Kainate-induced Epilepsy: Dephosphorylation of NF2 (Merlin at Ser 10) and PAK1 activation癲癇（てんかん）を巡って、NF2 (Merlin) とPAKが （正反対に）関与している！

Epilepsy has been known to be among PAK1-dependent neuronal diseases such as AD (Alzheimer) and PD (Parkinson).
According to a recent (2023) article by a Korean group led by Prof. Tae-Cheon Kang in South Korea, Kainate induces epilepsy in mice, and as a consequence, NF2 (Merlin) is dephosphorylated at Ser 10, and PAK1 is auto-phosphorylated at Ser 204, leading to its activation, through PLPP/CIN (Pyridoxal-5'-phosphate phosphatase/chronophin) signalling pathway, which causes the de-phosphorylation of NF2 at Ser 10．
Thus, it is most likely that NF2 phosphorylated at Ser 10 is a “potent” inhibitor of PAK1.
Furthermore, Ser 204 of PAK1 is the C-terminus of “PAK18” which is essential for binding to the SH3 domain of PIX . Thus, there is a high possibility that this “auto-phosphorylated” form (or Glu 204 mutant) of PAK1 would bind more tightly to PIX for its further activation.
Reference: JE Kim, DS Lee, TH Kim, et al (2023). PLPP/CIN-mediated NF2 S10 dephosphorylation distinctly regulates kainate-induced seizure susceptibility and neuronal death through PAK1-NF-κB-COX-2-PTGES2 signaling pathway。J Neuroinflammation.;　20:　99.
結論: ＰＡＫ　は　癲癇　（てんかん）　を助長し、NF2 (Merlin)　は（逆に）抑制している！
従って、癲癇は "PAK遮断剤" で治療しうるが、NF2患者には、癲癇が発生する可能性あり！