ArticleEBioMedicine2019
Inhibition of Nwd1 activity attenuates neuronal hyperexcitability and GluN2B phosphorylation in the hippocampus.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
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- Quantitative Proteomic and Phosphoproteomic Analyses Reveal a Role of Death-Associated Protein Kinase 1 in Regulating Hippocampal Synapse.Molecular neurobiology · 2024Article
- Inhibition of ANXA2 activity attenuates epileptic susceptibility and GluA1 phosphorylation.CNS neuroscience & therapeutics · 2023Article
- LncRNA MALAT1 Targets miR-9-3p to Upregulate SAP97 in the Hippocampus of Mice with Vascular Dementia.Biochemical genetics · 2023Article
- Transcriptome Sequencing in the Preoptic Region of Rat Dams Reveals a Role of Androgen Receptor in the Control of Maternal Behavior.International journal of molecular sciences · 2021Article
- Roles of N-Methyl-D-Aspartate Receptors (NMDARs) in Epilepsy.Frontiers in molecular neuroscience · 2021Review
- Integrative Analysis of lncRNA and mRNA and Profiles in Postoperative Delirium Patients.Frontiers in aging neuroscience · 2021Article
- cGAS/STING Pathway Activation Contributes to Delayed Neurodegeneration in Neonatal Hypoxia-Ischemia Rat Model: Possible Involvement of LINE-1.Molecular neurobiology · 2020Article
- Nwd1 Regulates Neuronal Differentiation and Migration through Purinosome Formation in the Developing Cerebral Cortex.iScience · 2020Article
- Programmed Cell Deaths and Potential Crosstalk With Blood-Brain Barrier Dysfunction After Hemorrhagic Stroke.Frontiers in cellular neuroscience · 2020Article
- MiR-181b suppresses the progression of epilepsy by regulation of lncRNA ZNF883.American journal of translational research · 2020Article
- Blood-Based Biomarkers for Predictive Diagnosis of Cognitive Impairment in a Pakistani Population.Frontiers in aging neuroscience · 2020Article
- A RareFrontiers in genetics · 2020Article
- Brain delivery of a virus to block seizures helps mice get a silent NACHT.EBioMedicine · 2019Article
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNACHT and WD repeat domain-containing protein 1 (Nwd1) is a member of the innate immune protein subfamily. Nwd1 contributes to the androgen receptor signaling pathway and is involved in axonal growth. However, the mechanisms that underlie pathophysiological dysfunction in seizures remain unclear.
methodsBiochemical methods were used to assess Nwd1 expression and localization in a mouse model of kainic acid (KA)-induced acute seizures and temporal lobe epilepsy (TLE) patients. Electrophysiological recordings were used to measure the role of Nwd1 in regulating synaptic transmission and neuronal hyperexcitability in a model of magnesium-free-induced seizure in vitro. Behavioral experiments were performed, and seizure-induced pathological changes were evaluated in a KA-induced seizure model in vivo. GluN2B expression was measured and its correlation with Tyr1472-GluN2B phosphorylation was analyzed in primary hippocampal neurons.
findingsWe demonstrated high protein levels of Nwd1 in brain tissues obtained from mice with acute seizures and TLE patients. Silencing Nwd1 in mice using an adeno-associated virus (AAV) profoundly suppressed neuronal hyperexcitability and the occurrence of acute seizures, which may have been caused by reducing GluN2B-containing NMDA receptor-dependent glutamatergic synaptic transmission. Moreover, the decreased activation of Nwd1 reduced GluN2B expression and the phosphorylation of the GluN2B subunit at Tyr1472.
interpretationHere, we report a previously unrecognized but important role of Nwd1 in seizure models in vitro and in vivo, i.e., modulating the phosphorylation of the GluN2B subunit at Tyr1472 and regulating neuronal hyperexcitability. Meanwhile, our findings may provide a therapeutic strategy for the treatment of epilepsy or other hyperexcitability-related neurological disorders. FUND: The funders have not participated in the study design, data collection, data analysis, interpretation, or writing of the report.
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