ArticleTranslational stroke research2020
PSD-93 Interacts with SynGAP and Promotes SynGAP Ubiquitination and Ischemic Brain Injury in Mice.
Article in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Differences in Src phosphorylation of PSD-93 and PSD-95 drive differences in scaffolding activity.Protein science : a publication of the Protein Society · 2026Article
- USP16 S-nitrosylation aggravates coronary microembolization-induced myocardial injury via repressing KDM1A-mediated glutathione homeostasis.Nature communications · 2025Article
- Post-ischemic ubiquitination at the postsynaptic density reversibly influences the activity of ischemia-relevant kinases.Communications biology · 2024Article
- Activity-Dependent Stabilization of Nascent Dendritic Spines Requires Nonenzymatic CaMKIIα Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Synaptic proteomics decode novel molecular landscape in the brain.Frontiers in molecular neuroscience · 2024Review
- Blocking postsynaptic density-93 binding to C-X3-C motif chemokine ligand 1 promotes microglial phenotypic transformation during acute ischemic stroke.Neural regeneration research · 2023Article
- Rho-Kinase/ROCK Phosphorylates PSD-93 Downstream of NMDARs to Orchestrate Synaptic Plasticity.International journal of molecular sciences · 2022Article
- Kynurenine/Aryl Hydrocarbon Receptor Modulates Mitochondria-Mediated Oxidative Stress and Neuronal Apoptosis in Experimental Intracerebral Hemorrhage.Antioxidants & redox signaling · 2022Article
- Excitatory Synaptic Transmission in Ischemic Stroke: A New Outlet for Classical Neuroprotective Strategies.International journal of molecular sciences · 2022Review
- Old but Still Hot Target, Glutamate-Mediated Neurotoxicity in Stroke.Translational stroke research · 2022Article
- Proteomics and weighted gene correlated network analysis reveal glutamatergic synapse signaling in diazepam treatment of alcohol withdrawal.Frontiers in pharmacology · 2022Article
- NOS1AP is a novel molecular target and critical factor in TDP-43 pathology.Brain communications · 2022Article
- Zinc provides neuroprotection by regulating NLRP3 inflammasome through autophagy and ubiquitination in a spinal contusion injury model.CNS neuroscience & therapeutics · 2021Article
- Proteomic insights into synaptic signaling in the brain: the past, present and future.Molecular brain · 2021Review
- Cyfip1 Regulates SynGAP1 at Hippocampal Synapses.Frontiers in synaptic neuroscience · 2020Article
- TMEM16F Aggravates Neuronal Loss by Mediating Microglial Phagocytosis of Neurons in a Rat Experimental Cerebral Ischemia and Reperfusion Model.Frontiers in immunology · 2020Article
- Resting-state EEG associated with clinical measures to predict upper limb motor recovery of subacute stroke.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Postsynaptic density protein-93 (PSD-93) plays an important role in ischemic brain injury through N-methyl-D-aspartate receptor (NMDAR)-triggered neurotoxicity. GTPase-activating protein for Ras (SynGAP) is a GAP specifically expressed in the central nervous system to regulate nerve development and synaptic plasticity. However, the link between PSD-93 and SynGAP and their role in ischemic brain injury remain elusive. Here, we showed that PSD-93 interacted with SynGAP and mediated SynGAP ubiquitination and degradation following ischemic brain injury. Proteasome inhibitor MG-132 could reverse the decrease of SynGAP protein level in wild-type mice following cerebral ischemia reperfusion through inhibiting SynGAP ubiquitination. Furthermore, NMDA receptor inhibitor MK801 could increase SynGAP protein level in wild-type mice following cerebral ischemia reperfusion. However, in PSD-93 knockout mice, MG-132 or NMDAR inhibitor had no significant effect on SynGAP expression. Both MG-132 and PSD-93 knockout reduced infarct volume and improved neurological deficit in mice at different time points after cerebral ischemia reperfusion. Furthermore, we identified that 670-685 amino acid sequence of SynGAP was essential to the binding of SynGAP to PSD-93, and designed a fusion peptide Tat-SynGAP (670-685aa) that could attenuate ischemic brain damage in wild-type mice. In conclusion, we provide the first evidence that PSD-93 directly interacts with SynGAP and mediates its ubiquitination and degradation to aggravate ischemic brain damage. Tat-SynGAP (670-685aa) may be considered as a candidate for treatment of acute ischemic stroke.
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