Fig. 3.
Fig. 3. Platelet activation, intracellular signaling, and secretion. / When a ligand or agonist such as thrombin interacts with its cognate receptor on the platelet membrane, phospholipase C is activated through a G-protein–dependent mechanism. Alternatively, when collagen interacts with platelets, phospholipase C is also activated but through other mechanisms (not shown). Phospholipase C cleaves PIP2to DAG, which activates protein kinase C. Phospholipase C also produces IP3, which releases Ca++ from the platelet dense tubular system. Increased intracellular Ca++ and protein kinase C work synergistically to induce platelet exocytosis. Protein kinase C phosphorylates secretory molecules such as PSP.

Platelet activation, intracellular signaling, and secretion.

When a ligand or agonist such as thrombin interacts with its cognate receptor on the platelet membrane, phospholipase C is activated through a G-protein–dependent mechanism. Alternatively, when collagen interacts with platelets, phospholipase C is also activated but through other mechanisms (not shown). Phospholipase C cleaves PIP2to DAG, which activates protein kinase C. Phospholipase C also produces IP3, which releases Ca++ from the platelet dense tubular system. Increased intracellular Ca++ and protein kinase C work synergistically to induce platelet exocytosis. Protein kinase C phosphorylates secretory molecules such as PSP.

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