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Figure 7 | BMC Neuroscience

Figure 7

From: GT1b-induced neurotoxicity is mediated by the Akt/GSK-3/tau signaling pathway but not caspase-3 in mesencephalic dopaminergic neurons

Figure 7

Schematic drawing of Akt/GSK-3β/tau signaling. Akt is activated in response to ILK or PI3 Kinase signaling, and subsequent activation of Akt. Akt is activated in response to ILK or PI3 kinase signaling, and subsequent activation of Akt. Activated Akt phosphorylates GSK-3β at Ser 9, leading to GSK-3β inactivation. Akt inactivation by GT1b induces dephosphorylation of GSK-3β, leading to GSK-3β activation. GSK-3β activation results in aberrant tau phosphorylation, axon instability, and neuronal death. Although we did not provide direct evidence of whether GT1b neuroxocicity is mediated by ILK or PI3K signaling or both, participation of GT1b in inhibition of Akt upstream signals, such as ILK or PI3K, is predicted.

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