Receptor tyrosine kinases transmit signals from outside the cell via the membrane into the cytosol. After activation by an external factor, the receptor monomers dimerize and phosphorylate each other’s intracellular domains. Cytosolic proteins bind to the phosphorylated domains and transmit the signal to other cytosolic proteins. In tumor cells, receptor tyrosine kinases can be dysregulated by various mechanisms, including increased levels of activating factors or mutation, amplification and overexpression of the corresponding receptor genes.

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