Cytosolic sialidase (neuraminidase 2; Neu2) is an enzyme whose expression increases during myoblast differentiation. Here we show that insulin-like growth factor 1 (IGF1)-induced hypertrophy of myoblasts notably increa-ses Neu2 synthesis by activation of the phosphatidylinositol 3-kinase/AKT/ mammalian target of rapamycin (P13K/AKT/mTOR) pathway, whereas the proliferative effect mediated by activation of the extracellular regulated kinase 1⁄2 (ERK1⁄2) pathway negatively contributed to Neu2 activity
