Figure 1.

GAS6/TAMs in hemostasis. During damage, growth-arrest-specific 6 (GAS6) is secreted by endothelial cells and its signaling upregulates the expression of adhesion molecules (P-selectin, VCAM-1 and ICAM-1) in the endothelium (grey). Thus, platelets (yellow) and leukocytes (purple), such as neutrophils, are recruited to damaged tissue allowing their interaction with the vessel intima. Besides, activation of platelets leads to phosphatidylserine (PtdSer) exposure and interaction with vitamin K-dependent proteins (VKDPs), including TAM ligands. Pro-coagulant Gla-proteins trigger coagulation cascade activation, while TAM activation promotes platelet aggregation and stabilization of clots by phosphoinositide 3-kinase (PI3K)-dependent phosphorylation of β3 integrin increasing affinity to fibrinogen and other ligands.