B6;129S-Ptgs2^tm1Jed/J

Stock number: 002476
Product name: COX-2-
Research areas: Developmental Biology Research, Immunology, Inflammation and Autoimmunity Research, Internal/Organ Research

Description

These Ptgs2 knock-out mice exhibit reduced viability with cardiac fibrosis and renal alterations characteristic of renal dysplasia. They are suitable for use in applications related to the study of mediators of inflammation.

Detailed description

Mice homozygous for the Ptgs2^tm1Jed 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.

Development

This strain was developed in the lab of Dr. Joe Dinchuk at Glenolden Laboratory, Dupont Merck Pharmaceutical Company. The transcription/translation start sites for the endogenous Ptgs2 gene have been removed. The 129S7-derived AB2.1 ES cell line was used. At The Jackson Laboratory, these mice were bred with B6129SF1/J (Stock No. 101043) to maintain the colony.

Allele

Symbol: Ptgs2^tm1Jed
Name: targeted mutation 1, Joe E Dinchuk
MGI accession ID: MGI:1857239
Generation method: Targeted
Attributes: Null/Knockout
Marker symbol: Ptgs2
Marker name: prostaglandin-endoperoxide synthase 2
Chromosome: 1
Strain of origin: 129S7/SvEvBrd-Hprt^b-m2
Molecular note: A 1.8 kb genomic fragment containing exon 1 and the transcription and translation start sites was replaced with a neomycin selection cassette. Northern blot analysis on RNA derived from embryonic fibroblasts derived from homozygous embryos demonstrated that no detectable transcript was produced from this allele.