Table 1.

Conditions where GSK-3β facilitates apoptosis.

System or stimulus	Mechanism
C(2) Ceramide-associated damage	Inhibits the phosphorylation of AKT and ERK pathways and through the dephosphorylation of GSK-3β [51]. GSK-3β inhibitors have been shown to inhibit apoptosis through inhibiting dephosphorylation of AKT and GSK-3β [52].
LPS-mediated endotoxic shock	While specific apoptotic studies have not been performed, LPS has been shown to stabilize apoptotic signal-regulating kinase-1 (ASK-1), a serine-threonine kinase associated with stress-induced apoptosis [53].
Immune system	Regulates in apoptosis of activated T-Cells [54].
HIV-mediated neuronal damage	Inhibits NF-κB [55–57].
Neurodegenerative disease-related toxicity and oxidative stress	Neuronal or oligodendrocyte injury or toxicity (including prion peptide) is associated with increased activity of GSK-3β[51, 58–64].
	Negative regulators of GSK-3β are associated with increased survival factors [51, 58–64] and neuroprotection [9, 38].
ER stress	ER stress can lead to dephosphorylation of pGSK-3β(S9), leading to stress-induced apoptosis through activated caspase-3 [12–14, 26, 28].
Hypoxia/ischemia	Activates mitochondrial death pathway [35, 65–68].