Dephosphorylation of Akt in C6 cells grown in serum-free conditions corresponds with redistribution of p85/PI3K to the nucleus.

摘要: Withdrawal of serum from cell cultures constitutes a useful model for the study mechanisms involved in regulation Akt function vitro. However, there have been several reports changes activity that are not fully explained by current phosphatidylinositol 3'-kinase (PI3K)/Akt signaling. We demonstrate expected loss phosphorylation C6 glioma cells cultured serum-free conditions, yet we also observed paradoxical increase PI3K-lipid kinase same cultures. These events corresponded with relocalization p85, regulatory subunit PI3K, to perinuclear region and local products. Treatment platelet-derived growth factor (PDGF) maintained association between p85 PDGF receptor during withdrawal restored production at plasma membrane. Although this protected dephosphorylation, it only slightly reversed cell-cycle arrest. effects were sensitive treatment epidermal factor, thus precluding generalized role factors. Our data suggest signaling, including may disrupt recruitment and/or anchoring an active p85(PI3K) complex membrane withdrawal, which could account concurrent function.