Figure 1 | Scientific Reports

Figure 1

From: mTOR-dependent alterations of Kv1.1 subunit expression in the neuronal subset-specific Pten knockout mouse model of cortical dysplasia with epilepsy

Figure 1

PI3K-Akt-mTOR signaling is hyperactivated in the hippocampus of NS-Pten KO mice. (A) Representative western blots from whole hippocampal homogenates from 6 week-old WT and NS-Pten KO mice probed with antibodies against Pten, p-S6 (S240/244; marker of mTORC1 activation), S6, p-AKT (S473; marker of mTORC2 activation), p-AKT (T308; marker of PI3K activation), AKT, and actin are shown. Full-length blots are presented in Supplemental Fig. 2. (B) Quantification of the western blots showed that Pten protein levels were significantly reduced while p-S6 (S240/244), p-AKT (S473), and p-AKT (T308) protein levels were significantly increased in NS-Pten KO compared to WT mice. n = 8 mice per group; *p < 0.05, ***p < 0.001 by Student’s t-test; errors bars are ± SEM. (C) Representative single optical sections of Pten and p-S6 (S240) co-immunostaining in 6 week-old WT and NS-Pten KO DG are shown. Arrows point to the areas that are enlarged in the insets. Arrowheads in the insets point to Pten-positive cells with basal p-S6 (S240) staining in WT DG and Pten-negative cells with elevated p-S6 (S240) staining in NS-Pten KO DG. (D) Quantification of Pten and p-S6 (S240) immunostaining intensity in the DG granule cell layer show significantly decreased Pten intensity and significantly increased p-S6 intensity in NS-Pten KO compared to WT mice. n = 3 mice per group. *p < 0.05 by Student’s t-test; errors bars are ± SEM. gcl, granule cell layer; ml, molecular layer.

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