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. 2017 Sep 20;10:295. doi: 10.3389/fnmol.2017.00295

Figure 4.

Figure 4

Impaired Akt-GSK3β signaling in Spin90-KO neurons is due to Akt-SPIN90 interaction. (A) DIV21 WT hippocampal neurons were treated with or without cLTD and lysates were harvested for immunoprecipitation with anti-SPIN90 antibody. SPIN90 interaction with pSer473-Akt, pan-Akt and GSK3β were assessed. (B) HeLa cells were harvested and immunoprecipitated with anti-SPIN90 antibody. Akt and SPIN90 binding was assessed. (C) Dose-dependent overexpression of GFP-SPIN90 in HeLa cells followed by immunoprecipitation with either pSer473-Akt, pSer9-GSK3β and GFP(SPIN90). pSer9-GSK3β activity was measured in vitro by a decrease in phosphorylation levels as dose of GFP-SPIN90 transfection reached from 5 ng to 20 ng. Data are expressed as mean ± SEM (*p < 0.05; n.s., non-significant).