Search Criteria: Research Area is "Developmental Biology Research: Internal/Organ Defects (heart)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008001 | 129S-Dvl2tm1Awb/J | Repository- Live |
| Half of homozygotes exhibit a perinatal lethal phenotype. Surviving homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Some newborn homozygotes fail to survive and exhibit breathing difficulties, cyanosis and reduced mobility. No gene product (protein) is detected by Western blot analysis of brain lystates. Some nonviable homozygotes display cardiac abnormalities. Most homozygotes (90%) have mild abnormalities of the ribs and vertebrae. 2 to 3% of the homozygous embryos display thoracic spina bifida and exencephaly. This mutant mouse strain may be useful in studies of bone and cardiac development, neural tube closure and spina bifida. | ||
| 007859 | 129S1/Sv-Sufutm1Aeb/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 an embryonic lethal phenotype, failing to develop past embryonic days 9.5 to 10. No gene product (protein) is detected by Western blot analysis. Truncated gene product (mRNA) is detected by Northern blot analysis. Homozygous embryos at 9 to 9.5 embryonic day exhibit growth retardation, incomplete embryonic turning, abnormal somite development, abnormal heart looping (due to abnormal left-right axial patterning) and open neural tubes. This mutant mouse strain may be useful in studies of the Hedgehog signaling pathway and embryonic development. | ||
| 006910 | B6.129-Crkltm1Hkp/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), Digeorge Syndrome (DGS) and Velocardiofacial Syndrome. | ||
| 007609 | B6.129S4-StrapGt(ROSA)71Sor/J | Repository- Live |
| Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes have an embryonic lethal phenotype, dying between E10.5 and E12.5. No gene product is detected in primary fibroblasts isolated from homozygous embryos (E9.5) by RT-PCR. Homozygous embryos have underdeveloped vasculature of the yolk sac, abnormal heart and somite development, and arrested neural tube closure and embryonic turning. Heterozygotes are viable and fertile. These Strap-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation. | ||
| 006470 | B6;129S-Hopxtm1Eno/J | Repository- Live |
| Homozygous mice are viable and fertile on this mixed genetic background. Absence of the targeted protein is confirmed in heart and brain tissues from homozygotes. The lacZ expression pattern is similar to that of the endogenous gene. Homozygous heart tissues show altered serum response factor (SRF)-associated gene expression. Mice homozygous for this null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. These mutant mice may be useful in studying cardiac growth and development. | ||
| 005130 | STOCK Gt(ROSA)26Sortm1(Smo/EYFP)Amc/J | Repository- Live |
| These mice contain an Enhanced Yellow Fluorescent Protein/Smoothened homolog (Drosophila) fusion gene inserted into the Gt(ROSA)26Sor locus. The mutant allele consists of a fusion product involving Enhanced Yellow Fluorescent Protein (EYFP) and the constitutively active W539L point mutation of the mouse smoothened homolog (Drosophila) gene (SmoM2). Expression of the Smo/EYFP fusion gene is blocked by a loxP-flanked STOP fragment placed between the Gt(ROSA)26Sor promoter and the Smo/EYFP sequence. When used in conjunction with a Cre recombinase-expressing strain, successful Cre-mediated excision results in the constitutive expression of mouse smoothened homolog (Drosophila) and unrestrained Hedgehog signaling in Cre-expressing tissues. Expression of the SmoM2 fusion protein can be monitored using EYFP-specific fluorescence protocols. Mice that are homozygous for the mutant allele are viable, fertile, normal in size and do not display any gross physical
..... For more information please see the full descriiption on the strain data sheet | ||
| 006578 | STOCK Myoz2tm1Eno/J | Repository- Live |
| Mice homozygous for this calsarcin-1 mutant allele are viable and fertile. Immunoblot of homozygous cardiac tissue shows no endogenous protein expression. Strong lacZ expression throughout all cardiac chambers mirrors the expression pattern of the endogenous gene, and marked skeletal muscles known to contain a high proportion of type I (slow) fibers. Homozygotes have skeletal muscle abnormalities in type I (slow) fibers and calcineurin activity. Echocardiography of homozygous mice reveals abnormal heart performance. Absence of gene function activates a cardiac hypertrophic fetal gene program (despite the absence of hypertrophy) and enhanced the cardiac growth response to pressure overload. These mutant mice may be useful in studying growth and gene expression of cardiac and skeletal muscle, as well as the pathogenesis of human cardiomyopathies. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic bac
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| 004526 | STOCK Smotm2Amc/J | Repository- Live |
| These mice possess loxP sites on either side of exon 1 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 bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the skin (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental epithelium. When bred to a strain with the targeted null allele (Stock No. 004288) and a strain expressing Cre recombinase in the nervous system (Stock No. 003771), this mutant mouse strain may be useful in studies of hedgehog signalling and cerebellar foliation. | ||
| 006473 | STOCK Smyd1tm1Dsr/J | Repository- Live |
| Mice heterozygous for this targeted mutation are viable and fertile. Mice homozygous for this targeted allele, however, die between embryonic day (E) 9.5 and 10.5 due to cardiomyocyte maturation defects, including an enlarged heart, single left-side ventricular chamber with tremendous extra cellular matrix expansion between the myocardial and endocardial layers, and defective Hand2 expression. No mRNA transcripts from the targeted mutant gene are detected in cardiac tissue from E9.5 homozygotes. These mutant mice may be useful in studying cardiomyocyte differentiation and cardiac morphogenesis. 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. | ||
| 000274 | TSJ/LeJ | Repository- Live |
| 004288 | 129X1-Smotm1Amc/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past 9.5 days post coitum. Homozygous mutant mice exhibit ventral cyclopia and holoprosencephaly. During development homozygous mice fail to undergo embryonic turning, closure of the ventral midgut and normal rightward looping of the heart. The embryonic heart remains a linear tube. This mutant mouse strain represents a model that may be useful in studies of tumors and neural tube defects due to disruption of the hedgehog pathways. When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004526) and a strain expressing Cre recombinase in the skin (Stock No. 004782), this mutant mouse strain may be useful in
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| 003360 | B6.129-Juptm1Kem/J | Repository-Cryopreserved |
| Plakoglobin Jup null-mutant embryos die from embryonic day 10.5 onward due to severe heart defects. Some mutant embryos develop further, especially on a C57BL/6 background. These mice die around birth, presumably due to cardiac dysfunction, and with skin blistering and subcorneal acantholysis. The skin phenotype in plakoglobin-deficient mice is reminiscent of the human blistering disease, epidermolytic hyperkeratosis. | ||
| 003334 | B6.129-Juptm1Ruiz/J | Repository-Cryopreserved |
| Plakoglobin (gamma catenin) is a constituent of the cytoplasmic plaque of desmosomes as well as of other adhering cell junctions, and is involved in anchorage of cytoskeletal filaments to specific cadherins. Homozygous null mutant animals die between days 12 - 16 of embryogenesis due to defects in heart function. The tissue instability correlates with absence of desmosomes in the heart. | ||
| 002463 | B6.129S-Itga4tm1Hyn/J | Repository-Cryopreserved |
| 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. | ||
| 008192 | B6.129S2-Nf1tm1Tyj/J | Repository-Cryopreserved |
| Heterozygous animals do not exhibit the classical symptoms of Human neurofibromatosis type 1, but are highly predisposed to the formation of various tumor types, notably phaeochromocytoma, a tumor of the neural crest-derived adrenal medulla, and myeloid leukemia. Homozygosity leads to abnormal cardiac development and mid-gestational embryonic lethality. This strain may be useful in studies of cancer and developmental biology. | ||
| 006142 | B6.129S4-Ppargtm1Rev/J | Repository-Cryopreserved |
| All mice homozygous for this targeted mutation die after gestational day 9.5 from severe placental defects and myocardial thinning. Heterozygotes are viable and fertile. White adipose tissue from heterozygous mice display approximately half the mRNA expression compared to wildtype. Tracer-determined glucose disposal rates and hepatic glucose production show that peripheral tissues and livers from heterozygotes are more sensitive to the effects of insulin than wildtype. This mutation eliminates both DNA-binding and ligand-binding functions of the endogenous gene, concomitantly generating a lacZ reporter that faithfully recapitulates the endogenous expression pattern. Heterozygous mice or homozygous embryo-derived cells may be useful in studies of embryo and placental development, diabetes, atherosclerosis, inflammation, and for beta-galactosidase reporter function of the endogenous gene. | ||
| 004267 | B6.129S6-Dnmt3ltm1Bes/J | Repository-Cryopreserved |
| Mice that are homozygous for this targeted allele are viable, normal in size, do not display any gross physical or behavioral abnormalities, but are sterile. Adult homozygous males display severe hypogonadism, Sertoli-cell-only phenotype and apoptotic death of spermatocytes prior to pachytene with loss of spermatogonia progressing to nonsyndromic azoospermia in later adulthood. Extreme abnormalities of meitotic pairing occur. There is a failure to methylate transposons in prospermatogonia with expression of very high levels of both LTR and non-LTR transposons in spermatogonia and spermatocytes. Homozygous females have normal oogenesis. Heterozygous progeny of homozygous females do not develop past 9.5 day post coitum, with pericardial edema with exencephaly and other neural tube defects. Maternally imprinted gene sequence that is usually heavily methylated in control oocytes is undermethylated in mutant mice oocytes. Paternally imprinted gene sequence is not effected and global genome
..... For more information please see the full descriiption on the strain data sheet | ||
| 006042 | B6.129S7-Efnb2tm2And/J | Repository-Cryopreserved |
| 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 bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 1 of the targeted gene is deleted in the tissue of interest. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. To test the effectiveness of this model, these mutant mice were bred to an endothelial-specific Cre-expressing transgenic mice, Tg(Tek-cre)12Flv (Stock No. 004128) . Offspring homozygous for the Cre-mediated exon 1 deletion show angiogenic remodeling defects and embryonic death identical to homozygous Efnb2tm1And mice (see Stock No. For more information please see the full descriiption on the strain data sheet | ||
| 004425 | B6;129-Gdf1tm1Sjl/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous null mice have an embryonic and perinatal lethal phenotype, most develop past embryonic day 14.5 with two thirds dying at birth and almost all not surviving beyond 48 hours after birth. Homozygous mutant newborn mice display a range of left-right axis defects such as visceral situs inversus, right pulmonary isomerism and cardiac anomalies including abnormal positioning of the aorta and pulmonary artery, and septal defects. Spleen and lungs were malformed in some homozygotes. This mutant mouse strain represents a model that may be useful in studies of situs inversus. | ||
| 002201 | B6;129S-Gja1tm1Kdr/J | Repository-Cryopreserved |
| Mice homozygous for the Gja1tm1Kdr targeted mutation die at birth. The cause of death is a failure in pulmonary gas exchange caused by a swelling and blockage of the right ventricular outflow tract from the heart. The cardiac abnormality involves a delay in the normal looping of the ascending limb of the heart tube, which includes the right ventricle and the outflow tract. This predisposes homozygous mutant mice to malformations of the subpulmonary outflow tract and tricuspid valve. The mutation also predisposes mice to lens cataracts and causes a severe reduction of germ cell numbers in homozygous mutant mice of both sexes. Both neonatal and adult mice heterozygous for the Gja1tm1Kdr targeted mutation have slower ventricular epicardial conduction of paced beats in the heart. | ||
| 003179 | STOCK Cdh2tm1Hyn/J | Repository-Cryopreserved |
| Mice that are heterozygous for the mutant allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. However, homozygous mice have an embryonic lethal phenotype, and die by embryonic day 10. The somites of the mutant embryos are small, irregularly shaped, and less cohesive compared with those of their wild-type littermates, and the epithelial organization of the somites is partially disrupted. Undulation of the neural tube is also observed in the mutant embryos. The mesodermal and endodermal cell layers of the yolk sac are separated in the mutants. The most dramatic cell adhesion defect is observed in the primitive heart; although myocardial tissue forms initially, the myocytes subsequently dissociate and the heart tube fails to develop normally. | ||
| 002906 | STOCK Evi1tm1Mmor/J | Repository-Cryopreserved |
| Evi1 mutant embryos die at E10.5 due to widespread hypocellularity, hemorrahaging, and disruption in the development of paraxial mesenchyme. In addition, defects in the heart, somites, and cranial ganglia were detected and the peripheral nervous system fails to develop. | ||
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