| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008104 | B6.129(FVB)-Ptgs2tm2.1(Ptgs1)Fun/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 have a longer period between successive pregnancies and reduced litter sizes. Ptgs1 gene product (protein), COX1, is increased approximately 5 fold in LPS-stimulated macrophages from homozygotes. Prostacyclin metabolite level in urine is reduced by 55% when compared to wildtype controls. No increase in prostaglandin-glycerol in mutant macrophages after LPS challenge is observed. Homozygotes exhibit reduced bradykinin-induced vasculature permeability and at 6 months of age have enlarged glomeruli due to increased inflammatory infiltrate. By 5 months of age, mutant mice develop chronic peritonitis and progressive renal cortex deterioration. This mutant mouse strain may be useful in studies of prostaglandin synthesis and inflammation. | ||
| 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 phenotype on the strain data sheet | ||
| 002476 | B6;129S-Ptgs2tm1Jed/J | Cryopreserved - Ready for recovery |
| Mice homozygous for the Ptgs2tm1Jed targeted mutation exhibit significant preweaning loss of homozygotes (original publication reports 30-40%). Homozygous mutant mice show polydipsia and polyuria due to a defect in renal development. Cardiac fibrosis is evident in approximately 50% of the mice. PTGS2 deficient mice do not show altered inflammatory responses to in several tests of paw and ear edema; however, cytoxicity of hepatic cells induced by endotoxin was strikingly mitigated in these homozygotes. Female homozygotes are infertile with defects in ovulation, fertilization, implantation, and decidualization. | ||
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