These F2r knock-out mice exhibit early mortality and may be useful in applications to develop therapeutics that will selectively block thrombin's different cellular actions.
Dr. Shaun Coughlin, U. of California at San Francisco
Thrombin activates platelets, endothelial cells, leukocytes and mesenchymal cells at sites of vascular injury. Disruption of the thrombin receptor in these F2r knock-out mice causes about half of the homozygotes to die at around embryonic day 9-10. Platelets from surviving homozygotes respond to thrombin while fibroblasts from the same mice are unable to respond to thrombin.
|Allele Name||targeted mutation 1, Andrew J Connolly|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Par1-; PAR-1-; Par1-; tr-|
|Gene Symbol and Name||F2r, coagulation factor II (thrombin) receptor|
|Strain of Origin||129S4/SvJae|
|Molecular Note||A neomycin resistance cassette replaced sequences in exon 2 encoding transmembrane domains 1-7. Northern blot analysis on RNA derived from E12 embryos and from embryonic fibroblasts demonstrated that no detectable transcript was produced from this allele. Furthermore, transcripts from this allele were not detected in various tissues of adult homozygous mice (data not shown).|
|Mutations Made By|| |
Dr. Andrew Connolly, Palo Alto Medical Foundation
Homozygous siblings may be bred. The litter size is reported to be about half of that normally expected from C57BL/6 mice. The expected coat color is black.
When using the tr- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002862 in your Materials and Methods section.