After treating human platelets with thrombin, it was found that higher levels of USP15 and FKBP5 were expressed; manipulating USP15 levels affected FKBP5 stability and function.
In experiments with mice lacking USP15 in their platelets, it was shown that this knockdown led to longer bleeding times and reduced thrombus formation, highlighting USP15's important role in regulating blood clotting.