ArticleJournal of neuroinflammation2023
PLPP/CIN-mediated NF2 S10 dephosphorylation distinctly regulates kainate-induced seizure susceptibility and neuronal death through PAK1-NF-κB-COX-2-PTGES2 signaling pathway.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- A Correlation between Inflammatory Factors and Epileptic Seizures: A Meta-analysis.Actas espanolas de psiquiatria · 2025Pooled it
- Pan-Cancer Analysis of the Immunomodulatory Roles and Prognostic Value of PDXP and Experimental Verification in SKCM.Cancer medicine · 2026Article
- Scutellarin Alleviates Neuronal Apoptosis After Ischemia and Hypoxia via the HIF-1α-CX3CR1 Axis.CNS neuroscience & therapeutics · 2026Article
- Development of pH-responsive gelatin/PVP nanogel by gamma radiation for controlled delivery of silibinin.Scientific reports · 2026Article
- Region-resolved proteomic map of the human brain: functional interconnections and neurological implications.Signal transduction and targeted therapy · 2026Article
- Compound Analysis and Mechanistic Exploration of Shen-Yan-Fang-Shuai Formula in Diabetic Kidney Disease: An UHPLC-MS/MS and Bioinformatics Study.Journal of diabetes research · 2026Article
- PAK1 Is Involved in Epileptogenesis by Regulating the Synaptic Plasticity of Hippocampal Neurons Through LIMK.Neurochemical research · 2025Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPyridoxal-5'-phosphate phosphatase/chronophin (PLPP/CIN) selectively dephosphorylates serine (S) 10 site on neurofibromin 2 (NF2, also known as merlin (moesin-ezrin-radixin-like protein) or schwannomin). p21-activated kinase 1 (PAK1) is a serine/threonine protein kinase, which is involved in synaptic activity and plasticity in neurons. NF2 and PAK1 reciprocally regulate each other in a positive feedback manner. Thus, the aim of the present study is to investigate the effects of PLPP/CIN-mediated NF2 S10 dephosphorylation on PAK1-related signaling pathways under physiological and neuroinflammatory conditions, which are largely unknown.
methodsAfter kainate (KA) injection in wild-type, PLPP/CIN
resultsPLPP/CIN overexpression increased PAK1 S204 autophosphorylation concomitant with the enhanced NF2 S10 dephosphorylation in hippocampal neurons under physiological condition. Following KA treatment, PLPP/CIN overexpression delayed the seizure on-set and accelerated PAK1 S204 phosphorylation, NF-κB p65 S276 phosphorylation, COX-2 upregulation and PTGES2 induction, which were ameliorated by PLPP/CIN deletion or IPA-3. Furthermore, IPA-3 pretreatment shortened the latency of seizure on-set without affecting seizure severity (intensity) and ameliorated CA3 neuronal death induced by KA.
conclusionsThese findings indicate that PLPP/CIN may regulate seizure susceptibility (the latency of seizure on-set) and CA3 neuronal death in response to KA through NF2-PAK1-NF-κB-COX-2-PTGES2 signaling pathway.
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