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. 2018 Nov 28;39:377–387. doi: 10.1016/j.ebiom.2018.11.040

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© 2018 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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Fig. 3 — GSK3 inhibitory phosphorylation correlates with GluA1 (S845) phosphorylation in temporal lobe epilepsy and focal cortical dysplasia samples. (a,b) Western blot was used to determine the levels P-GluA1 (S845), P-GluA1 (S831), GluA1, P-GSK3α (S21), P-GSK3β (S9), GSK3α and GSK3β in samples from patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS) and in clinical malformations of cortical development (FCD and hippocampi adjacent to FCD). Tubulin is shown as a loading control. (c) Correlation analysis of P-GluA1 (S831)/GluA1 or P-GluA1 (S845)/GluA1 and P-GSK3β (S9)/GSK3β or P-GSK3α (S21)/GSK3α. The data were analyzed as Pearson and Spearman correlation coefficients (r).