Paradoxical Activation of c-Src as a Drug-Resistant Mechanism

Abstract

Highlights d Binding of ATP-competitive inhibitors to c-Src relieves its auto-inhibition d Inhibitor-bound c-Src in an open state forms a complex with FAK d Reduction of inhibitor concentration activates c-Src and the FAK-Grb2-Erk cascade d Inhibitors activate drug-resistant c-Src mutant and the cascade