Figure 7.
Figure 7. Model depicting the mechanism and the function of tyrosine phosphorylation of PKCδ following PAR stimulation in human platelets. Thrombin acts through PAR1 and PAR4 receptors and causes activation of the Gq/PLC pathways. PLC activation leads to generation of IP3, which mobilizes intracellular calcium. Increase in calcium directly or indirectly leads to increase in Src activity and subsequently tyrosine phosphorylation of PKCδ. DAG leads to phosphorylation of the threonine 505 residues, which is required for the dense granule secretion. Tyrosine phosphorylation of the Y311 residue mediated through the Src family PTKs is required for thromboxane A2 generation downstream of PAR agonists.

Model depicting the mechanism and the function of tyrosine phosphorylation of PKCδ following PAR stimulation in human platelets. Thrombin acts through PAR1 and PAR4 receptors and causes activation of the Gq/PLC pathways. PLC activation leads to generation of IP3, which mobilizes intracellular calcium. Increase in calcium directly or indirectly leads to increase in Src activity and subsequently tyrosine phosphorylation of PKCδ. DAG leads to phosphorylation of the threonine 505 residues, which is required for the dense granule secretion. Tyrosine phosphorylation of the Y311 residue mediated through the Src family PTKs is required for thromboxane A2 generation downstream of PAR agonists.

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