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Fig. 9 | Cell Communication and Signaling

Fig. 9

From: γ-Enolase enhances Trk endosomal trafficking and promotes neurite outgrowth in differentiated SH-SY5Y cells

Fig. 9

Model of Trk trafficking under γ-enolase-induced neurotrophic signalling. In differentiated SH-SY5Y cells, γ-enolase is translocated to the plasma membrane with γ1-syntrophin, where it associates with the intracellular domain of the Trk receptor. Treating differentiated SH-SY5Y cells with the biological active C-terminal peptide of γ-enolase (γ-Eno peptide) triggers Trk receptor internalisation by clathrin-mediated endocytosis, and thence its trafficking to late endosomes, which leads to Rap1 activation. As well as γ-Eno-peptide-mediated activation of the PI3-K/Akt and MAPK/ERK signalling pathways, these signals are required for γ-Eno-peptide-induced cell survival and neurite outgrowth

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Cell Communication and Signaling

ISSN: 1478-811X