These Plaur knock-out mice exhibit no overt phenotypic abnormalities with no compromise in fertility, development, or hemostasis.
Dr. Thomas Bugge, NIH/NIDCR
Homozygous mice are born and survive to adulthood with no overt phenotypic abnormalities. No Plaur gene product (protein) is detected. In addition, activated peritoneal macrophages collected from homozygous mice fail to promote plasminogen activation in vitro. The loss of the receptor also results in a redistribution of uPA in some tissues but has no impact on pro-PLAU activation in the urogenital tract. Thus, in the absence of other challenging factors such as infection, injury, or other functional deficits, PLAUR deficiency does not compromise fertility, development, or hemostasis. These mice provide a means to test the proposed function of PLAU/PLAUR in wound repair, atherogenesis, and tumor cell invasion in vivo.
This mutation was generated by replacing exon 3 with a vector containing Hprt. The 129P2-derived E14TG2a ES cell line was used.
|Allele Name||targeted mutation 1, Jay L Degen|
|Allele Type||Targeted (Null/Knockout)|
|Allele Synonym(s)||Plaurtm1; uPAR-|
|Gene Symbol and Name||Plaur, plasminogen activator, urokinase receptor|
|Strain of Origin||129P2/OlaHsd|
|Molecular Note||Exon 3, encoding the second half of the amino-terminal uPA binding domain, was replaced by an HPRT minigene.|
Homozygotes are viable and fertile. The expected coat color is black.
When using the uPAR- mouse strain in a publication, please cite the originating article(s) and include JAX stock #002829 in your Materials and Methods section.