Search Criteria: Research Area is "Cardiovascular Research: Vascular Defects (Thrombosis)"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 007937 | B6.129-Tyro3tm1Grl/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain lysate. Homozygotes exhibit decreased sensitivity to induced pathological thrombosis resulting in reduced fatal pulmonary embolism (25% of wild-type). Platelet aggregation and clot retraction after thrombin treatment is impaired. Platelet signaling and secretion is also defective. Activity induced seizures can occur in mutant mice over the age of seven months. This mutant mouse strain may be useful in studies of thrombosis and platelet aggregation. | ||
| 008101 | B6.129S6(FVB)-Ptgs2tm1.1Fun/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Female homozygotes are not fertile. The protein gene product does not have cyclooxygenase activity while the peroxidase activity is normal as measured by LPS induction of macrophages derived from mutant mice. Mutant mice are more sensitive to collagen treatment resulting in reduction of platelet numbers (indicating enhanced thrombogenesis) and exhibit a higher frequency of sudden death due to thromboxane receptor agonist treatment. No prolonged bleeding time from LPS administration is observed. Prostaglandin E metabolite levels are diminished in urine. Three month old mutant mice have elevated systolic blood pressure (measured by the tail cuff method). Homozygotes exhibit undersize, pale kidneys with atrophic cortices, interstitial inflammation, hypoplastic glomeruli and glomerulosclerosis.
This mutant mouse strain may be useful in studies of
..... For more information please see the full descriiption on the strain data sheet | ||
| 002830 | B6.129P2-Plgtm1Jld/J | Repository-Cryopreserved |
| Mice homozygous for the Plgtm1 targeted mutation are viable and fertile. They show a progressive multi-organ pathology and die around 6 months of age. The pathology is characterized by wasting, rectal prolapse, impaired skin wound healing, gastointestinal ulceration, and thrombosis. No details of mammary gland morphology have been provided. | ||
| 006184 | B6.129P2-Tbxas1tm1Swl/J | Repository-Cryopreserved |
| Homozygotes are viable and fertile with no gross physical or behavioral abnormalities. Northern blot show absence of a full length transcript in homozygous spleen and thymus. Homozygous mice exhibit prolonged bleeding time, defective platelet aggregation, and are protected from arachidonic acid induced-shock. These mice may be useful in studies of vascular biology, including hemostasis and thrombosis, as well as human TXAS-deficiency. | ||
| 004371 | B6.129S2(D2)-Vtntm1Dgi/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 (protein) was immunodetected. Serum from mutant mice has no plasma plasminogen activator inhibitor 1 (PAI-1) binding capacity and can not support cell spreading on tissue culture plastic surface. Thrombosis rate after arterial injury is enhanced and angiogenesis in response to tissue injury is decreased in mutant mice. This mutant mouse strain represents a model that may be useful in studies of the in vivo function of vitronectin. | ||
| 004042 | B6.129S2-Alox12tm1Fun/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals. | ||
| 006182 | B6;129S6-Ptgs1tm1Fun/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. Reduced gene product (protein) levels, 10% of wildtype levels, are detected by Western blot analysis of nonstimulated peritoneal macrophages. RT-PCR analysis of stomach and kidney tissue reveals that gene product (mRNA) levels are reduced by 70-73%. This allele is a hypomorph. Mutant mice have a reduced response to arachidonic acid and capsaicin evoked ear inflammation and to carrageenan induced paw edema. Platelet aggregation is impaired as indicated by resistance to arachidonic acid induced thrombosis in vivo, and failure to aggregate in response to arachidonic acid in vitro. Mutant mice exhibit lengthened bleeding time. This mutant mouse strain may be useful in studies related to inflammatory immune response and thrombosis. | ||
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