 006555 | A.129(B6)-Tg(APPSw)40Btla/Mmjax | Transferred |
| 012695 | B6(129S4)-Et(EGFP/cre)16053Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as:
nearly ubiquitous; with fewer cells in granule cell layer, olfactory bulb, striatum, and layer 4 of neocortex.
Cre recombinase activity is also observed in many other tissues (including thigh muscle, pancreas, tail skin, tail muscle, liver, spleen, adrenal gland, kidney, bladder, trachea, thymus, heart, lung, seminal vesicle, prostate, and testis. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-med ..... For more information please see the full phenotype on the strain data sheet | ||
| 012696 | B6(129S4)-Et(EGFP/cre)16055Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Deep neocortical layers, prefrontal cortex, CA2 of dorsal, CA1 of ventral hippocampus; might be specific for some amygdalar nuclei and ventromedial nucleus of hypothalamus. Scattered cells in midbrain, pons, medulla, neocortex. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of th ..... For more information please see the full phenotype on the strain data sheet | ||
| 012697 | B6(129S4)-Et(EGFP/cre)16059Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Scattered cells in most areas: Few purkinje and granule cells, few cells in neocortex, hippocampus, thalamus, midbrain, pons, medulla, hypothalamus. Prefrontal cortex has no staining in some sections. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cr ..... For more information please see the full phenotype on the strain data sheet | ||
| 012698 | B6(129S4)-Et(EGFP/cre)16102Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted. Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: all areas stained; fewer cells in layers 1 and 3 of neocortex, striatum and CA1 region of hippocampus. Cre recombinase activity is also observed in many other tissues (including thigh muscle, pancreas, tail skin, tail muscle, liver, spleen, adrenal gland, kidney, bladder, trachea, thymus, heart, lung, mammary gland, uterus, and ovary. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will ..... For more information please see the full phenotype on the strain data sheet | ||
| 012699 | B6(129S4)-Et(EGFP/cre)16218Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Staining is in layer 4 of neocortex, subiculum and a few cells in the medulla. All other areas are nearly blank. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. | ||
| 012700 | B6(129S4)-Et(EGFP/cre)16250Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Scattered cells in all areas. More cells in thalamus, layer 2 of olfactory cortex, midbrain, and hypothalamus. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. | ||
| 012701 | B6(129S4)-Et(EGFP/cre)16255Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Cells in all areas; more cells in layers 4, 5, and 6 of neocortex, hypothalamus, midbrain, pons, and medulla. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. | ||
| 012702 | B6(129S4)-Et(EGFP/cre)16261Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Nice staining in deep cortical layers (possibly 5&6); scattered cells in all other areas. Many granule cells and some purkinje cells. No Cre recombinase activity is reported in other tested tissues. The donating investigator did not characterize fluorescent expression of the EGFP portion of the fusion protein. When these enhancer trap lentiviral transgenic mice are bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the floxed sequence(s) in cre-expressing tissues in the offspring. For characterizati ..... | ||
| 012703 | B6(129S4)-Et(EGFP/cre)16279Rdav/Mmmh | Transferred |
| Mice hemizygous for this enhancer trap transgene are viable and fertile, with expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFP/Cre) gene under control of the promoter/enhancer regions surrounding the site where the enhancer trap transgene randomly inserted.
Specifically, the donating investigator reports Cre recombinase activity in brain tissues as: Staining in layers 2, 4, and 6 of neocortex, sparse cells in striatum and cerebellum. Very dense staining in amygdala, hippocampus, anterior olfactory nucleus, retrosplenial cortical area, and a few nuclei in the hypothalamus (including the VMH). Low level of staining in most other areas; Fewer cells in CA3 region in dorsal hippocampus and fewer cells in CA2 of ventral hippocampus. Cre recombinase activity is also observed in many other tissues (including thigh muscle, pancreas, tail skin, tail muscle, liver, spleen, adrenal gland, kidney, bladder, trachea, thymus, heart, lung, mammary ..... For more information please see the full phenotype on the strain data sheet | ||
| 005300 | B6.129-Tg(APPSw)40Btla/Mmjax | Transferred |
| 008710 | B6.129P2(129S4)-Hprttm10(Ple162-EGFP/cre)Ems/Mmjax | Transferred |
| These Ple162-EGFPCre;mEMS954 mice have the Ple162-EGFPCre transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human paired-like homeodomain 3 (PITX3) gene directing expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFPCre). These Ple162-EGFPCre;mEMS954 mice may be useful in studying PITX3-expressing cells in the brain and diseases affecting the brain, including mesocorticolimbic dopamine system function in the drug and natural reward circuitry of the brain, cognition, motivation, drug addiction, and psychiatric disorders.
For Ple162-EGFPCre;mEMS954 expression information, see The Pleiades Promoter Project website (Ple162 Promoter (pEMS1148)). The donating ..... | ||
| 008877 | B6.129P2(129S4)-Hprttm12(Ple177-EGFP/cre)Ems/Mmjax | Transferred |
| These Ple177-EGFPCre;mEMS762 mice have the Ple177-EGFPCre transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human regulator of G-protein signaling 16 (RGS16) gene directing expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFPCre) to hippocampus, cortex, and cerebellum. These Ple177-EGFPCre;mEMS762 mice may be useful in studying RGS16-expressing cells in the brain and diseases affecting the brain.
For Ple177-EGFPCre;mEMS762 expression information, see The Pleiades Promoter Project website (Ple177 Promoter (pEMS1089)). The donating investigator reports: | ||
| 009114 | B6.129P2(129S4)-Hprttm14(Ple103-EGFP/cre)Ems/Mmjax | Transferred |
| These Ple103-EGFP/cre;mEMS675 mice have the Ple103-EGFP/cre transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human huntingtin-associated protein 1 (HAP1) gene directing expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFPCre). These Ple103-EGFP/cre;mEMS675 mice may be useful in studying HAP1-expressing cells in the brain and diseases affecting the brain.
For Ple103-EGFP/cre;mEMS675 expression information, see The Pleiades Promoter Project website (Ple103 Promoter (pEMS1083)). The donating investigator reports: | ||
| 009116 | B6.129P2(129S4)-Hprttm16(Ple167-EGFP/cre)Ems/Mmjax | Transferred |
| These Ple167-EGFP/cre;mEMS681 mice have the Ple167-EGFP/cre transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human pogo transposable element with ZNF domain (POGZ) gene directing expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFPCre). These Ple167-EGFP/cre;mEMS681 mice may be useful in studying POGZ-expressing cells in the brain and diseases affecting the brain.
For Ple167-EGFP/cre;mEMS681 expression information, see The Pleiades Promoter Project website (Ple167 Promoter (pEMS1091)). The donating investigator reports: | ||
| 008709 | B6.129P2(129S4)-Hprttm9(Ple178-EGFP/cre)Ems/Mmjax | Transferred |
| These Ple178-EGFPCre;mEMS756 mice have the Ple178-EGFPCre transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human regulator of G-protein signaling 16 (RGS16) gene directing expression of an enhanced green fluorescent protein/Cre recombinase fusion protein (EGFPCre). These Ple178-EGFPCre;mEMS756 mice may be useful in studying RGS16-expressing cells in the brain and diseases affecting the brain.
For Ple178-EGFPCre;mEMS756 expression information, see The Pleiades Promoter Project website (Ple178 Promoter (pEMS1090)). The donating investigator reports: | ||
| 009113 | B6.129P2(Cg)-Hprttm13(Ple54-EGFP)Ems/Mmjax | Transferred |
| These Ple54-EGFP/NLS;mEMS1927 mice have the Ple54-EGFP/NLS transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human doublecortin (DCX) gene directing expression of an enhanced green fluorescent protein (EGFP). These Ple54-EGFP/NLS;mEMS1927 mice may be useful in studying DCX-expressing cells in the brain and diseases affecting the brain. For Ple54-EGFP/NLS;mEMS1927 expression information, see The Pleiades Promoter Project website (Ple54 Promoter (pEMS1200)). The EGFP expression pattern is described by the donating investigator as: | ||
| 009115 | B6.129P2(Cg)-Hprttm15(Ple111-EGFP)Ems/Mmjax | Transferred |
| These Ple111-EGFP;mEMS1774 mice have the Ple111-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human hypocretin (orexin) neuropeptide precursor (HCRT) directing expression of an enhanced green fluorescent protein (EGFP). These Ple111-EGFP;mEMS1774 mice may be useful in studying HCRT -expressing cells in the brain and diseases affecting the brain. For Ple111-EGFP;mEMS1774 expression information, see The Pleiades Promoter Project website (Ple111 Promoter (pEMS1417)). The donating investigator reports: | ||
| 009348 | B6.129P2(Cg)-Hprttm17(Ple48-lacZ)Ems/Mmjax | Transferred |
| These Ple48-lacZ;mEMS3961 mice have the Ple48-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human dopamine beta-hydroxylase (dopamine beta-monooxygenase) [DBH] gene directing expression of β-galactosidase (lacZ). These Ple48-lacZ;mEMS3961 mice may be useful in studying DBH-expressing cells in the brain and diseases affecting the brain. For Ple48-lacZ;mEMS3961 expression information, see The Pleiades Promoter Project website (Ple48 Promoter (pEMS1519)). The donating investigator reports that Ple48 expression is enriched in noradrenergic nuclei but additional expression is observed in exogenous regions including the cortex. Interestingly, lacZ staining overlaps wit ..... | ||
| 009118 | B6.129P2(Cg)-Hprttm18(Ple90-EGFP)Ems/Mmjax | Transferred |
| These Ple90-EGFP;mEMS1899 mice have the Ple90-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human glial fibrillary acidic protein (GFAP) gene directing expression of enhanced green fluorescent protein (EGFP). These Ple90-EGFP;mEMS1899 mice may be useful in studying GFAP-expressing cells in the brain and diseases affecting the brain.
For Ple90-EGFP;mEMS1899 expression information, see The Pleiades Promoter Project website (Ple90 Promoter (pEMS1377)). The donating investigator reports: | ||
| 012572 | B6.129P2(Cg)-Hprttm19(Ple88-lacZ)Ems/Mmjax | Transferred |
| These Ple88-lacZ;mEMS3672 mice have the Ple88-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Glial fibrillary acidic protein (GFAP) gene directing expression of β-galactosidase (lacZ). These Ple88-lacZ;mEMS3672 mice may be useful in studying GFAP-expressing cells in the brain and diseases affecting the brain. For Ple88-lacZ;mEMS3672 expression information, see The Pleiades Promoter Project website (Ple88 Promoter (pEMS1559)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia).
..... | ||
| 009353 | B6.129P2(Cg)-Hprttm20(Ple53-EGFP)Ems/Mmjax | Transferred |
| These Ple53-EGFP;mEMS1892 mice have the Ple53-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human doublecortin (DCX) gene directing expression of enhanced green fluorescent protein (EGFP). These Ple53-EGFP;mEMS1892 mice may be useful in studying DCX-expressing cells in the brain and diseases affecting the brain.
For Ple53-EGFP;mEMS1892 expression information, see The Pleiades Promoter Project website (Ple53 Promoter (pEMS1199)). The donating investigator reports: | ||
| 009596 | B6.129P2(Cg)-Hprttm33(Ple183-EGFP)Ems/Mmjax | Transferred |
| These Ple183-EGFP;mEMS2742 mice have the Ple183-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human S100 calcium binding protein B (S100B) gene directing expression of an enhanced green fluorescent protein (EGFP). These Ple183-EGFP;mEMS2742 mice may be useful in studying S100B-expressing cells in the brain and diseases affecting the brain. For Ple183-EGFP;mEMS2742 expression information, see The Pleiades Promoter Project website (Ple183 Promoter (pEMS1382)). The donating investigator reports: | ||
| 010770 | B6.129P2(Cg)-Hprttm34(Ple186-EGFP)Ems/Mmjax | Transferred |
| These Ple186-EGFP;mEMS2748 mice have the Ple186-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human S100 calcium binding protein B (S100B) gene directing expression of an enhanced green fluorescent protein (EGFP). These Ple186-EGFP;mEMS2748 mice may be useful in studying S100b-expressing cells in the brain and diseases affecting the brain
For Ple186-EGFP;mEMS2748 expression information, see The Pleiades Promoter Project website (Ple186 Promoter (pEMS1385)). The donating investigator reports: | ||
| 012574 | B6.129P2(Cg)-Hprttm38(Ple17-lacZ)Ems/Mmjax | Transferred |
| These Ple17-lacZ;mEMS4619 mice have the Ple17-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the RIKEN cDNA 3110035E14 (C8ORF46) gene
directing expression of β-galactosidase (lacZ). These Ple17-lacZ;mEMS4619 mice may be useful in studying C8ORF46-expressing cells in the brain and diseases affecting the brain. For Ple17-lacZ;mEMS4619 expression information, see The Pleiades Promoter Project website (Ple17 Promoter (pEMS1487)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). | ||
| 008706 | B6.129P2(Cg)-Hprttm4(Ple88-EGFP)Ems/Mmjax | Transferred |
| These Ple88-EGFP;mEMS1671 mice have the Ple88-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human glial fibrillary acidic protein (GFAP) gene directing expression of enhanced green fluorescent protein (EGFP). These Ple88-EGFP;mEMS1671 mice may be useful in studying GFAP-expressing cells in the brain and diseases affecting the brain.
For Ple88-EGFP;mEMS1671 expression information, see The Pleiades Promoter Project website (Ple88 Promoter (pEMS1375)). The donating investigator reports: | ||
| 012576 | B6.129P2(Cg)-Hprttm40(Ple34-lacZ)Ems/Mmjax | Transferred |
| These Ple34-lacZ;mEMS4613 mice have the Ple34-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Claudin 5 (CLDN5) gene directing expression of β-galactosidase (lacZ). These Ple34-lacZ;mEMS4613 mice may be useful in studying CLDN5-expressing cells in the brain and diseases affecting the brain. For Ple34-lacZ;mEMS4613 expression information, see The Pleiades Promoter Project website (Ple34 Promoter (pEMS1505)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). | ||
| 010805 | B6.129P2(Cg)-Hprttm41(Ple160-lacZ)Ems/Mmjax | Transferred |
| These Ple160-lacZ;mEMS4135 mice have the Ple160-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human paired-like homeodomain 3 (PITX3) gene directing expression of β-galactosidase (lacZ). These Ple160-lacZ;mEMS4135 mice may be useful in studying PITX3-expressing cells in the brain and diseases affecting the brain.
For Ple160-lacZ;mEMS4135 expression information, see The Pleiades Promoter Project website (Ple160 Promoter (pEMS1631)). The lacZ expression pattern is described by the donating investigator as: | ||
| 012331 | B6.129P2(Cg)-Hprttm42(Ple131-lacZ)Ems/Mmjax | Transferred |
| These Ple131-lacZ;mEMS4655 mice have the Ple131-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human antigen identified by monoclonal antibody Ki-67 (MKI67) gene directing expression of β-galactosidase (lacZ). These Ple131-lacZ;mEMS4655 mice may be useful in studying MKI67-expressing cells in the brain and diseases affecting the brain. For Ple131-lacZ;mEMS4655 expression information, see The Pleiades Promoter Project website (Ple131 Promoter (pEMS1602)). These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). | ||
| 012577 | B6.129P2(Cg)-Hprttm43(Ple140-lacZ)Ems/Mmjax | Transferred |
| These Ple140-lacZ;mEMS4485 mice have the Ple140-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Orphan nuclear receptor NR2E1 (NR2E1) gene directing expression of β-galactosidase (lacZ). These Ple140-lacZ;mEMS4485 mice may be useful in studying NR2E1-expressing cells in the brain and diseases affecting the brain. For Ple140-lacZ;mEMS4485 expression information, see The Pleiades Promoter Project website (Ple140 Promoter (pEMS1612)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbi ..... | ||
| 010709 | B6.129P2(Cg)-Hprttm44(Ple49-lacZ)Ems/Mmjax | Transferred |
| These Ple49-lacZ;mEMS3682 mice have the Ple49-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human dopamine beta-hydroxylase (dopamine beta-monooxygenase) [DBH] gene directing expression of β-galactosidase (lacZ). These Ple49-lacZ;mEMS3682 mice may be useful in studying DBH-expressing cells in the brain and diseases affecting the brain.
For more information, see The Pleiades Promoter Project website (Ple49 Promoter (pEMS1520)). The donating investigator reports: | ||
| 012333 | B6.129P2(Cg)-Hprttm45(Ple67-lacZ)Ems/Mmjax | Transferred |
| These Ple67-lacZ;mEMS3906 mice have the Ple67-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the FEV (ETS oncogene family) (FEV) gene directing expression of β-galactosidase (lacZ). These Ple67-lacZ;mEMS3906mice may be useful in studying FEV-expressing cells in the brain and diseases affecting the brain. For Ple67-lacZ;mEMS3906expression information, see The Pleiades Promoter Project website (Ple67 Promoter (pEMS1539)). The lacZ expression pattern is described by the donating investigator as: Of note, Ple67-EGFP mice (also see Stock No. 009349 ..... | ||
| 012733 | B6.129P2(Cg)-Hprttm53(CAG-lacZ)Ems/Mmjax | Transferred |
| These CAG-lacZ;mEMS3960 mice have the CAG-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the CAG promoter directing expression of β-galactosidase (lacZ). These CAG-lacZ;mEMS3960 mice have widespread expression of lacZ throughout all tested brain tissue and are a positive control for experiments using lacZ-expressing Pleiades Promoter Project lines. For CAG-lacZ;mEMS3960 expression information, see The Pleiades Promoter Project website (CAG Promoter (pEMS1488)). These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). | ||
| 010789 | B6.129P2(Cg)-Hprttm54(Ple233-EGFP)Ems/Mmjax | Transferred |
| These Ple233-EGFP;mEMS3251 mice have the Ple233-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human troponin T type 1 (skeletal, slow) [TNNT1] gene directing expression of an enhanced green fluorescent protein (EGFP). These Ple233-EGFP;mEMS3251 mice may be useful in studying TNNT1-expressing cells in the brain and diseases affecting the brain.
The donating investigator reports: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). | ||
| 012578 | B6.129P2(Cg)-Hprttm56(Ple25-lacZ)Ems/Mmjax | Transferred |
| These Ple25-lacZ;mEMS4627 mice have the Ple25-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Gastrin/cholecystokinin type B receptor (CCKBR) gene directing expression of β-galactosidase (lacZ). These Ple25-lacZ;mEMS4627 mice may be useful in studying CCKBR-expressing cells in the brain and diseases affecting the brain. For Ple25-lacZ;mEMS4627 expression information, see The Pleiades Promoter Project website (Ple25 Promoter (pEMS1496)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbi ..... | ||
| 012579 | B6.129P2(Cg)-Hprttm58(Ple119-lacZ)Ems/Mmjax | Transferred |
| These Ple119-lacZ;mEMS4054 mice have the Ple119-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the 5-hydroxytryptamine 1A receptor (HTR1A) gene directing expression of β-galactosidase (lacZ). These Ple119-lacZ;mEMS4054 mice may be useful in studying HTR1A-expressing cells in the brain and diseases affecting the brain. For Ple119-lacZ;mEMS4054 expression information, see The Pleiades Promoter Project website (Ple119 Promoter (pEMS1590)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). ..... | ||
| 012580 | B6.129P2(Cg)-Hprttm59(Ple123-lacZ)Ems/Mmjax | Transferred |
| These Ple123-lacZ;mEMS4556 mice have the Ple123-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the isoprenylcysteine carboxyl methyltransferase (ICMT) gene directing expression of β-galactosidase (lacZ). These Ple123-lacZ;mEMS4556 mice may be useful in studying ICMT-expressing cells in the brain and diseases affecting the brain. For Ple123-lacZ;mEMS4556 expression information, see The Pleiades Promoter Project website (Ple123 Promoter (pEMS1594)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of Br ..... | ||
| 012581 | B6.129P2(Cg)-Hprttm62(Ple153-lacZ)Ems/Mmjax | Transferred |
| These Ple153-lacZ;mEMS3735 mice have the Ple153-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Oxytocin-neurophysin 1 precursor (OXT) gene directing expression of β-galactosidase (lacZ). These Ple153-lacZ;mEMS3735 mice may be useful in studying OXT-expressing cells in the brain and diseases affecting the brain.
For Ple153-lacZ;mEMS3735 expression information, see The Pleiades Promoter Project website (Ple153 Promoter (pEMS1624)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia) ..... | ||
| 012342 | B6.129P2(Cg)-Hprttm63(Ple12-lacZ)Ems/Mmjax | Transferred |
| These Ple12-lacZ;mEMS3916 mice have the Ple12-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the arginine vasopressin (AVP) gene directing expression of β-galactosidase (lacZ). These Ple12-lacZ;mEMS3916 mice may be useful in studying AVP-expressing cells in the brain and diseases affecting the brain. For Ple12-lacZ;mEMS3916 expression information, see The Pleiades Promoter Project website (Ple12 Promoter (pEMS1482)). The lacZ expression pattern is described by the donating investigator as: Of note, Ple12-EGFP mice have expression of EGFP directed by the same minipromoter. The Ple12-EGFP mice are de ..... | ||
| 012347 | B6.129P2(Cg)-Hprttm64(Ple170-lacZ)Ems/Mmjax | Transferred |
| These Ple170-lacZ;mEMS4316 mice have the Ple170-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Pogo transposable element with ZNF domain (POGZ) gene directing expression of β-galactosidase (lacZ). These Ple170-lacZ;mEMS4316 mice may be useful in studying POGZ-expressing cells in the brain and diseases affecting the brain. For Ple170-lacZ;mEMS4316 expression information, see The Pleiades Promoter Project website (Ple170 Promoter (pEMS1641)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Col ..... | ||
| 012582 | B6.129P2(Cg)-Hprttm67(Ple238-lacZ)Ems/Mmjax | Transferred |
| These Ple238-lacZ;mEMS4323 mice have the Ple238-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the thyrotropin releasing hormone (TRH) gene directing expression of β-galactosidase (lacZ). These Ple238-lacZ;mEMS4323 mice may be useful in studying TRH-expressing cells in the brain and diseases affecting the brain. For Ple238-lacZ;mEMS4323 expression information, see The Pleiades Promoter Project website (Ple238 Promoter (pEMS1710)). The lacZ expression pattern is described by the donating investigator as: Of note, Ple238-EGFP mice have expression of EGFP directed by the same minipromoter. The Ple2 ..... | ||
| 012583 | B6.129P2(Cg)-Hprttm68(Ple127-lacZ)Ems/Mmjax | Transferred |
| These Ple127-lacZ;mEMS4442 mice have the Ple127-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the Amine oxidase [flavin-containing] A (MAOA) gene directing expression of β-galactosidase (lacZ). These Ple127-lacZ;mEMS4442 mice may be useful in studying MAOA-expressing cells in the brain and diseases affecting the brain. For Ple127-lacZ;mEMS4442 expression information, see The Pleiades Promoter Project website (Ple127 Promoter (bEMS84)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Columbia). ..... | ||
| 008707 | B6.129P2(Cg)-Hprttm7(Ple185-EGFP)Ems/Mmjax | Transferred |
| These Ple185-EGFP;mEMS1627 mice have the Ple185-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human S100 calcium binding protein B (S100B) gene directing expression of enhanced green fluorescent protein (EGFP). These Ple185-EGFP;mEMS1627 mice may be useful in studying S100β-expressing cells in the brain and diseases affecting the brain.
The donating investigator reports: | ||
| 012656 | B6.129P2(Cg)-Hprttm70(Ple240-lacZ)Ems/Mmjax | Transferred |
| These Ple240-lacZ;mEMS4100 mice have the Ple240-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the UDP galactosyltransferase 8 (UGT8) gene directing expression of β-galactosidase (lacZ). These Ple240-lacZ;mEMS4100 mice may be useful in studying UGT8-expressing cells in the brain and diseases affecting the brain. For Ple240-lacZ;mEMS4100 expression information, see The Pleiades Promoter Project website (Ple240 Promoter (pEMS1712)). Of note, Ple240-EGFP;mEMS2810 mice have expression of EGFP directed by the same minipromoter. The Ple240-EGFP;mEMS2810 mice are described by the donating investigator as: | ||
| 012657 | B6.129P2(Cg)-Hprttm71(Ple155-lacZ)Ems/Mmjax | Transferred |
| 012659 | B6.129P2(Cg)-Hprttm73(Ple142-lacZ)Ems/Mmjax | Transferred |
| These Ple142-lacZ;mEMS4751 mice have the Ple142-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the nuclear receptor subfamily 2, group E, member 1 (NR2E1) gene directing expression of β-galactosidase (lacZ). These Ple142-lacZ;mEMS4751 mice may be useful in studying NR2E1-expressing cells in the brain and diseases affecting the brain. For Ple142-lacZ;mEMS4751 expression information, see The Pleiades Promoter Project website (Ple142 Promoter (bEMS86)). The lacZ expression pattern is described by the donating investigator as: These mice were created and deposited by The Pleiades Promoter Project (Centre for Molecular Medicine and Therapeutics, University of British Colum ..... | ||
| 012734 | B6.129P2(Cg)-Hprttm74(Ple232-lacZ)Ems/Mmjax | Transferred |
| These Ple232-lacZ;mEMS3756 mice have the Ple232-lacZ transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human troponin T type 1 (skeletal, slow) [TNNT1] gene directing expression of β-galactosidase (lacZ). These Ple232-lacZ;mEMS3756 mice may be useful in studying TNNT1-expressing cells in the brain and diseases affecting the brain.
For Ple232-lacZ;mEMS3756 expression information, see The Pleiades Promoter Project website (Ple232 Promoter (pEMS1704)). The lacZ expression pattern is not yet described by the donating investigator. Of note, Ple232-EGFP mice have expression of EGFP directed by the same minipromoter. The ..... | ||
| 008708 | B6.129P2(Cg)-Hprttm8(Ple151-EGFP)Ems/Mmjax | Transferred |
| These Ple151-EGFP;mEMS1615 mice have the Ple151-EGFP transgene targeted as a single copy "knockin" into the upstream region of hypoxanthine guanine phosphoribosyl transferase (Hprt) locus on the X chromosome. Heterozygous females and hemizygous males are viable and fertile, with the promoter/regulatory regions of the human oligodendrocyte transcription factor 1 (OLIG1) gene directing expression of enhanced green fluorescent protein (EGFP). These Ple151-EGFP;mEMS1615 mice may be useful in studying OLIG1-expressing cells in the brain and diseases affecting the brain.
The donating investigator reports: | ||
| 006406 | B6.129S4-Tg(APPSwLon)96Btla/Mmjax | Transferred |
| 009126 | B6.Cg-Nos2tm1Lau Tg(Thy1-APPSwDutIowa)BWevn/Mmjax | Transferred |
| 008730 | B6.Cg-Tg(APPSwFlLon,PSEN1*M146L*L286V)6799Vas/Mmjax | Transferred |
| 007051 | B6.Cg-Tg(tetO-APPSwInd)102Dbo/Mmjax | Transferred |
| 007052 | B6.Cg-Tg(tetO-APPSwInd)107Dbo/Mmjax | Transferred |
| 007049 | B6.Cg-Tg(tetO-APPSwInd)885Dbo/Mmjax | Transferred |
| 004807 | B6;129-Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa/Mmjax | Transferred |