ArticleMolecular neurobiology2025
DeSUMOylation of Spastin Enhances AMPA Receptor Recycling and Synaptic Plasticity via IST1-Dependent Endosomal Sorting.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Gadd45α silencing alleviates cerebral ischemia-reperfusion injury by suppressing FOXO1 signaling.Scientific reports · 2026Article
- miR-132 and Its Exosomal Form in Alzheimer's Disease: Linking Epigenetic Regulation to Neurodegeneration.Molecular neurobiology · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
The trafficking of AMPA receptors (AMPARs), including internalization, recycling, and membrane reinsertion, is critical for maintaining synaptic plasticity. Our previous work showed that the microtubule-severing protein Spastin regulates AMPAR surface expression, but the underlying mechanisms remain to be fully elucidated. Here, we demonstrate that deSUMOylated Spastin (Spastin-K427R) enhanced GluA1 recycling and membrane reinsertion and is associated with dendritic spine maturation and excitatory synaptic transmission. Overexpression of Spastin-K427R increased surface GluA1 expression, spine density, and miniature excitatory synaptic currents (mEPSC) amplitude and frequency, with stronger effects than wild-type Spastin. While wild-type Spastin directed GluA1 to both recycling and late endosomes, Spastin-K427R preferentially promoted its localization to Syntaxin 13-associated recycling endosomes and reduced LAMP1-associated degradation. We further identified IST1, an ESCRT-III complex component, as a key mediator of Spastin's effect. Co-overexpression of IST1 with Spastin enhanced synaptic transmission and spine maturation, whereas IST1 knockdown reduced GluA1 surface levels and abolished Spastin's effects. Notably, Spastin-K427R exhibited enhanced binding to IST1 than wild-type Spastin. These findings reveal a post-translational mechanism by which the deSUMOylation of Spastin facilitates IST1-dependent AMPAR recycling, contributing to synaptic plasticity regulation.
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Registered trials
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 Socratic graph.