Figure 7
Figure 7. Model depicting the functional role of PKC-θ downstream of GPVI and PAR activation in platelets. Collagen and CRP act through GPVI, whereas thrombin, SFLLRN (PAR1), and AYPGKF (PAR4) act via PARs and cause activation of the Gq/PLC pathways. PLC activation leads to generation of IP3, which mobilizes calcium from intracellular stores. Increased DAG leads to the translocation to the membrane and subsequent phosphorylation of the threonine 538 residues on PKC-θ. Activated PKC-θ has a significant role in granule secretion via mediating syntaxin-4 phosphorylation and thromboxane generation via regulating ERK phosphorylation. Furthermore, PKC-θ is involved in both inside-out and outside-in αIIbβ3 signaling pathways.

Model depicting the functional role of PKC-θ downstream of GPVI and PAR activation in platelets. Collagen and CRP act through GPVI, whereas thrombin, SFLLRN (PAR1), and AYPGKF (PAR4) act via PARs and cause activation of the Gq/PLC pathways. PLC activation leads to generation of IP3, which mobilizes calcium from intracellular stores. Increased DAG leads to the translocation to the membrane and subsequent phosphorylation of the threonine 538 residues on PKC-θ. Activated PKC-θ has a significant role in granule secretion via mediating syntaxin-4 phosphorylation and thromboxane generation via regulating ERK phosphorylation. Furthermore, PKC-θ is involved in both inside-out and outside-in αIIbβ3 signaling pathways.

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