ArticleCell reports2018
PRRT2 Regulates Synaptic Fusion by Directly Modulating SNARE Complex Assembly.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- Article
- Proline-Rich Transmembrane Protein 2 Is Variably Expressed Across Excitatory and Inhibitory Neurons in Mouse Motor Circuits.The Journal of comparative neurology · 2026Article
- Identification of Copy Number Variations in Familial Hemiplegic Migraine Genes in Suspected Hemiplegic Migraine Patients.Biomedicines · 2026Article
- Clinical spectrum and treatment responses in.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Highly stable planar asymmetric suspended membranes for investigating protein dynamics and membrane fusion.Nature protocols · 2025Review
- Current Trends in Pediatric Migraine: Clinical Insights and Therapeutic Strategies.Brain sciences · 2025Review
- Loss of SynDIG4/PRRT1 alters distribution of AMPA receptors in Rab4- and Rab11-positive endosomes and impairs basal AMPA receptor recycling.Frontiers in pharmacology · 2025Article
- Proline-rich transmembrane protein 2 regulates the magnitude and frequency of dopamine release by repetitive neuronal stimuli in the striatum of L-dopa-treated mice.Neuropsychopharmacology reports · 2024Article
- SNARE mimicry by the CD225 domain of IFITM3 enables regulation of homotypic late endosome fusion.bioRxiv : the preprint server for biology · 2024Article
- Paroxysmal Kinesigenic Dyskinesia: Genetics and Pathophysiological Mechanisms.Neuroscience bulletin · 2024Review
- Deciphering the Role of Rapidly Evolving Conserved Elements in Primate Brain Development and Exploring Their Potential Involvement in Alzheimer's Disease.Molecular biology and evolution · 2024Article
- Allelic heterogeneity and abnormal vesicle recycling inFrontiers in molecular neuroscience · 2024Article
- Rapid Quantification of First and Second Phase Insulin Secretion Dynamics using an In vitro Platform for Improving Insulin Therapy.Cell calcium · 2023Article
- A Push-Pull Mechanism Between PRRT2 and β4-subunit Differentially Regulates Membrane Exposure and Biophysical Properties of NaV1.2 Sodium Channels.Molecular neurobiology · 2023Article
- A high-content endogenous GLUT4 trafficking assay reveals new aspects of adipocyte biology.Life science alliance · 2023Article
- Functional regulation of syntaxin-1: An underlying mechanism mediating exocytosis in neuroendocrine cells.Frontiers in endocrinology · 2023Review
- Trafficking regulator of GLUT4-1 (TRARG1) is a GSK3 substrate.The Biochemical journal · 2022Article
- PRRT2 Mutation and Serum Cytokines in Paroxysmal Kinesigenic Dyskinesia.Current medical science · 2022Article
- Clinical characteristics and genetics of ten Chinese children with PRRT2-associated neurological diseases.Frontiers in pediatrics · 2022Article
- Synaptopathies in Developmental and Epileptic Encephalopathies: A Focus on Pre-synaptic Dysfunction.Frontiers in neurology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in proline-rich transmembrane protein 2 (PRRT2) are associated with a range of paroxysmal neurological disorders. PRRT2 predominantly localizes to the pre-synaptic terminals and is believed to regulate neurotransmitter release. However, the mechanism of action is unclear. Here, we use reconstituted single vesicle and bulk fusion assays, combined with live cell imaging of single exocytotic events in PC12 cells and biophysical analysis, to delineate the physiological role of PRRT2. We report that PRRT2 selectively blocks the trans SNARE complex assembly and thus negatively regulates synaptic vesicle priming. This inhibition is actualized via weak interactions of the N-terminal proline-rich domain with the synaptic SNARE proteins. Furthermore, we demonstrate that paroxysmal dyskinesia-associated mutations in PRRT2 disrupt this SNARE-modulatory function and with efficiencies corresponding to the severity of the disease phenotype. Our findings provide insights into the molecular mechanisms through which loss-of-function mutations in PRRT2 result in paroxysmal neurological disorders.
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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 OpenQuestion graph.