The urokinase-type plasminogen activator receptor (uPAR) gene was disrupted in mice in
order to explore the role of cell surface-associated plasminogen activation in development
and hemostasis. Homozygous, uPAR−/− mice were born and survived to adulthood with no
overt phenotypic abnormalities. There was no indication of loss of fetal animals based on the
Mendelian pattern of transmission of the mutant uPAR gene. uPAR−/− mice carried no
detectable uPAR in lung, spleen, and other tissues when measured both immunologically by …