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New discoveries with mice mutant in endothelial and platelet selectins.
Persistence of platelet thrombus formation in arterioles of mice lacking both von Willebrand factor and fibrinogen.
Control of thrombus embolization and fibronectin internalization by integrin alpha IIb beta 3 engagement of the fibrinogen gamma chain.
Formation of platelet strings and microthrombi in the presence of ADAMTS-13 inhibitor does not require P-selectin or beta3 integrin.
Glycoprotein Ibalpha and von Willebrand factor in primary platelet adhesion and thrombus formation: lessons from mutant mice.
ADAMTS13: a new link between thrombosis and inflammation.
Inflammation induces hemorrhage in thrombocytopenia.
Platelets adhere to and translocate on von Willebrand factor presented by endothelium in stimulated veins.
Platelet granule secretion continuously prevents intratumor hemorrhage.
Decreased plasma fibronectin leads to delayed thrombus growth in injured arterioles.
Increased thrombogenesis and embolus formation in mice lacking glycoprotein V.
PADGEM-dependent adhesion of platelets to monocytes and neutrophils is mediated by a lineage-specific carbohydrate, LNF III (CD15).
Oxidative stress activates ADAM17/TACE and induces its target receptor shedding in platelets in a p38-dependent fashion.
PADGEM protein: a receptor that mediates the interaction of activated platelets with neutrophils and monocytes.
The role of platelet adhesion receptor GPIbalpha far exceeds that of its main ligand, von Willebrand factor, in arterial thrombosis.
Platelets and platelet adhesion support angiogenesis while preventing excessive hemorrhage.
Systemic antithrombotic effects of ADAMTS13.
Plasma fibronectin promotes thrombus growth and stability in injured arterioles.
von Willebrand factor-mediated platelet adhesion is critical for deep vein thrombosis in mouse models.
ARC15105 is a potent antagonist of von Willebrand factor mediated platelet activation and adhesion.