Search Criteria: Research Area is "Research Tools: Sensorineural Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 005379 | B6(A)-Rpe65rd12/J | Repository- Live |
| 008087 | B6.129S1-Bchetm1Loc/J | Repository- Live |
| 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
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| 007557 | B6.129S2-Oprd1tm1Kff/J | Repository- Live |
| Mice homozygous for this delta-opioid receptor mutant allele (DOR-) are viable and fertile. DOR-selective ligand binding is absent in vitro on brain membranes from homozygous mice. Unlike mutant mice deficient in kappa- or mu-opioid receptors (Stock No. 007558 or 007559, respectively), homozygous DOR- mutants exhibit increased anxiety and depressive-like behavior but no alteration of spontaneous pain perception. Homozygous DOR- mice also have increased ethanol self-administration and increased inflammatory pain. These DOR mutant mice may be useful in studying the biological activity of opioids andanalgesics, mechanical nociception, inflammatory pain, and emotional disorders.
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 ch
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| 007558 | B6.129S2-Oprk1tm1Kff/J | Repository- Live |
| Mice homozygous for this kappa-opioid receptor mutant allele (KOR-) are viable and fertile. KOR-selective ligand binding is absent on brain membranes from homozygous mice. In contrast to mutant mice deficient of delta- or mu-opioid receptors (Stock No. 007557 or 007559), KOR- homozygotes have normal mechanical pain thresholds, but greatly increased sensitivity to chemical visceral pain. KOR- homozygotes also exhibit normal spontaneous stress responses (unlike delta-opioid receptor null mice). Homozygous KOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. These KOR mutant mice may be useful in studying biological activity of opioids, analgesics, spinally mediated thermal nociception and chemical visceral pain thresholds. 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. These mut
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| 007559 | B6.129S2-Oprm1tm1Kff/J | Repository- Live |
| Mice homozygous for this mu-opioid receptor mutant allele (MOR-) are viable and fertile. MOR-selective ligand binding is absent on brain membranes from homozygous mice. Homozygous MOR- mice exhibit a lack of morphine analgesia, reward, and withdrawal. This is accompanied by decreased mechanical, thermal, and chemical pain thresholds. Homozygous MOR- mice also show decreased ethanol self-administration and decreased THC-conditioned place aversion. In contrast to mutant mice deficient of delta- or kappa-opioid receptors (Stock No. 007557 or 007558, respectively), MOR- homozygotes exhibit hypolocomotive spontaneous stress responses. Indeed, the reduced anxiety and depressive-like behavior observed in MOR- mutants is in stark contrast to kappa-opioid receptor deficient mice. These MOR mutant mice may be useful in studying the biological activity of opioids, analgesics, and responses to mechanical, chemical and thermal nociception at a supraspinal level. In an attempt to offer alleles
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| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 003684 | B6.C3Ga-Mfrprd6/J | Repository- Live |
| Male and female mice homozygous for rd6develop a slowly progressive retinal degeneration affecting both rod and cone cells beginning at 3-4 weeks of age, soon after the retina develops. Ophthalmoscopic examination reveals small, evenly distributed white spots throughout the retina from the time the mice are 8 weeks old. The spots remain clearly visible until about 7 months, when clinical signs of retinal degeneration first become evident, and become less easily distinguishable as degeneration progresses. Retinal blood vessels appear pale and attenuated by 7 months and are undetectable by 15 months, when the fundus appears mottled, lightly pigmented and granular. Aberrations of the photoreceptor layer are histologically evident at 3-4 weeks; by one year, only one to three cell layers (of the normal 10-12) remain. The time and distribution of the ophthalmoscopically detectable retinal spots correlate with histologic observation of putative phagocytic cells in the subretinal space
..... For more information please see the full phenotype on the strain data sheet | ||
| 006576 | B6.FVB-Tg(GNAT2-Dta)98Wwk/J | Repository- Live |
| Mice hemizygous for this "Trc-Tox176" transgene (also called "h-GNAT2pro-DTA") are viable and fertile. Expression of diphtheria toxin (DTA) from the transgene is similar to that of endogenous GNAT2, leading to ablation of both rod and cone photoreceptor development in the ventral retina (the abnormality is a result of abnormal cellular development rather than a consequence of retinal degeneration). The dorsal retina has nearly normal development of rods, but the development of cones is limited to about 10%. These transgenic mice exhibit an absence of cone photoreceptors in the retina, as well as the concomitant absence of rod photoreceptors in the ventral retina. The mice may be useful in studies of photoreceptor development, photoreceptor-related retinal diseases, and to profile photoreceptor genes in adult and in developmental stages. | ||
| 006401 | B6;129P-Trpa1tm1Kykw/J | Repository- Live |
| Homozygous mice are viable and fertile. The donating investigator reports a dramatic loss of fecundity after 5-6 months of age. The targeting vector contains an endoplasmic reticulum (ER) retention signal (KDEL), which is reported to sequester the potential truncated mRNA product in the ER. The vector also contains an IRES-PLAP reporter gene, allowing extracellular antibody staining/chromogenic development tracking of cells normally expressing the endogenous gene. Homozygous mice display behavioral deficits in response to mustard oil, cold, and punctate mechanical stimuli. These mice have a normal startle reflex to loud noise, a normal sense of balance, a normal auditory brainstem response, and normal transduction currents in vestibular hair cells. These mutants may be useful in neurobiological studies involving dorsal root ganglion neurons and cells of the inner ear, as well as for auditory, temperature, or chemical irritant trials. | ||
| 006675 | B6;129P2-Olfr151tm25Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 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. | ||
| 006676 | B6;129P2-Olfr151tm26Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 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. | ||
| 006596 | B6;129P2-Olfr160tm4Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 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. | ||
| 006595 | B6;129P2-Olfr17tm1Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 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. | ||
| 006667 | B6;129P2-Omptm3Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by GFP. The targeted mutation results in a knockout. Mature olfactory sensory neurons express GFP at high levels. These neurons can be revealed by the intrinsic fluorescence of GFP, or by immunofluorescence with anti-GFP antibodies. Homozygous mice are subfertile. | ||
| 006668 | B6;129P2-Omptm4(cre)Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by Cre. The targeted mutation results in a knockout. Mature olfactory sensory neurons express the Cre recombinase at high levels. Homozygous mice are subfertile. As an example, when crossed to a strain with widespread expression of GFP and a loxP-flanked Bgeo reporter (see Stock No. 004178), this mutant mouse strain may be useful in lineage tracing. | ||
| 006594 | B6;129S2-Omptm1Mom/MomJ | Repository- Live |
| The coding region and part of the 3' non-translated region of the Omp gene was replaced by taulacZ, a fusion protein of the microtubule-binding protein tau (from bovine origin) and beta-galactosidase. The targeted mutation results in a knockout. Mature olfactory sensory neurons express beta-galactosidase at high levels. These neurons can be revealed by histochemistry of beta-galactosidase enzymatic activity, or by immunofluorescence with anti-beta-galactosidase antibodies. Homozygous mice are subfertile. | ||
| 001979 | C3A.BLiA-Pde6b+.O20-Prph2Rd2/J | Repository- Live |
| 006579 | C57BL/6-Tg(Camk2a-Bdnf)A9Stl/J | Repository- Live |
| 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. | ||
| 006912 | C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J | Repository- Live |
| Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4+ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco
..... For more information please see the full phenotype on the strain data sheet | ||
| 007674 | STOCK Esrrbtm1.1Nat/J | Repository- Live |
| 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 | ||
| 006677 | STOCK Olfr151tm28Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr151 also co-express the Cre recombinase by virtue of IRES-mediated co-translation. | ||
| 006678 | STOCK Olfr160tm6Mom/MomJ | Repository- Live |
| Olfactory sensory neurons that express the olfactory receptor Olfr160 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. | ||
| 004510 | STOCK Rom1tm1Mci/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and normal in size. When heterozygous mice are bred together, homozygous animals occur at a greatly reduced frequency (~6%). No gene product (protein) is detected in retinal tissue from homozygotes by Western blot analysis. Onset of progressive retinal degeneration occurs at 2 months of age beginning with a thinning of the outer nuclear layer of retinal cells. Rod outer segments in 2 month old mice display disorganized arrangement, irregular gaps and amorphous aggregates. At 4 months of age organization of rod outer segments improves. TUNEL assay of mutant retinal tissue show photoreceptor degeneration is due to apoptotic cell death. Ultra structural organization of rod outer segment disks is disorganized, often with patches of enlarged disks. Electroretinogram a-wave analysis of photoreceptor function reveals a diminished maximal photoreceptor response (50% lower than wildtype). This mutant mouse strain may be useful in stu
..... For more information please see the full phenotype on the strain data sheet | ||
| 007577 | STOCK Tg(Gt(ROSA)26Sor-BCHE*G117H)837Loc/J | Repository- Live |
| 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 | ||
| 005987 | 129-Achetm1Loc/J | Repository-Cryopreserved |
| Homozygous mice have 25% fetal mortality. Those born have retarded growth, fine motor tremors, unusual posture and gait, no righting reflex, malformed pinna, and sealed eyelids. These mice die emaciated and dehydrated by 3 weeks of age. Enriched diets for the nursing female and pups allow homozygous mice to survive to adulthood. Males exhibit no breeding behavior. Homozygous females can become pregnant when bred to heterozygous or wildtype males, but both female and pups do not survive. Acetylcholinesterase (AChE) activity is completely abrogated in serum and tissue from homozygous mice, and approximately half in heterozygotes. Many symptoms of organophosphate poisoning are observed in homozygous mice, including pulsating paws, body tremor, abnormal gait, pinpoint pupils, muscle weakness, and early death following seizure. When restrained, a white mucus forms on the eyes and seizures may occur. Mice also have several developmental delays, low body mass, decreased pain response, sexual
..... For more information please see the full phenotype on the strain data sheet | ||
| 007766 | B6.129P2(Cg)-Olfr160tm6Mom/MomJ | Repository-Cryopreserved |
| 007767 | B6.129P2-Olfr17tm1Mom/MomJ | Repository-Cryopreserved |
| 003462 | B6.129S1-Thrbtm1Df/J | Repository-Cryopreserved |
| Mice homozygous for the Thrbtm1Df targeted mutation are viable and fertile displaying normal growth rates. Homozygous mutant mice exhibit goiter and elevated levels of both thyroid hormone and thyroid stimulating hormone. Defects in liver responses to thyroid hormone and subtle behavioral abnormalities are observed. The mice fail to develop normal hearing, as assessed by impaired auditory-evoked brainstem responses, and are susceptible to audiogenic seizures. This strain provides a recessive model for the human syndrome of generalized thyroid hormone resistance (GTHR). | ||
| 007768 | B6.129S2-Omptm1Mom/MomJ | Repository-Cryopreserved |
| 003823 | B6.129S4-Ttpatm1Far/J | Repository-Cryopreserved |
| 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. | ||
| 005970 | B6.129S7-Atoh1tm2Hzo/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mutant mice have a perinatal lethal phenotype and die shortly after birth. No gene product (protein) is detected in resting chondrocytes by immunohistochemical analysis of embryonic age 18.5 homozygotes. Beta-galactosidase X-gal staining of neural tissue from embryonic day 14.5 and newborn (postnatal day 0) aged homozygous and heterozygous mice mimicks the endogenous expression pattern. Mice homozygous for this mutation exhibit a phenotype similar to the phenotype observed in mice homozygous for the null (loss of function) targeted mutation. Homozygotes lack cerebellar granule neurons, cochlear and ventricular hair cells, and the pontine nuclei in the brain stem. This mutant mouse strain may be useful in studies of brain and inner ear development. | ||
| 004160 | B6.129X1-Pon1tm1Lus/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No paraoxonase activity is detected in blood plasma. Homozygous animals are extremely sensitive to the toxic effects of the chlorpyrifos and its active form, chlorpyrifos oxon, a potent cholinesterase inhibitor. When fed a high-fat, high-cholesterol diet, homozygous mice are more susceptible to atherosclerosis when compared to wildtype littermates. In vitro studies indicate that high-density lipoproteins derived from homozygous animals are unable to prevent low-density lipoprotein oxidation. This mutant mouse strain represents a model that may be useful in studies related to toxicology (particularly insecticide poisoning) and factors regulating susceptibility to atherosclerosis. | ||
| 006689 | B6;129P2-Olfr151tm19Mom/MomJ | Repository-Cryopreserved |
| 004946 | B6;129P2-Omptm2(spH)Mom/J | Repository-Cryopreserved |
| 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 | ||
| 004953 | B6;129S6-Gucy2etm1Gar/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of eye tissue. Progressive loss of electroretinograms (ERGs) of cone cells from homozygotes begins at age 3 to 5 weeks. ERGs are completely lost in mice older than 8 weeks of age. Histological analysis of mutants between 4 and 5 weeks of age reveals retinal cone cell atrophy and a reduction in the number of cone cells. Isolated retinal rod cells exhibit reduced a-wave and b-wave ERGs, and impaired photoresponse. This mutant mouse strain may be useful in studies of incomplete achromatopsia, progressive cone-rod dystrophy, retinitis pigmentosa and Leber congenital amaurosis. | ||
| 006160 | B6;129X1-Avpr1btm1Wsy/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable, fertile, normal in size, exhibit apparently normal sexual behavior, and do not display any gross physical abnormalities. Homozygous mice exhibit less social agression, altered chemoinvestigatory behavior, and impaired social recognition. These mice may be useful in studies of agressive behavior, social motivation, and appropriate behavioral responses, and may be potential models of autism and agression accompanying dementia and traumatic brain injury. | ||
| 001957 | C3A Pde6brd1.O20/A-Prph2Rd2/J | Repository-Cryopreserved |
| 005095 | C57BL/6J-nmf240/J | Repository-Cryopreserved |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf240 entry. | ||
| 001981 | O20/A-Prph2Rd2/J | Repository-Cryopreserved |
| 006702 | STOCK Ntstm1Mom/MomJ | Repository-Cryopreserved |
| 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. | ||
| 006645 | STOCK Olfr151tm12(Olfr16)Mom/MomJ | Repository-Cryopreserved |
| The coding region of the olfactory receptor Olf151 was replaced by that of the mouse olfactory receptor Olfr16. Olfactory sensory neurons that express the mutated locus co-express taulacZ 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. | ||
| 006691 | STOCK Olfr151tm14(Adrb2)Mom/MomJ | Repository-Cryopreserved |
| 006635 | STOCK Olfr151tm15(V1rb2)Mom/MomJ | Repository-Cryopreserved |
| The coding region of the olfactory receptor Olfr151 (formerly M71) was replaced by that of the V1rb2 vomeronasal receptor (termed VRi2 in Rodriguez et al.,1999, Cell 97, 199-208). Olfactory sensory neurons that express the mutated locus co-express taulacZ by virtue of IRES-mediated co-translation. These neurons can be revealed by histochemistry of b-galactosidase enzymatic activity, or by immunofluorescence with anti-b-galactosidase antibodies. | ||
| 006692 | STOCK Olfr151tm16(Olfr160/161)Mom/MomJ | Repository-Cryopreserved |
| 006693 | STOCK Olfr151tm17Mom/MomJ | Repository-Cryopreserved |
| 006688 | STOCK Olfr151tm18(GFP)Mom/MomJ | Repository-Cryopreserved |
| 006694 | STOCK Olfr151tm20Mom/MomJ | Repository-Cryopreserved |
| 006695 | STOCK Olfr151tm21Mom/MomJ | Repository-Cryopreserved |
| 006690 | STOCK Olfr151tm23Mom/MomJ | Repository-Cryopreserved |
| 006652 | STOCK Olfr160tm2(GFP)Mom/MomJ | Repository-Cryopreserved |
| 006696 | STOCK Olfr160tm3Mom/MomJ | Repository-Cryopreserved |
| 006669 | STOCK Olfr17tm7Mom/MomJ | Repository-Cryopreserved |
| Olfactory sensory neurons that express the olfactory receptor Olfr17 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. | ||
| 006631 | STOCK V1rb2tm1Mom/MomJ | Repository-Cryopreserved |
| Vomeronasal sensory neurons that express the vomeronasal receptor V1rb2 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. | ||
| 006632 | STOCK V1rb2tm2Mom/MomJ | Repository-Cryopreserved |
| 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. | ||
| 006633 | STOCK V1rb2tm3Mom/MomJ | Repository-Cryopreserved |
| 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. | ||
| 006657 | STOCK Vmn2r26tm1Mom/MomJ | Repository-Cryopreserved |
| 005105 | STOCK Tg(Chx10-EGFP/cre-ALPP)2Clc/J | Repository-Cryopreserved |
| 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 | ||
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IMPORTANT NOTE: Price information is on the strain data sheet which can be viewed by clicking on the strain name.
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 005296 | C57BL/6J-nmf246/J | Research Strain |
| View strain phenotype and additional information on the Neuroscience Mutagenesis Facility web page for nmf246 entry. | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
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New Strains Under DevelopmentThe Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion. Strains "Under Development" fall into two categories depending on the anticipated demand from the scientific community.
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- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
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