Skip to main content
. Author manuscript; available in PMC: 2015 Nov 30.
Published in final edited form as: Prog Mol Biol Transl Sci. 2015 Jan 30;131:409–434. doi: 10.1016/bs.pmbts.2014.11.010

Figure 2. Translational control pathways involved in hyperalgesic priming.

Figure 2

mTORC1 phosphorylates 4EBPs, negative regulators of eIF4F formation. This results in its dissociation from eIF4E, allowing the binding of eIF4E to eIF4G. Phosphorylation of eIF4E (via ERK/MNK1/2) or eIF4G (via mTORC1) enhances the formation of the eIF4F complex, promoting translation. Phosphorylation of CPEB by CamKIIα enhances translation efficiency by increasing the length of the poly A tail in mRNAs containing a CPE sequence. Taken together, eIF4F complex formation enhances cap-dependent translation, which is necessary for the induction of priming via translational control of gene expression in sensory afferents.