ArticleNeuropharmacology2013
Nedd4 is a specific E3 ubiquitin ligase for the NMDA receptor subunit GluN2D.
Article in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Regulation of Synaptic NMDA Receptor Activity by Post-Translational Modifications.Neurochemical research · 2025Review
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- Rabphilin-3A undergoes phase separation to regulate GluN2A mobility and surface clustering.Nature communications · 2023Article
- Disruption of the Ubiquitin-Proteasome System and Elevated Endoplasmic Reticulum Stress in Epilepsy.Biomedicines · 2022Review
- Protein quality control ofFrontiers in cellular neuroscience · 2022Review
- Historical perspective and progress on protein ubiquitination at glutamatergic synapses.Neuropharmacology · 2021Review
- Regulation of the NMDA receptor by its cytoplasmic domains: (How) is the tail wagging the dog?Neuropharmacology · 2021Review
- Blocking the Spinal Fbxo3/CARM1/KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Proteomic insights into synaptic signaling in the brain: the past, present and future.Molecular brain · 2021Review
- Role of the Ubiquitin System in Chronic Pain.Frontiers in molecular neuroscience · 2021Review
- Evidence for an Interaction BetweenFrontiers in psychiatry · 2021Article
- Regulation of NMDA glutamate receptor functions by the GluN2 subunits.Journal of neurochemistry · 2020Review
- Transcriptome analysis of rat dorsal hippocampal CA1 after an early life seizure induced by kainic acid.Epilepsy research · 2020Article
- Article
- NMDA receptor C-terminal signaling in development, plasticity, and disease.F1000Research · 2019Review
- Protein Modifications with Ubiquitin as Response to Cerebral Ischemia-Reperfusion Injury.Translational stroke research · 2018Review
- Possible divergence of serum- and glucocorticoid-inducible kinase function in ischemic brain injury.Neural regeneration research · 2016Article
- Role of serum- and glucocorticoid-inducible kinases in stroke.Journal of neurochemistry · 2016Article
- Dynamic Regulation of N-Methyl-d-aspartate (NMDA) and α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid (AMPA) Receptors by Posttranslational Modifications.The Journal of biological chemistry · 2015Review
- Synaptotagmins interact with APP and promote Aβ generation.Molecular neurodegeneration · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
NMDA receptors are a family of glutamate-gated ion channels that regulate various CNS functions such as synaptic plasticity and learning. However hypo- or hyper-activation of NMDA receptors is critically involved in many neurological and psychiatric conditions such as pain, stroke, epilepsy, neurodegeneration, schizophrenia, and depression. Thus, it is important to identify mechanisms (such as by targeted ubiquitination) that regulate the levels of individual subtypes of NMDA receptors. In this study, we used a series of tagged, carboxy terminal constructs of GluN2D to identify associating proteins from rat brain. Of seven different GluN2D C-terminal fragments used as bait, only the construct containing amino acids 983-1097 associated with an E3 ubiquitin ligase, Nedd4. A direct interaction between GluN2D and Nedd4 was confirmed both in vivo and in vitro. This association is mediated by an interaction between GluN2D's C-terminal PPXY motif and the 2nd and 3rd WW domains of Nedd4. Of the four GluN2 subunits, Nedd4 directly interacted with GluN2D and also weakly with GluN2A. Nedd4 coexpression with GluN2D enhances GluN2D ubiquitination and reduces GluN1/GluN2D NMDA receptor responses. These results identify Nedd4 as a novel binding partner for GluN2D and suggest a mechanism for the regulation of NMDA receptors that contain GluN2D subunits through ubiquitination-dependent downregulation. This article is part of the Special Issue entitled 'Glutamate Receptor-Dependent Synaptic Plasticity'.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.