Protein kinase B (AKT) upregulation and Thy-1-α v β 3  integrin-induced phosphorylation of Connexin43 by activated AKT in astrogliosis.

Here, we identify changes in the PI3K/AKT molecular signaling network and show how they participate in astrogliosis by regulating the HC protein Cx43. Moreover, because HC opening and ATP release are important in astrocyte reactivity, the phosphorylation of Cx43 by AKT and the associated increase in ATP release identify a potential therapeutic window of opportunity to limit the adverse effects of astrogliosis.