Platelet activation on the injured vessel wall is induced by multiple signaling pathways and leads to extensive cytoskeletal rearrangements that are crucial for conversion from discoid to spheric shape, granule secretion, spreading and, at later time points clot retraction. Many of these processes are controlled by proteins of the Rho family of small GTPases, like RhoA, Rac1, and Cdc42 and their downstream effector molecules such as the WiskottAldrich syndrome proteins, formins and p21-activated kinases. In addition, cytoskeletal adaptor proteins such Platelets are small anucleated cell fragments derived from the cytoplasm of bone marrow megakaryocytes. At sites of vascular injury, platelets adhere and aggregate on the exposed subendothelial extracellular matrix and thereby form a plug that seals the wound. This process is essential for normal Etidronate hemostasis, but in diseased vessels it may lead to pathological thrombus formation and infarction of vital organs. Platelet activation on the injured vessel wall is induced by multiple signaling pathways and leads to extensive cytoskeletal rearrangements that are crucial for conversion from discoid to spheric shape, granule secretion, spreading and, at later time points clot retraction. Many of these processes are controlled by proteins of the Rho family of small GTPases, like RhoA, Rac1, and Cdc42 and their downstream effector molecules such as the WiskottAldrich syndrome proteins, formins and p21-activated kinases. In addition, cytoskeletal adaptor proteins such as talin1 and kindlin-3 are crucial for platelet function by linking the actin cytoskeleton to integrins thereby enabling their shift from low to high affinity for their ligands and thus stable platelet adhesion and aggregation. Elevation of cytosolic Ca2+ is a central step during platelet activation. It is induced through the release of Ca2+ from intracellular stores and subsequent Ca2+ entry through the plasma membrane, a process called store-operated Ca2+ entry, which represents the major influx pathway of extracellular Ca2+ in platelets. This process is regulated by the endoplasmic reticulum membrane-bound protein stromal interaction molecule 1 that senses Ca2+ depletion in intracellular stores via its EF hand motifs and Orai1, the major SOCE Butylparaben channel in the plasma membrane.