Search Criteria: Research Area is "Cardiovascular Research: Heart Abnormalities"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 002684 | B6.129P2-Nos3tm1Unc/J | Level 2 |
| Mice homozygous for the Nos3tm1Unc targeted mutation are viable and fertile. They have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues. | ||
| 005704 | B6.129-Fbn1tm2Rmz/J | Repository- Live |
| Both heterozygous and homozygous "mgR" mutant mice are viable with no phenotypic abnormalities at birth. The protein expressed from this mutant allele is the same size as wild-type. Skin tissues show an intermediate reduction in transcript levels compared to wild-type and the mg-delta null allele. Thus the "mgR" mutation does not completely ablate gene function (resulting in rapid death). Instead, expression is hypomorphic and conducive to studying the clinical stages precursive to animal lethality. Homozygotes develop medial calcification, the inflammatory-fibroproliferative response, and inflammation-mediated elastolysis in the natural history of dissecting aneurysm and die between 2-6 month of age with Marfan syndrome (MFS)-like manifestations. | ||
| 006243 | B6.129S4-Timp1tm1Pds/J | Repository- Live |
| Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genet
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| 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. | ||
| 002044 | B6Ei.Cg-Atp7aMo-blo/J | Repository- Live |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs.. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to
..... For more information please see the full phenotype on the strain data sheet | ||
| 003810 | STOCK Adrb1tm1Bkk Adrb2tm1Bkk/J | Repository- Live |
| Mice that are homozygous null for the Adrb1 and Adrb2 genes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Stimulation of beta adrenergic receptor function in these mice by agonists or exercise reveals significant impairments in chronotropic range, vascular reactivity and metabolic rate. A severely attenuated chronotropic and hypotensive response is observed after administration of the non-selective beta adrenergic receptor agonist isoproterenol. An abnormal response to epinephrine is also seen, with bradycardia and a monophasic hypertensive blood pressure change being observed rather than the tachycardia and biphasic hypertensive/ hypotensive response seen in wildtype mice. When exercised, heart rates in null mice are lower than that of wild type mice. No difference is noted in the resting heart rate. | ||
| 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
..... | ||
| 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. | ||
| 004374 | 129-Npr1tm1Gar/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) was detected. Homozygous mutant mice have elevated systolic, diastolic and mean blood pressure when compared to wildtype. Heterozygous mutant mice display systolic, diastolic and mean blood pressure that are slightly elevated above wildtype levels. Blood pressure in mutant mice remains elevated independent of salt content in diet. Infusion treatment of atrial natriuretic peptide in mutant mice does not result in the increased urine output or sodium excretion response seen in wildtype mice. Plasma volume expansion to release natriuretic/diuretic factors from the heart fails to induce increased urine output, sodium excretion and cyclic GMP excretion in the mutant. The same plasma volume expansion in wildtype mice results in a 12-fold increase in urine output, a 6-fold increase in sodium excretion and a 4-fold increase in c
..... For more information please see the full phenotype on the strain data sheet | ||
| 004367 | B6.129-Adra2atm1Bkk/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Expression of the receptor in the brain was significantly reduced as assessed by antagonist binding, which indicated a 90% reduction. The antagonist binding assay is not entirely specific for the receptor, as the residual 10% binding was attributable to a different subtype of receptor. Mutant mice exhibit a resting tachycardia of more than 180 beats/min greater than normal. Although mutant mice do not have elevated blood pressure, administration of the hypotensive agonist, dexmedetomidine, does not reduce blood pressure. Electrical stimulation of isolated heart atria at frequencies mimicking physiological sympathetic nerve activity results in increased release of noradrenaline at high frequencies and inhibited release at low frequencies. Noradrenaline release from isolated wildtype atria is higher at high frequencies than at low frequencies. I
..... For more information please see the full phenotype on the strain data sheet | ||
| 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. | ||
| 003537 | B6.129-Kif3atm1Gsn/J | Repository-Cryopreserved |
| Ciliary formation appears to be crucial in developing left-right asymmetry in early mouse embryonic development. One of the necessary cilia components is the Kif3a gene product. Homozygous Kif3a knockout mice die at 10 days postcoitum, exhibit randomized establishment of left-right asymmetry and display numerous structural abnormalities. Cardiac looping is randomized, often retarded. Growth is severely retarded with caudal truncation. A neural tube closure defect is also apparent. Scanning electron microscopy indicates the absence of embryonic cilia. A small percentage of heterozygotes exhibit morphological abnormalities. | ||
| 006833 | B6.129-Sgcbtm1Kcam/2J | Repository-Cryopreserved |
| Homozyous mice are viable and fertile. They develop severe muscular dystrophy and cardiomyopathy with focal areas of necrosis. Severe dystrophic changes including necrosis, dystrophic calcification, fatty infiltration, central nucleation, fibrosis, atrophy and hypertrophy are detected in diaphragm and calf/thigh muscle. Some of these changes occur in 4-week-old animals and accumulate with age. At 20 weeks of age, several regions of focal myocardial necrosis have been observed; small areas of necrotic myocardiocytes may be observed as early as 9 weeks of age. At 30 weeks of age, large areas of fibrosis are detected. Sarcoglycan-sarcospan and dystroglycan complexes are disrupted in skeletal, cardiac, and smooth muscle membranes. Loss of the sarcoglycan-sarcospan complex in vascular smooth muscle results in vascular irregularities in heart, diaphragm, and kidneys. Vascular constrictions in skeletal muscle, cardiac muscle and kidneys is observed. For more information please see the full phenotype on the strain data sheet | ||
| 004582 | B6.129-Sgcdtm1Mcn/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. No gene product (protein) is immunodetected in skeletal muscle microsomal preparations. At 8 weeks of age there is an onset of sudden mortality, with a 50% survival rate at 28 weeks. Elevated creatine kinase serum levels are indicative of striated muscle degeneration. Histopathology of skeletal muscle tissue reveals degeneration and regeneration of muscle fibers, inflammatory infiltrate, perivascular fibrosis and calcification. At 12 weeks of age, cardiac muscle tissue also begins to show degeneration, inflammatory infiltration and perivascular fibrosis. Myofiber membranes have permeability defects as assessed by Evans blue dye uptake into myofiber cytoplasm. Skeletal muscle of mutant mice have an enhanced sensitivity to mechanically induced sarcolemmal damage. This mutant mouse strain may be useful in studies of limb girdle muscular dystrophy and cardiomyopathy. | ||
| 002689 | B6.129P2-Acetm3Unc/J | Repository-Cryopreserved |
| The entire angiotensin converting gene is duplicated in this strain by homologous recombination (gap repair gene targeting). Mice that are heterozygous for this mutation have three functional genes. Mice that are homozygous for this mutation have four functional genes. This permits examination of the effects of having two (wildtype), three or four functional copies of the targeted gene in its normal chromosomal location. Serum ACE activities increased progressively from 62% in one copy mice to 144% of normal in three copy animals. Blood pressures did not differ significantly; however, heart rates, heart weights and renal tubulointerstitial volumes decreased significantly with increasing copy number. This mutant mouse strain may be useful in studies of cardiovascular and renal disease. | ||
| 004159 | B6.129P2-Adra1btm1Cta/J | Repository-Cryopreserved |
| Mice that are homozygous null for the targeted allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Adra1b transcripts are detected. The amount of alpha 1 adrenergic recptor binding activity as measured by radioligand assays is dramatically decreased in homozygous liver, heart and cerebral cortex. The blood pressure response induced by increasing doses of phenylephrine is reduced by 45% in comparison to wild type mice. Similarly, phenylephrine-induced contraction of aortic tissue is diminished 25%. This mutant mouse strain represents a model that may be useful in studies related to blood pressure regulation. | ||
| 003461 | B6.129P2-Thratm1Ven/J | Repository-Cryopreserved |
| The Thra gene encodes the T3 receptor TRa1 (alpha 1) and a non-T3 bindng product TRa2 (alpha 2), generated by alternative splicing in the C-terminal region. This Thra mutant is deleted for the T3 receptor TRa1 (ALPHA ONE) but retains TRa2. These mutants have an average heart rate 20% lower than that of control animals, prolonged QTend and QRS durations, body temperatures 0.5 degrees C lower than that of control animals. A mild hypothyrodism is present but is restricted to males. | ||
| 002270 | B6.129S-Fn1tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Fn1tm1Hyn targeted mutation die during early embryonic development. Blastocyst development and implantation of homozygotes is normal. Gastrulation is initiated and appears normal, including extensive mesodermal movement. From embryonic day 8 onwards homozygous mutant embryos deteriorate through the 10th and 11th days of gestation. Homozygous mutant embryos have a shortened anterior-posterior axes, fail to develop a notochord or somites, and have abnormal development of the heart, blood vessels, and yolk sac indicating a general deficiency in mesodermally derived tissues. Heterozygous mice are viable for at least 2 years and appear healthy and approximately the same size as wild-type littermates. Plasma levels of fibronectin in heterozygotes are 50% lower than normal wildtype siblings. | ||
| 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. | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches. | ||
| 002777 | B6.129S2-Adra2atm1Lel/J | Repository-Cryopreserved |
| Mice homozygous for this mutation are viable and fertile. They exhibit loss of physiological functions evoked by alpha1-adrenergic receptor agonists and display increased susceptibility to kindling-induced seizures. | ||
| 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. | ||
| 002719 | B6.129S4-Wt1tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Wt1tm1Jae targeted mutation die between embryonic days 13 and 15. They fail to develop a kidney or gonads. The hearts of homozygous mutant mice also fail to develop properly. Hearts are smaller than wildtype controls and possess a rounded apex. The right ventricular wall is thin and the left ventricle is reduced in size. There appears to be normal development of the aortic, pulmonary, mitral and tricuspid valves. Development of the diaphragm is also incomplete resulting in incomplete separation of the thoracic and abdominal cavities. Homozygous mutant lungs are also markedly smaller than wild type lungs. Heterozygous mice appear normal and show no tumor development (mice followed until 10 months of age). | ||
| 002646 | B6.129S6-Nf1tm1Fcr/J | Repository-Cryopreserved |
| Mice homozygous for the Nf1tm1Fcr targeted mutation die during embryonic development due to severe heart malformation (~E13). They also show hyperplasia of neural crest-derived sympathetic ganglia. Heterozygotes do not exhibit any overt disease symptoms. However, as noted in a another targeted mutation deleting the same exon of the Nf1 gene (Jacks, et al., Nat Genetics 7:353-361, 1994), they do show a predisposition to many types of tumors and were recently shown to have deficits in learning and memory (Silva, et al., Nat Genetics 15:281-284, 1997). | ||
| 000535 | B6.Cg-Atp7aMo-blo/J | Repository-Cryopreserved |
| Female mice heterozygous for the blotchy alleles (Atp7aMo-blo) are viable and fertile. They have irregular patches of light-colored fur. Hemizygous males and homozygous females have reduced viability and many are infertile. Hemizygotes and homozygotes are light all over with no blotching, are usually small, and occasionally have deformed hindlegs. Most hemizygotes and homozygotes have defective elastin in the aorta and usually die with aortic aneurysm. Hemizygous males have enlarged air spaces in the lung (emphysema), probably because of defective elastin and collagen. Skin collagen and aortic elastin have defective crosslinking at the step at which lysine residues are converted to aldehydes. Hemizygous males have a deficiency of noradrenalin in the brain, probably because a deficiency of copper shown to exist in the brain causes defective activity of the enzyme dopamine-beta-hydroxylase. Copper absorption from the gut and hepatic copper concentration are reduced to 6
..... For more information please see the full phenotype on the strain data sheet | ||
| 004264 | B6;129-Cycstm1Wlm/J | Repository-Cryopreserved |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 004362 | B6;129-Scarb1tm1Kri Apoetm1Unc/J | Repository-Cryopreserved |
| At birth, mice homozygous for both targeted alleles are viable, normal in size and do not display any gross physical or behavioral abnormalities. All double mutants die between 5 to 8 weeks following birth, exhibiting hypercholesterolemia and significantly lower body weights compared to control mice. Mice display an altered appearance several days before death, displaying ruffled fur, an abnormal gate and sometimes labored breathing. Hearts from double mutants are enlarged, exhibit evidence of myocardial infarction and are functionally impaired. Histological examination reveals extensive coronary artery disease characterized by atherosclerotic plaques with evidence of cholesterol clefts and fibrin deposition. As with other Scarb1 homozygous null mutants, females are infertile while the fertility of homozygous males remains intact. This double mutant mouse strain offers a model that may be a useful tool in studies related to coronary heart disease. | ||
| 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. | ||
| 002992 | B6;129S1-Vcam1tm1Roml/J | Repository-Cryopreserved |
| Mice homozygous for the Vcam1tm1Roml targeted mutation are not viable and exhibit either of two phenotypes. Approximately half the VCAM-deficient embryos die prior to embryonic day 11.5 exhibiting a severe defect in placental development in which the allantois failed to fuse with the chorion. The other half of the VCAM-deficient embryos survive to embryonic day 11.5-12.5 and display several heart abnormalities. Significant amounts of blood is found in the heart and pericardial space and embyros lack an epicardium. | ||
| 002495 | B6;129S4-Col1a1tm1Jae/J | Repository-Cryopreserved |
| Homozygous mice are viable and develop to young adulthood without obvious differences from wildtype mice. As the mice age they develop fibrosis in the dermis characterized by a thickening and roughening of the skin, which is similar to that seen in human scleroderma. Homozygous females develop postpartum abnormalities of the uterus caused by a failure of collagen resorption. They have slightly reduced litter sizes and significantly fewer litters than normal wildtype mice. A secondary collagenase cleavage site was found in the mutant protein that could be cleaved by rat collagenase but not by human collagenase. | ||
| 002332 | B6;129S4-Wt1tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Wt1tm1Jae targeted mutation die between embryonic days 13 and 15. They fail to develop a kidney or gonads. The hearts of homozygous mutant mice also fail to develop properly. Hearts are smaller than wildtype controls and possess a rounded apex. The right ventricular wall is thin and the left ventricle is reduced in size. There appears to be normal development of the aortic, pulmonary, mitral and tricuspid valves. Development of the diaphragm is also incomplete resulting in incomplete separation of the thoracic and abdominal cavities. Homozygous mutant lungs are also markedly smaller than wild type lungs. Heterozygous mice appear normal and show no tumor development (mice followed until 10 months of age). | ||
| 003266 | B6;129S7-Epas1tm1Rus/J | Repository-Cryopreserved |
| Mice homozygous for the Epas1tm1Rus targeted mutation develop normally until embryonic day 11.5. Beginning at embryonic day 12.5 the ratio of homozygous embryos begins to decline and by day 16.5 there are no viable mutant embryos. Overall morphological development, including the circulatory system, is normal. Of particular interest however, is a pronounced bradycardia in homozygous mutant mice. Catecholamine levels in homozygous mutant mice are also significantly lower than wildtype controls. Administration of the catecholamine precursor DOPS to pregnant females rescues approximately 40% of mutant embryos. Embryos that survive to birth appear runted, fail to nurse, and die within 24 hours of birth. These results suggest a pivotal role of EPAS1 in catecholamine homeostasis. Heterozygous mice from this strain contain a modified lacZ gene in the targeting construct. This characteristic makes this strain useful as a marker for endothelial cells. | ||
| 002640 | B6;SJL-Tg(Myh6-ADRBK1)27Wjk/J | Repository-Cryopreserved |
| Mice carrying this transgene overexpress a truncated form of the bovine beta-adrenergic receptor kinase-1 containing only the last 194 amino acids of the ADRBK1 protein. The truncated protein inhibits endogenous beta-adrenergic receptor kinase-1 by blocking beta-adrenergic receptor desensitization. This myocardial inhibition increases cardiac function of homozygotes under basal conditions and leads to supersensitization to beta-agonists. This strain may serve as a model for increased left ventricular performance, a novel method of positive intropy, and enhanced beta-adrenergic signalling. | ||
| 002637 | B6SJL-Tg(CAMalpha1b)7Wjk/J | Repository-Cryopreserved |
| Mice carrying the CAMalpha1b transgene display stable myocardial specific hypertrophy with ensuing markers of hypertrophy being elevated. In addition, alpha 1 adrenergic receptor signaling through the Gq-phospholipase C-protein kinase C signaling pathway is enhanced. | ||
| 002639 | B6SJL-Tg(Myh6-ADRBK1)12Wjk/J | Repository-Cryopreserved |
| Mice carrying this transgene show a 3 to 5 fold overexpression of bovine beta-adrenergic receptor kinase-1. Myocardial beta-adrenergic receptors are hyperphosphorylated and desensitized in hemizygotes resulting in attenuated cardiac function in response to beta-agonists. | ||
| 002638 | B6SJL-Tg(WTbeta2)4Wjk/J | Repository-Cryopreserved |
| These transgenic mice exhibit increased basal myocardial adenylyl cyclase activity, enhanced atrial contractility, and increased left ventricular function in vivo; these parameters at baseline in the transgenic animals were equal to those observed in control animals maximally stimulated with isoproterenol. Mice carrying this transgene display a marked overexpression of the human beta-2 adrenergic receptor (~200 fold increase). | ||
| 002197 | C57BL/6-Col1a1Mov13/J | Repository-Cryopreserved |
| The integration of the M-MuLV genome near the 5' end of the Col1a1 gene blocks transcription of the gene from this locus. Mice homozygous for this mutation suffer from arrested development at day 12 and die at about embryonic day 13-14. Heterozygotes in our colony rarely survived to 8 months of age. Many died at less than 3 months of age. | ||
| 006423 | C57BL/6J-Hlb468/J | Repository-Cryopreserved |
| For information on Hlb468 view the web page on the Mouse Heart, Lung, Blood and Sleep Disorders Center site. | ||
| 008265 | C57BL/6J-hlb233/J | Repository-Cryopreserved |
| 008266 | C57BL/6J-hlb495/J | Repository-Cryopreserved |
| 008267 | C57BL/6J-hlb520/J | Repository-Cryopreserved |
| 008268 | C57BL/6J-hlb521/J | Repository-Cryopreserved |
| 005863 | C57BL/6J-Tg(ACTB-DDAH1)1Jpck/J | Repository-Cryopreserved |
| Hemizygous mice are viable and fertile with no anatomic abnormalities. Transgene expression is observed in aorta, heart, and brain. Transgenic dimethylarginine dimethylaminohydrolase (DDAH) activity is reflected in a reduction of plasma asymmetric dimethylarginine (ADMA). Nitric oxide synthase (NOS) activity is significantly increased in transgenic skeletal and cardiac muscle. Transgenic mice have lower blood pressure and higher heart rate. Transgenic mice may be useful in studies of atherosclerosis, hypertension, hyperlipidemia, hypercholesterolemia, hyperhomocystinemia, diabetes mellitus, stroke, renal failure, preeclampsia, and other conditions associated with vascular pathophysiology and/or cardiovascular disease. | ||
| 006817 | D2.129S4(Cg)-Wt1tm1Jae/EiJ | Repository-Cryopreserved |
| 005059 | FVB.129-Kcnj12tm1Swz/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 (mRNA or protein) is detected by Northern blot analysis of cardiac tissue or Southern blot analysis. Cardiac ventribular myocytes isolated from homozygotes exhibit a 50% reduction in inwardly rectifying potassium ion currents under physiological and elevated extracellular potassium ion concentration levels. This mutant mouse strain may be useful in studies of potassium ion dependent cardiac electrophysiology. | ||
| 005057 | FVB.129-Kcnj2tm1Swz/J | Repository-Cryopreserved |
| 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. | ||
| 002535 | FVB/N-Tg(ANX6)2Agh/J | Repository-Cryopreserved |
| Mice carrying the human annexin VI transgene display a phenotype similar to congestive heart failure. They show alterations in the contractility and calcium dynamics in cardiomyocytes, and these cells also have reduced basal calcium levels. Mice homozygous for the transgene die by 4 weeks of age while hemizygous mice live to about 1 year of age. | ||
| 000220 | LPT/LeJ | Repository-Cryopreserved |
| 006021 | NOD.Cg-H2-Ab1tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ | Repository-Cryopreserved |
| The NOD transgenic HLA DQ8, H2-Ab1deficient mouse is diabetes resistant but develops cardiomyopathy resulting in early death from heart failure in both males and females. Histological exam indicates hearts are 3-4x larger than wildtype. Pathology results from an autoimmune response against normal cardiomyocytes in the atrial and ventricular walls, as well as against myocytes present in the outermost muscle layer surrounding the pulmonary veins. Disease progression can be blocked by cyclosporin A treatment and is accelerated with Complete Freund’s Adjuvant (Elliott et al, 2003, PNAS) . This model is useful for studying autoimmune myocarditis, idiopathic dilated cardiomyopathy and heart failure and to understand the role of MHC class II in autoimmunity.. | ||
| 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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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 |
| 005350 | B6.CAST(Cg)-Largevls/Pjn | Research Strain |
| Mice homozygous for the veils (Largevls) allele appear runted with muscle wasting. By five months of age, mild to moderate multifocal areas of cardiomyocyte degeneration are observed in the myocardium of homozygotes. Homozygote mice exhibit extensive ocular abnormalities including: retinal dysplasia, a disorganized ganglion cell layer, thinning of the inner nuclear layer, a progressive diminution of photoreceptor cells with aging, as well as, defects in the inner limiting membrane and outer plexiform layer. (Lee Y, et al., 2005) | ||
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How to Register Interest
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
Select the strain name to link to the strain data sheet.
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.
- Receive periodic updates on the status of the colony UNDER DEVELOPMENT
- Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available
- Provide input affecting speed and quantity of availability
It is VERY IMPORTANT that you register interest in strains Under Development. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain Under Development. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.
- Strains that will be made available from a live distribution colony at The Jackson Laboratory.
These strains are designated as: "Under Development for Distribution Colony"- Strains that will be made available through the Cryopreservation Repository.
These strains are designated as: "Under Development for Cryopreservation Repository"
Send questions to our Technical Support team using the Express Technical Support Form.
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