Activating mutations in the Met receptor overcome the requirement for autophosphorylation of tyrosines crucial for wild type signaling.

Abstract excerpt

Mutations in Met have been identified in human cancer, and we have previously shown that these mutations deregulate the enzymatic activity of this tyrosine kinase receptor, thereby unleashing its oncogenic potential. Signal transduction via wild type Met has been shown to require the autophosphorylation of two tyrosine doublets; Y8,9 which functions to enhance enzymatic activity, and Y14,15 which provides docking...

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