A new role for Bcl-3 in the regulation of integrin αIIbβ3-dependent platelet clot contraction. Clot contraction mediated by binding of polymerized fibrin to activated αIIbβ3 is inhibited in Bcl-3–deficient mice and enhanced in Bcl-3–overexpressing cell lines. The anticancer drug, rapamycin, acting at mammalian target of rapamycin (mTOR) impairs de novo synthesis of Bcl-3 in human platelets and also blocks clot contraction.
