Abstract
Under physiological conditions, circulating platelets are discoid in shape. On these platelets, the fibrinogen receptor (integrin αIIbβ3) is in a low-affinity state, unable to bind soluble fibrinogen (Fg). Activation by agonists such as ADP and thrombin leads to a change in the conformation of the integrin αIIbβ3 through a process known as inside-out signaling. This enables the integrin to bind soluble Fg, which initiates a cascade of events referred to as outside-in signaling. Outside-in signaling control processes such as platelet spreading and clot retraction by regulating small G-proteins such as RhoA, Rac and cdc42.