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In KRAS-driven adenocarcinomas, CaM with pTyr99 acts by fully activating PI3Ka through binding of the pTyr99 to the two SH2 domains of PI3Ka. The CaM pTyr99 binding site acts as the RTK pYXXM motif, substituting for the missing RTK signal, thus stimulating the PI3Ka/Akt/mTOR pathway.
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