ArticleProceedings of the National Academy of Sciences of the United States of America2014
Sorting Nexin 27 regulates basal and activity-dependent trafficking of AMPARs.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 88 citations in OpenAlex.
- Retromer-targeted therapy for neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Comprehensive High-Depth Proteomic Analysis of Plasma Extracellular Vesicle-Containing Preparations in CDKL5 Deficiency Disorder.Biomedicines · 2026Article
- Novel Variants Identified in Families With SNX27 -Related Neurodevelopmental Disorder, Aiding in Characterizing Its Genotypic and Phenotypic Spectrum.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2026Article
- SNX6-mediated subunit-specific secretory trafficking of AMPA receptors regulates synaptic function and plasticity.Communications biology · 2025Article
- Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity.Neuroscience · 2025Article
- Membrane Trafficking in Psychiatric Disorders: Bridging Cellular Dysfunction and Mental Health-A Narrative Review.Molecular neurobiology · 2025Review
- The neuropathy-linked protein TECPR2 is a Rab5 effector that regulates cargo recycling from early endosomes.Nature communications · 2025Article
- Dynamic extracellular interactions with AMPA receptors.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity.The Journal of cell biology · 2025Article
- The schizophrenia risk gene C4 induces pathological synaptic loss by impairing AMPAR trafficking.Molecular psychiatry · 2025Article
- Tumor suppressor p53 modulates activity-dependent synapse strengthening, autism-like behavior and hippocampus-dependent learning.Molecular psychiatry · 2023Article
- Recruitment of the SNX17-Retriever recycling pathway regulates synaptic function and plasticity.The Journal of cell biology · 2023Article
- Kaixin-San improves Aβ-induced synaptic plasticity inhibition by affecting the expression of regulation proteins associated with postsynaptic AMPAR expression.Frontiers in pharmacology · 2023Article
- Review
- SNX27-Retromer directly binds ESCPE-1 to transfer cargo proteins during endosomal recycling.PLoS biology · 2022Article
- Article
- Glutamatergic Synapse Dysfunction inFrontiers in molecular neuroscience · 2022Article
- Retromer dependent changes in cellular homeostasis and Parkinson's disease.Essays in biochemistry · 2021Review
- Infantile spasms-linked Nedd4-2 mediates hippocampal plasticity and learning via cofilin signaling.EMBO reports · 2021Article
- Sorting Out Sorting Nexins Functions in the Nervous System in Health and Disease.Molecular neurobiology · 2021Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Activity-dependent changes in synaptic strength have long been postulated as cellular correlates of learning and memory. Long-term potentiation (LTP), a well characterized form of synaptic plasticity, is often expressed as an increase in the number of postsynaptic AMPA-type glutamate receptors (AMPARs). Although the precise molecular mechanisms governing LTP remain elusive, this study identifies one member of the sorting nexin family, Sorting Nexin 27 (SNX27), as a critical component in this process. The ability of sorting nexins to bind specific phospholipids as well as their propensity to form protein-protein complexes, points to a role for these proteins in membrane trafficking and protein sorting. Here, we demonstrate that SNX27 binds to AMPARs, and that this interaction is regulated in an activity-dependent manner. Furthermore, we provide evidence that SNX27 is synaptically enriched and its level of expression regulates targeting of AMPARs to the neuronal surface. Loss of SNX27 abolishes recruitment of surface AMPARs during chemical LTP. Collectively, our data suggest a role for SNX27 in modulating synaptic plasticity through regulated interaction with AMPARs.
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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.