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A proposed mechanism for activated Ras-induced and ERK1/2- and PIN1-dependent FAK Y397 dephosphorylation by PTP-PEST. Activated Ras results in ERK1/2-dependent phosphorylation of PTP-PEST S571 and FAK S910 and subsequent recruitment of PIN1 for cis-trans isomerization of both PTP-PEST and FAK. This leads to increased interaction between PTP-PEST and FAK, dephosphorylation of FAK Y397, and enhanced tumor cell migration, invasion, and metastasis.
