Activation of protein synthesis in cardiomyocytes by the hypertrophic agent phenylephrine requires the activation of ERK and involves phosphorylation of tuberous sclerosis complex 2 (TSC2)

Insulin activates protein synthesis by the PI3K pathway, which involves the activation of PKB/Akt. However, the effects of PE are mediated through the classical MAPK pathway and results presented in this study indicate that ERK1/2 activity is required to activate protein synthesis and mTOR signalling. It is probable that a kinase downstream of ERK, such as p90RSK, phosphorylates TSC2, alleviating its inhibition of Rheb. This results in the activation of the mTOR pathway and S6 kinases and the inhibition of 4E-BP1 activity; both of these events activate protein synthesis. The Mnks also contribute to the activation of protein synthesis by PE, probably through the phosphorylation of eIF4E and perhaps of other substrates.

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Activation of protein synthesis in cardiomyocytes by the hypertrophic agent phenylephrine requires the activation of ERK and involves phosphorylation of tuberous sclerosis complex 2 (TSC2). (2005) Mark Rolfe, et al. Biochem J. 2005 Jun 15;388(Pt 3):973-984. Figure: F8. All organisms Drosophila melanogaster Homo sapiens

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