Search Criteria: "Facebase: models"
New Strains Awaiting Transfer from the Donor
Additional Register Interest Strains/a>
JAX® Mice Strains
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000646 | A/J | Level 2 |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A/J inbred strain is widely used in cancer and immunology research. It is highly susceptible to cortisone-induced congenital cleft palate. It has a high incidence of spontaneous lung adenomas, and lung tumors readily develop in response to carcinogens. A high percentage of mammary adenocarcinomas (a large proportion of acinar-type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. A/J mice fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid, and 15% fat) fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, ..... | ||
| 000647 | A/WySnJ | Repository- Live |
| Developed by LC Strong in 1921 from a cross between a Cold Spring Harbor albino and a Bagg albino, the A inbred strain is used widely used in cancer and immunology research. It is highly susceptible to induction of congenital cleft palate by cortisone. It has a high incidence of spontaneous lung adenomas and lung tumors readily develop in response to carcinogens. High percentage of mammary adenocarcinomas (a large proportion acinar type) develop in multiparous females. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in The Jackson Laboratory substrains. Unlike A/J mice, A/WySnJ mice carry a spontaneous mutation in Tnfrsf13c and exhibit a significant loss of mature B cells (Miller, et al., 1991, Lentz et al., 1996, Shulga-Morskaya et al., 2004). | ||
| 010525 | B6.129S-Notch2tm3Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exon 3 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 exon 3 deleted in the cre-expressing tissue(s).
When bred to a strain with early embryonic Cre recombinase expression (see Stock No. 003755 for example), this mutant mouse strain may be useful in studies of the Notch pathway during development. When bred to a strain expressing Cre recombinase in embryos, in particular, cardiac neural crest cells (see Stock No. 005549 for example), this mutant mouse strain may be useful in studies of vascular smooth muscle development and the cardiovascular defects associated with Alagille syndrome ..... | ||
| 010616 | B6.129S1-Jag1tm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA or protein) is detected by RT-PCR or Western blot analysis of homozygous embryos, aged embryonic day 10. Homozygotes have an embryonic lethal phenotype, with defective vasculature formation in the embryo and yolk sac and widespread hemorrhaging at embryonic day 10.5. Heterozygotes exhibit iris coloboma, irregular/off center pupils and corneal opacity. | ||
| 010546 | B6.129S1-Jag2tm1Grid/J | Repository- Live |
| Mice that are homozygous for this targeted mutation have a perinatal lethal phenotype, dying shortly after birth due to craniofacial defects (cleft palate, due to fusion of unelevated palatal shelves with the tongue). Embryos homozygous for the mutation and aged embryonic day 10.5-11.5, display a hyperplastic thick apical ectodermal ridge of the limb buds. Homozygous neonates have bilateral cleft of the secondary palate and syndactyly (fused digits) of both forelimbs and hindlimbs, although the hindlimbs are more affected. The number of inner ear hair cells is increased in mutants. Histological analysis reveals an increased number of inner ear hair cells and disorganized stereocilia bundles in mutants. Homozygotes exhibit abnormal thymic morphology and decreased gamma-delta T cell number. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Heterozygotes have abnormal inner ear morphology (increased number of hair c ..... For more information please see the full phenotype on the strain data sheet | ||
| 010620 | B6.129S1-Notch2tm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Due to alternative splicing, 2 in-frame gene products (mRNA) are detected by RT-PCR analysis of homozygous embryos. The mutant transcripts would produce proteins with one or two EGF repeats deleted. Levels of the mutant transcripts are similar to the wildtype transcript level. This targeted allele is a hypomorph. Homozygotes are neonatal lethal due to developmental defects in the kidney, heart and eye vasculature. Homozygous neonates exhibit hypoplastic kidneys, with vasculature lesions at the cortical surface, and lack mature glomeruli. Bilateral microphthalmia, with retrolenticular hyperplasia, is observed in homozygotes. At age embryonic day 11.5, some homozygous embryos exhibit delayed growth, pericardial effusion and widespread hemorrhaging. Homozygous embryos that survive past embryonic day 11.5 display myocardial hy ..... For more information please see the full phenotype on the strain data sheet | ||
| 009386 | B6.129S1-Osr2tm1Jian/J | Repository- Live |
| The Osr2-lacZ mutation abolishes endogenous gene function and expresses a β-galactosidase fusion protein (fused in-frame with the N-terminal 15 amino acid residues of the endogenous protein). Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wild-type gene (for example, β-galactosidase expression during embryogenesis is detected by E9.5 in the mesonephric vesicles). Homozygous mice die shortly after birth with open eyelids, bilateral cleft of the secondary palate, and thickened tympanic rings. Heterozygotes are viable and fertile. These Osr2-lacZ mice may be useful as a lacZ reporter for Osr2 expression or as a knockout model for studying developmental biology (craniofacial, limb, and kidney). | ||
| 010621 | B6.129S1-Snai1tm2.1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice have an embryonic lethal phenotype, failing to develop past gastrulation. Homozygotes exhibit a phenotype similar to mice homozygous for the Snai1del1 allele, with abnormal mesoderm with cavities or lacunae, and lined with cells exhibiting a polarized, columnar epithelium morphology. | ||
| 010617 | B6.129S1-Snai2tm1Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, subfertile, and smaller in size compared to wildtype controls. These mice express a beta galactosidase fusion protein with 120 amino acids from the first half of the endogenous protein. The beta galactosidase staining pattern mimics the endogenous gene expression pattern in the embryonic limb buds and extraembryonic tissue. Homozygous adults develop eye infections (suppurative conjunctivitis) due to swollen eyelids. When challenged with UV radiation exposure, homozygotes exhibit decreased inflammation, lower skin tumor burden and fewer spindle cell tumors compared to wildtype. | ||
| 003755 | B6.129S4-Meox2tm1(cre)Sor/J | Repository- Live |
| This strain expresses Cre recombinase under the control of the endogenous Meox2 promoter. Expression of Cre recombinase is observed in epiblast-derived tissues as early as embryonic day 5. The insertion creates a null allele for the Meox2 gene. Homozygous mice are viable on this background but exhibit an overall reduction in muscle mass and the absence of specific muscles resulting in abnormal limb posture and reduced motility. This phenotype is variable. As many as 80% of homozygotes are severely affected, fail to thrive and die before weaning. Some homozygotes (10%) exhibit clefting of the secondary palate. These mice can be utilized as a deleter strain for loxP flanked DNA and provide an alternative to tetraploid embryo analysis. | ||
| 016902 | B6.129S5-Irf6Gt(OST398253)Lex/J | Repository- Live |
| In this strain a gene construct (VICTR48), containing a neomycin resistance (neo), integrated downstream of the splice donor site of the interferon regulatory factor 6 (Irf6) gene. Mice that are heterozygous for the gene trap mutation are viable and fertile. Homozygotes have a perinatal lethal phenotype. IRF6 is a transcription factor involved in keratinocyte, epidermal, and epithelial cell proliferation as well as craniofacial development. IRF6 is expressed in the skin and oral epithelium from E17.5. Heterozygotes have mild oral adhesions between epithelial layers of the maxilla and mandible. Homozygous embryos have taut, shiny skin, lack external ears and have snouts and jaws shorter and more rounded than their wild-type littermates. They also have short forelimbs that lacked visible digits, a single caudal projection that lacked visible hindlimbs and tail, and a cleft secondary palate. Their skeleton also exhibits a split xiphoid process, shortened sternum, delayed oss ..... For more information please see the full phenotype on the strain data sheet | ||
| 012843 | B6.129X1(Cg)-Slc32a1tm1.1Bgc/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have perinatal lethal phenotype due to respiratory failure. No gene product (mRNA) is detected by RT-PCR analysis of brain tissue from homozygous embryos aged E16.5. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern. Neonate homozygotes exhibit lack of movement, hunched posture, cleft secondary palate, umbilical hernia, and bumps of displaced brown fat deposits in the dorsal cervical area. The Donating Investigator reports that adult heterozygous males on the C57BL/6J background have seizures starting approximately at age 6 months. | ||
| 012844 | B6.Cg-Gad1tm1.1Bgc/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have a lethal phenotype. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern. All newborn homozygotes have cleft palate, and 85% of neonate homozygotes exhibit umbilical hernia. | ||
| 004293 | B6;129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet ..... | ||
| 012603 | B6;129-Tgfbr2tm1Karl/J | Repository- Live |
| These TβRII floxed mutant mice possess loxP sites flanking exon 4 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 exon 4 deleted in cre-expressing tissues. This strain may be useful for studying the cellular and mechanical role of TGF-β in regulating development, hematopoiesis, wound healing, and immune function.
For example, when crossed to a strain expressing Cre recombinase in the neural tube, midbrain and dorsal spinal cord (see Stock No. 007807), this mutant mouse strain may be useful in studies of DiGeorge syndrome. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. > ..... | ||
| 010618 | B6;129S-Jag1tm2Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exon 4, which encodes the DSL (Delta-Serrate-Lag2) domain, 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 exon 4 deleted in the cre-expressing tissue(s). The exon 4-deleted allele produces a nonfunctional JAG1 protein.
When bred to a strain with Cre recombinase expression during development in the telencephalon and discrete head structures, such as the otocyst (see Stock No. 006084 for example), this mutant mouse strain may be useful in studies of developmental inner ear defects. When bred to a strain with Cre recombinase expression in endothelial cells during embryogenesis and adulthood (see Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 010686 | B6;129S-Snai1tm2Grid/J | Repository- Live |
| These mice possess loxP sites on either side of exons 2 and 3 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 exon 2 and 3 deleted in the cre-expressing tissue(s). | ||
| 009389 | B6;129S1-Bambitm1Jian/J | Repository- Live |
| Mice homozygous for this Bambiflox allele are viable and fertile, with loxP sites flanking exon 1 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous signal peptide deleted in the cre-expressing tissue(s); this is expected to produce a null allele. These mutant mice may be useful in generating conditional mutations for studying the role of Bambi in developmental biology and the TGF-beta pathway. | ||
| 010619 | B6;129S1-Lfngtm1Grid/J | Repository- Live |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. At birth, homozygotes exhibit shortened trunk and tails. Severely affected homozygotes soon die due to respiratory difficulties related to malformed rib cages. Less severely affected homozygotes survive into adulthood. By age embryonic day 8.5, homozygotes exhibit defective somite formation, with indistinct boundaries and irregular shape and size. Vertebral column formation is disrupted, and ribs are bifurcated and fused. Although sclerotome cells condense, the metameric pattern is not maintained. Fusions in the dorsal root ganglia and axonal patterning defects are revealed by histological analysis. | ||
| 010547 | B6;129S1-Notch3tm1Grid/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 blot analysis of brain, lung and heart tissue or Western blot analysis of lung and brain tissue from homozygotes. Homozygotes exhibit disorganized artery wall morphology, and thin vascular smooth muscle cell coat and processes. | ||
| 010544 | B6;129S1-Notch4tm1Grid/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) is detected by RT-PCR analysis of lung and kidney tissue from homozygous adult animals, and in situ hybridization of homozygous embryos. Homozygotes exhibit a slightly elevated systolic blood pressure. | ||
| 010722 | B6;129S1-Snai2tm2Grid/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, subfertile, and are smaller in size than wildtype controls. Homozygotes have diluted coat color and areas of depigmentation, sometimes exhibiting white forehead blaze and spots on tails and feet. From birth to weaning age (approximately 3 weeks), homozygotes exhibit slowed growth rate and by 3 weeks of age weigh approximately 70% of wildtype control. After weaning, mutant growth rates are similar to wildtype, but mutants remain small in size. Homozygous adults develop eye infections (suppurative conjunctivitis and blepharitis). Homozygous males have reduced testes size due to reduced seminiferous tubules and are slightly subfertile, producing smaller litters sizes. Approximately 15% of homozygous males are infertile. Spermatogenesis is normal, however, in fertile homozygotes. Homozygotes exhibit macrocytic anemia, decreased hematocrit and leukocyte numbers. T cell differentiation is impaired and thymus size is dimi ..... For more information please see the full phenotype on the strain data sheet | ||
| 012463 | B6;129S4-Foxd1tm1(GFP/cre)Amc/J | Repository- Live |
| Heterozygous mice are viable and fertile, normal in size and do not display any gross physical or behavioral abnormalities. The DI states that the strain is homozygous lethal. The FoxD1GC allele expresses an eGFPCre fusion protein (EGFP and cre fusion protein) from the Foxd1 promoter/enhancer elements. When Foxd1 is induced, EGFP immunofluorescence is observed during kidney development in metanephric mesenchyme in cells fated to become stromal cells of the kidney. When FoxD1GC mice are bred with mice containing loxP-flanked sequence, Cre-mediated recombination will result in deletion of the floxed sequences in the Foxd1-expressing cells of the offspring. These mice may be useful for studying therapeutic strategies directly targeting pericyte differentiation in vivo and may productively impact fibrotic kidney disease. | ||
| 012655 | FVB.A-Irf6clft1/BeiJ | Repository- Live |
| Mice that are homozygous for this hypomorphic allele are characterized by an abnormal adhesion between the tongue and palate. Approximately 63% of E18.5 mutants exhibit a partial fusion of the anterior palate, the remaining mutants exhibit a complete cleft of the secondary palate. Oral adhesions between the palate and tongue are first observed by E12.5. In addition, a small number of mutants exhibit syndactyly, short forelimbs, curly tail, and hind limbs that appear fused to the body.
This mutant mouse strain may be useful in studies of cleft palate and Van der Woude Syndrome.
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. | ||
| 017437 | FVB/N-Ckap5TgTn(sb-cHS4,Tyr)2320F-1Ove/J | Repository- Live |
| These OVE2320F-1 (OVE#2320F-1) mice harbor a mutation created by random insertion of the SB-cHS4core-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2229). Using inverse PCR analysis, the lentiviral integration site was identified in intron 26 of the cytoskeleton associated protein 5 gene (Ckap5) on chromosome 2. The 5'-LTR is linked to the (-) strand of DNA at position 91,408,998 bp [NCB137/mm9; 5'-91,408,998(-)]. The lentivirus is inserted in the sense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: small with cleft palate. | ||
| 017438 | FVB/N-MidnTg(Tyr)2261EOve/J | Repository- Live |
| These OVE2261E (OVE#2261E) mice harbor a mutation created by random insertion of the Tyro-WPRE-FUGW lentiviral transgene (LV2177). Using inverse PCR analysis, the lentiviral integration site was identified in intron 4 of the midnolin gene (Midn) on chromosome 10. The 3'-LTR is linked to the (-) strand of DNA at position 79,614,557 bp [NCB137/mm9; 3'-79,614,557(-)]. The lentivirus is inserted in the antisense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: cleft palate, and females have small ovaries. | ||
| 017436 | FVB/N-Tapt1TgTn(sb-cHS4,Tyr)2508GOve/J | Repository- Live |
| These OVE2508G (OVE#2508G) mice harbor a mutation created by random insertion of the SB-cHS4core-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2229). Using inverse PCR analysis, the lentiviral integration site was identified in intron 11 of the transmembrane anterior posterior transformation 1 gene (Tapt1) on chromosome 5. The 3'-LTR is linked to the (+) strand of DNA at position 44,574,289 bp [NCB137/mm9; 3'-44,574,289(+)]. The lentivirus is inserted in the antisense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: cleft palate, possible anemia. | ||
| 017434 | FVB;B6-Cramp1lTgTn(sb-rtTA,Tyr)2447AOve/J | Repository- Live |
| These OVE2447A (OVE#2447A) mice harbor a mutation created by random insertion of the SB-sa-IRES-rtTA-pA-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2223). Using inverse PCR analysis, the lentiviral integration site was identified in intron 3 of the cramped-like [Drosophila] gene (Cramp1l) on chromosome 17. The 5'-LTR is linked to the (-) strand of DNA at position 25,135,745 bp [NCB137/mm9; 5'-25,135,745(-)]. The rtTA is inserted in the sense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: cleft palate. | ||
| 017609 | FVB/N-Rr16Tn(sb-Tyr)1HCebOve/J | Under Development - Now Accepting Orders |
| These BART6-TP1H mice harbor a transposition-induced mutation near the bone morphogenetic protein 4 locus (Bmp4) on mouse chromosome 14.
The transposed integration site is reported to be at 46,829,514 [NCB137/mm9] on chromosome 14: this is ~150 kb away from Bmp4. The transposed integration site is tightly linked with the original integration site.
The donating investigator reports they have been unable to identify a transposon-induced deletion near Bmp4 and the mutation is not found within the BMP4 coding sequences. The mutation results in altered BMP4 expression (presumably via a transposition-induced inversion that leads to loss-of-function of an enhancer that is required for expression of BMP4 in the optic vesicle).
Heterozygous and homozygous mice from this line exhibit light grey/medium grey coat color. All homozygous mice exhibit congenital absence of both eyes (anophthalmia) due to defects in lens induction. Homozygous mice are fertile, although ~ ..... For more information please see the full phenotype on the strain data sheet | ||
| 017598 | FVB/N-Sdccag8Tn(sb-Tyr)2161B.CA1C2Ove/J | Under Development - Now Accepting Orders |
| These OVE2161B-CA1C-2 mice harbor a mutation created by random insertion of the pT2-BART3 transposon transgene. Using inverse PCR analysis, the integration site was identified between exons 12-13 of the serologically defined colon cancer antigen 8 gene (Sdccag8) on chromosome 1. The transgene is linked to the (+) strand of DNA at position 178,833,225 bp [NCB137/mm9; L:SV40:178,833,225(+)]. The donating investigator reports that homozygous mice have complete absence of Sdccag8 transcript. All homozygous mice exhibit cleft palate, with open palate observed by embryonic day (E)15. Homozygous mice die shortly after birth with complications from cleft palate (cannot suckle). In addition, the donating investigator reports that homozygous mice exhibit preaxial polydactyly and polycystic kidney disease. Hemizygous and homozygous mice of line OVE2161B-CA1C-2 exhibit very light tan coat color and red eyes. | ||
| 016870 | FVB/NJ-Ap2b1Tg(Tyr)427Ove/EtevJ | Under Development - Now Accepting Orders |
| These OVE427 mice harbor a mutation created by random insertion of two head-to-tail copies of the tyrosinase minigene (TYBS) transgene into the Ap2b1 (adaptor protein complex 2 β1 subunit) gene on chromosome 11. This results in a knockout allele; no β2-adaptin mRNA or protein is expressed from the mutant allele. Homozygous OVE427 mice exhibit complete clefting of the secondary palate (autosomal recessive nonsyndromic cleft palate) and die shortly after birth. Coronal cross-sections of the secondary palate of embryonic day (E)17 and E18 homozygous embryos display evidence of palatal shelf elevation and the apparent failure of the shelves to fuse. Ap2β1-deficiency also leads to reduced levels of another adaptor protein-2 (AP-2) complex protein, α-adaptin (Ap2a1). No craniofacial dysmorphology or any anomalies involving the limbs or developing skeleton are reported for OVE427 homozygotes. Other than cleft palate, additional histological examinati ..... For more information please see the full phenotype on the strain data sheet | ||
| 017435 | FVB;B6-SlmapTn(sb-rtTA)2426B.SB4Ove/J | Under Development - Now Accepting Orders |
| These OVE2426B-SB4 (OVE#2426B-SB4) mice harbor a mutation created by random insertion of the SB-sa-IRES-rtTA-pA-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2223), and the transposon was subsequently mobilized via exposure to sleeping beauty transposase (SB10) to generate the mutation. Using inverse PCR analysis, the transposon integration site was identified in intron 20 of the sarcolemma associated protein gene (Slmap) on chromosome 14. The right IR/DR is linked to the (-) strand of DNA at position 27,244,452 bp [NCB137/mm9; R3-27,244,452(-)]. The rtTA is inserted in the sense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: cleft palate. | ||
| 007664 | 129S-Efnb1tm1Sor/J | Cryopreserved - Ready for recovery |
| These mice possess loxP sites flanking exons 2 through 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 2 through 5 deleted in the cre-expressing tissue(s). These Efnb1 conditional mutant mice may be useful in studying cellular signaling in embryonic development and adult mice; specifically receptor tyrosine kinases. For example, when crossed to a strain expressing Cre recombinase in epiblast-derived tissues (see Stock No. 003755), this mutant mouse strain may be useful in embryogenesis research. For example, when bred to a strain expressing Cre recombinase in midbrain/dorsal spinal cord (see Stock No. 007807 or For more information please see the full phenotype on the strain data sheet | ||
| 005709 | B6.129-Skitm1Cco/J | Cryopreserved - Ready for recovery |
| This mutant was created on a mixed (129 x C57BL/6J) background. Greater than 80% of mice on this mixed background had severe neural tube closure defects (such as exencephaly) while less than 16% exhibited facial clefting. The penetrance of these phenotypes has segregated with further backcross to C57BL/6J. The congenic mutant described here was backcrossed 12-14 times to wildtype C57BL/6J. Mice homozygous for the targeted mutation die before or shortly after birth due to developmental defects. Null mice are distinguishable from wildtype and heterozygous littermates at embryonic day 8.5 (E8.5) with delayed, but complete, cranial neural tube closure (incomplete at the normal E9.5). Ninety percent of null mice alive at E18.5 exhibit facial clefting. Other highly penetrant phenotypes include flattened snout, depressed nasal bridge, excessive orbital separation, elongated subventricular zones, vestigial polydactyly, and malformations of the olfactory bulb, iris, and ventral septum. Heterozy ..... For more information please see the full phenotype on the strain data sheet | ||
| 002619 | B6.129-Tgfb3tm1Doe/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Tgfb3tm1Doe mutation are not viable. Mice exhibit cleft palate and possibly developmental defects in the lung. | ||
| 007453 | B6.129P2(Cg)-Dhcr7tm1Gst/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Dhcr7Ex8 allele lack the exon 8 coding sequence and flanking splice acceptor site of the targeted gene, resulting in the truncated DHCR7 mutation most frequently observed in Smith-Lemli-Opitz/RSH Syndrome (SLOS) patients (IVS8-1G > C). Although a truncated product is transcribed from the targeted gene, no mRNA containing the deleted 3'-coding region is detected in homozygous liver or brain tissue. Homozygous mice exhibit the same biochemical defects as observed with SLOS patients, including markedly reduced tissue cholesterol and total sterol levels, and 30- to 40-fold elevated concentrations of 7-dehydrocholesterol. Newborn homozygotes have difficulty breathing, do not suckle, and die soon after birth with immature lungs, enlarged bladder, and, frequently, cleft palate. These Dhcr7Ex8 mutant mice may be useful in studying Smith-Lemli-Opitz/RSH Syndrome (SLOS; a birth-defect mental-retardation syndrome) or other metabolic disorders invol ..... For more information please see the full phenotype on the strain data sheet | ||
| 009387 | B6.129S1-Osr1tm1Jian/J | Cryopreserved - Ready for recovery |
| The Osr1tm1Jian (Odd1-LacZ) mutation abolishes endogenous gene function and expresses a β-galactosidase fusion protein (fused in-frame with the N-terminal 16 amino acid residues of the endogenous protein). Under control of the upstream promoter/enhancer elements, lacZ expression is directed to the same tissues as the wild-type gene (for example, β-galactosidase expression during embryogenesis is detected at E7.5 in the intermediate mesoderm, is expanded to the gut endoderm, lung bud mesenchyme and myocardial cells by E9.5, and is activated in developing branchial arches and limb buds by E10.5). Almost all (`95%) of homozygous mice die in utero between E11.5-E12.5 from circulation distress; exhibiting malformed atrial septum, dilated atria with hypoplastic venous valves, and blood backflow from the heart into systemic veins. Homozygotes also exhibit complete agenesis of adrenal glands, metanephric kidneys, gonads, and defects in pericard ..... For more information please see the full phenotype on the strain data sheet | ||
| 003865 | B6.129S2-Itgavtm1Hyn/J | Cryopreserved - Ready for recovery |
| The majority (80%) of homozygous null Itgav mice die during embryonic days 9.5-11.5. These mice are characterized by pericardial edema and retarded growth probably due to placental defects. Mice surviving this period die at birth exhibiting intracranial and intestinal hemorrhaging. Angiogenesis in other tissues is normal. Cleft palate is also observed. | ||
| 003336 | B6.129S7-Cdkn1ctm1Sje/J | Cryopreserved - Ready for recovery |
| Mice lacking the Cdkn1c gene have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochrondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; lens cell hyperproliferation and apoptosis. The targeted gene is imprinted. The phenotype differs depending on whether the targeted allele is transmitted from the dam or the sire; maternal inheritance of the null allele is lethal. This is a model for the human Beckwith-Wiedemann syndrome. | ||
| 000026 | B6.C3-Gli3Xt-J/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the extra toes-J spontaneous mutation (Gli3Xt-J) have varying numbers of extra digits on preaxial side of feet. Homozygous mutant mice die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube are evident at E9. Homologous to Grieg's cephalopoly-syndactyly, a rare multi-system syndrome in humans. | ||
| 004275 | B6.Cg-Fignfi/Frk | Cryopreserved - Ready for recovery |
| 006382 | B6;129-Casktm1Sud/J | Cryopreserved - Ready for recovery |
| Homozygous floxed mice are viable and fertile, but females do not thrive. The body size of mutants is significantly smaller than littermate controls and they exhibit a slightly increased mortality. Knock-in mice are hypomorphs and protein is expressed at less than 30% of normal levels. Crossing of the floxed mutants with mice expressing cre recombinase in the male germline excises the floxed exon and a neomycin resistance gene cassette to create a complete knockout of the gene. Knockout homozygotes die within a few hours of birth. They exhibit a partially penetrant cleft palate syndrome and increased apoptosis in the thalamus, but display no other major developmental changes or deficits in basic electrical properties of their neurons.
When bred to a strain expressing Cre recombinase in the male germline (see Stock No. 003328 or 007252 for example), this mutant mouse str ..... | ||
| 002711 | B6;129-Gabrb3tm1Geh/J | Cryopreserved - Ready for recovery |
| The gamma-Aminobutyric acid type A receptors mediate the majority of rapid inhibitory synaptic transmission in the CNS. The beta3 subunit is an essential component of these receptors in many brain regions, especially during development, and is implicated in several pathophysiologic processes. The majority of mice homozygous for the Gabrb3tm1Geh mutation (or beta3-/-) die at birth with ~60% displaying cleft palate and the remaining ~35% die for unidentified reasons. Homozygous females that survive are fertile but do not care for their pups. Survivors have frequent myoclonus and occasional epileptic seizures, are hypersensitive to external stimuli and handling, have a lack of coordination and display altered responses to certain anesthesias. In addition, the observed behavioral deficits (especially regarding social behaviors) indicate that mutant mice may be a useful model of autism spectrum disorders. Of note, several strains bearing gamma-aminobutyric acid (GABA-A) ..... | ||
| 003277 | B6;129S7-Acvr2atm1Zuk/J | Cryopreserved - Ready for recovery |
| Activin receptor IIA deficient mice are viable. Homozygous males are fertile, while homozygous females are infertile. Follicle-stimulating hormone levels are reduced in mutant mice. Some skeletal and facial abnormalities, including micrognathia, cleft palate and defects in Meckel's cartilage are observed. These defects are reminiscent of Pierre-Robin syndrome in humans. Severe defects occasionally result in the perinatal or in utero death of a small number of homozygous mutant embryos. | ||
| 002788 | B6;129S7-Fsttm1Zuk/J | Cryopreserved - Ready for recovery |
| Homozygous mice die within hours after birth due to a failure to breathe. They are smaller in size than normal wildtype siblings and show craniofacial, musculoskeletal, and skin defects. | ||
| 002990 | B6;129S7-Inhbatm1Zuk/J | Cryopreserved - Ready for recovery |
| Homozygous mice die within 24 hours of birth. They show craniofacial defects including a cleft palate. | ||
| 000523 | B6By.Cg-Eh/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the hairy ears mutation die within a day of birth. The palatal shelves fail to fuse resulting in complete clefting of the secondary palate, and the tympanic rings are shortened and deformed. Heterozygotes can be identified by tufts of hair on the inner ear and smaller than normal ear pinnae. | ||
| 000278 | B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J | Cryopreserved - Ready for recovery |
| 000515 | B6CBACa Aw-J/A-SfnEr/J | Cryopreserved - Ready for recovery |
| This mutation shows complete penetrance in heterozygotes. These mice grow a normal appearing but probably somewhat dry first coat until the age of about 13 days; then hair loss begins and continues until the fur becomes sparse. Repeated growth and re-epilation follow without a definite pattern. Heterozygotes are slightly reduced in size and some may die before weaning, but adults are fully viable and fertile. Homozygotes die at birth from inability to breathe because of a closed oral cavity. At embryonic day 17 the skin of homozygotes is extremely thin and smooth with few vibrissae and hair follicles. The snout is truncated and the mouth closed. The limbs and tail are greatly shortened and held close to the trunk and the anal and urogenital orifices are closed. There are marked skeletal abnormalities and cleft palate. Homozygotes can be recognized at 13 days of gestation by their blunt limbs and stumpy tail. Between 13 and 15 days the nares and oral opening close, resulting in marked c ..... For more information please see the full phenotype on the strain data sheet | ||
| 001434 | C3HeB/FeJ x STX/Le-Mc1rE-so Gli3Xt-J Zeb1Tw/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the twirler mutation (Zeb1Tw) display head-shaking and circling behavior but are not deaf. There are morphological abnormalities of the inner ear which consist of irregularities in the outline of the semicircular canals, sometimes amounting to branching, and reduction or absence of otoliths. Moderate astrocytosis in the vestibular nuclei and cerebellar white matter has been reported. Homozygotes have cleft lip and palate or cleft palate only. They die within 24 hours after birth. Viability and fertility are normal except that adults tend to become obese and may then become sterile. Penetrance is incomplete. This strain is also carrying the sombre (Mc1rE-so) and extra toes-Jackson (Gli3St-J) mutations. Extra toes-J heterozygotes have varying numbers of extra digits on preaxial side of feet. Homozygotes die in utero with multiple abnormalities. Excessively large pharyngeal arches and an open neural tube a ..... For more information please see the full phenotype on the strain data sheet | ||
| 000252 | DC/LeJ | Cryopreserved - Ready for recovery |
| Mice heterozygous for the semidominant dancer mutation exhibit head tossing and circling behavior. Heterozygotes are not deaf, but have defects in the vestibular region (Wenngren et al., 1989). Homozygotes die at birth with cleft lip and cleft palate (Deol et al., 1966). Strain background influences cleft lip/palate expression in heterozygotes (Trasler et al., 1982). Positional cloning of Dc revealed a 3.3 kb insertion of the Tebp gene into the first intron of Tbx10. The insertion causes ectopic expression of a Tebp-Tbx10 chimeric transcript (Bush et al., 2004). | ||
| 005057 | FVB.129-Kcnj2tm1Swz/J | Cryopreserved - Ready for recovery |
| Mice that are homozygous for the targeted mutation have a complete cleft of the secondary palate and die within 12 hours of birth. Heterozygotes 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 blot analysis of cardiac tissue or Southern blot analysis. Inwardly rectifying potassium ion currents are absent in cerebral artery myocytes and cardiac ventribular myocytes isolated from homozygote neonates. Elevated external potassium ion concentrations do not dilate isolated neonatal cerebral arteries. Homozygotes exhibit altered electrocardiogram profiles indicative of reduced heart rate and bradycardia. This mutant mouse strain may be useful in studies of potassium ion dependent vasodilation, cardiac arrythmia such as Anderson syndrome, cleft palate and developmental bone malformation. | ||
| 013100 | FVB.C-Prdm16csp1/J | Cryopreserved - Ready for recovery |
| Mice heterozygous for the csp1 ENU-induced mutation, are viable, fertile, and normal in size. Homozygous mutants exhibit the cleft palate (CP) phenotype and perinatal lethality with respiratory failure. The occurrence of the CP phenotype in homozygous csp1 mice drops to 9% after backcrossing onto the C57BL/6J background for four generations, although 93% of these mice still die shortly after birth and still exhibit respiratory failure. Approximately 6% of heterozygous mutant mice exhibit the (CP) phenotype. These csp1 mice possess a C to A mutation within intron 6 of the PR domain containing 16 (Prdm16) gene, resulting in vairable absence of exon 7 and early termination within exon 8. It is unclear if this truncated PRDM16 protein is stable in csp1. The CP phenotype of these csp1 mice is exhibited by micrognathia and failed palate shelf elevation due to physical obstruction by the tongue, resembling human Pierre Robin sequence (PRS)-like ..... For more information please see the full phenotype on the strain data sheet | ||
| 003318 | STOCK Shhtm1Amc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Shhtm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.
When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e ..... | ||
| 003102 | STOCK Tgfb2tm1Doe/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Tgfb2tm1Doe targeted mutation exhibit perinatal mortality. Homozygous mutant mice exhibit a wide range of developmental defects including cardiac, lung, craniofacial, limb, spinal column, eye, inner and urogenital defects. | ||
| 008469 | STOCK Wnt9btm1.2Amc/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Wnt9bc allele are viable and fertile, with loxP sites flanking exon 2 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region deleted in the cre-expressing tissue(s). Such deletion is predicted to result in out-of-frame splicing of exon 1 to exon 3, and consequently a mutant transcript that would encode a nonfunctional peptide comprising the first 27 amino acids of Wnt9b that includes the signal peptide. These Wnt9bc mice may be useful in generating conditional mutations for studying the role of Wnt9b (and other Wnt family members) in development and canonical Wnt signaling cascades, including metanephric kidney and urogenital system development. | ||
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