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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: J Neurochem. 2019 Mar 15;149(1):98–110. doi: 10.1111/jnc.14668

Figure 8. Summary.

Figure 8.

HIV-1 Tat-dependent increases in [Ca2+]i activate both GSK3β (by dephosphorylating p-GSK3β at S9) and CaMKIIβ (by phosphorylating CaMKIIβ at T287). In mature OLs, large amounts of activated, cytoplasmic CaMKIIβ inhibit GSK3β (┴), which protects OLs from death. Conversely, in immature OLs, higher levels of activated GSK3β are present. The low levels of activated CaMKIIβ, which are preferentially distributed within OL cellular processes but not the cell body (┴), are inadequate to sufficiently inhibit GSK3β activation. Overactivation of GSK3β triggers signaling events leading to immature OL death.