The study investigates how PYK2 nuclear translocation regulates neuronal responses to glutamate and contributes to neurotoxicity during epilepsy. PYK2 interacts with MBD2 and influences chromatin modifications and transcriptional responses in hippocampal neurons.
PYK2 promoted glutamate-induced nuclear localization of MBD2 and influenced chromatin modifications and neuronal gene expression. PYK2 deficiency reduced glutamate-induced neuronal death and decreased aberrant synaptic sprouting and CA3 neuronal death following pilocarpine-induced status epilepticus.
Ptk2b^flox/flox conditional Knockout mouse — genOway-developed, generated by flanking exons 15b–18 with LoxP sites. For this study, the floxed line was crossed with a ubiquitous Cre deleter to generate Ptk2b^-/- mice lacking PYK2 in all cell types. The deletion disrupts the protein kinase domain and prevents PYK2 expression.
Epilepsy, status epilepticus, neurotoxicity, neuronal cell death, hippocampus, glutamate signaling, synaptic plasticity, chromatin regulation
Ptk2b conditional Knockout, floxed exons 15b–18, LoxP sites, homologous recombination, Cre-mediated deletion, pilocarpine-induced status epilepticus, hippocampal neuron culture
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