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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: PLPP/CIN-mediated NF2 S10 dephosphorylation distinctly regulates kainate-induced seizure susceptibility and neuronal death through PAK1-NF-κB-COX-2-PTGES2 signaling pathway

Fig. 2

Effects of PLPP/CIN overexpression on phosphorylations of NF2 and PAK1 following KA injection. PLPP/CIN overexpression delays seizure on-set and increases its intensity in response to KA, which are which are reversed by its deletion. Two hours after KA injection, PLPP/CIN overexpression reduces NF2 S10 phosphorylation in a coupled with enhanced PAK1 S204 phosphorylation. a Representative EEG (upper panels) and frequency-power spectral temporal mans (lower panels) in response to KA in PLPP/CIN+/+, PLPP/CINTg and PLPP/CIN−/− mice. bd Quantitative analyses of the latency of seizure on-set, total EEG power and behavioral seizure severity in response to KA (*p < 0.05 vs. WT mice; n = 7, respectively). e Representative Western blot data of phosphorylations of NF2 and PAK1 in the whole hippocampus. fh Quantifications of PLPP/CIN expression, NF2 S10 and PAK1 S204 phosphorylations based on Western blot data (*p < 0.05 vs. WT animals and #p < 0.05 vs. control animals with Newman-Keuls post-hoc test, n = 7, respectively). (ij) Linear regression analyses between NF2 S10 and PAK1 S204 phosphorylations in WT and PLPP/CINTg mice

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