ArticleThe EMBO journal2006
Rabphilin regulates SNARE-dependent re-priming of synaptic vesicles for fusion.
Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed.
- Disruption of the LRRK2 substrate RAB12 facilitates neurotransmission and causes hyperactivity in mice.NPJ Parkinson's disease · 2026Article
- Metaplastic sleep regulation inbioRxiv : the preprint server for biology · 2026Article
- Article
- Multiple Transcriptomic Analyses Explore Potential Synaptic Biomarker Rabphilin-3A for Alzheimer's Disease.Scientific reports · 2024Article
- Rabphilin-3A undergoes phase separation to regulate GluN2A mobility and surface clustering.Nature communications · 2023Article
- Rabphilin 3A binds the N-peptide of SNAP-25 to promote SNARE complex assembly in exocytosis.eLife · 2022Article
- Rabphilin3A reduces integrin-dependent growth cone signaling to restrict axon regeneration after trauma.Experimental neurology · 2022Article
- Studies on anti-rabphilin-3A antibodies in 15 consecutive patients presenting with central diabetes insipidus at a single referral center.Scientific reports · 2022Article
- The Role of DNA Damage in Neural Plasticity in Physiology and Neurodegeneration.Frontiers in cellular neuroscience · 2022Review
- cAMP-Dependent Synaptic Plasticity at the Hippocampal Mossy Fiber Terminal.Frontiers in synaptic neuroscience · 2022Review
- In vivo Roles of Rab27 and Its Effectors in Exocytosis.Cell structure and function · 2021Review
- C1QL3 promotes cell-cell adhesion by mediating complex formation between ADGRB3/BAI3 and neuronal pentraxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Haploinsufficiency of X-linked intellectual disability gene CASK induces post-transcriptional changes in synaptic and cellular metabolic pathways.Experimental neurology · 2020Article
- Spermidine protects from age-related synaptic alterations at hippocampal mossy fiber-CA3 synapses.Scientific reports · 2019Article
- Unbiased Thiol-Labeling and Top-Down Proteomic Analyses Implicate Multiple Proteins in the Late Steps of Regulated Secretion.Proteomes · 2019Article
- Gβγ SNARE Interactions and Their Behavioral Effects.Neurochemical research · 2019Review
- Novel Cellular Functions of Very Long Chain-Fatty Acids: Insight From ELOVL4 Mutations.Frontiers in cellular neuroscience · 2019Review
- The Electrophysiology of Presynaptic Congenital Myasthenic Syndromes With and Without Facilitation: From Electrodiagnostic Findings to Molecular Mechanisms.Frontiers in neurology · 2019Review
- Presynaptic congenital myasthenic syndrome with altered synaptic vesicle homeostasis linked to compound heterozygous sequence variants in RPH3A.Molecular genetics & genomic medicine · 2018Article
- Homozygous Expression of Mutant ELOVL4 Leads to Seizures and Death in a Novel Animal Model of Very Long-Chain Fatty Acid Deficiency.Molecular neurobiology · 2018Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Synaptic vesicle fusion is catalyzed by assembly of synaptic SNARE complexes, and is regulated by the synaptic vesicle GTP-binding protein Rab3 that binds to RIM and to rabphilin. RIM is a known physiological regulator of fusion, but the role of rabphilin remains obscure. We now show that rabphilin regulates recovery of synaptic vesicles from use-dependent depression, probably by a direct interaction with the SNARE protein SNAP-25. Deletion of rabphilin dramatically accelerates recovery of depressed synaptic responses; this phenotype is rescued by viral expression of wild-type rabphilin, but not of mutant rabphilin lacking the second rabphilin C2 domain that binds to SNAP-25. Moreover, deletion of rabphilin also increases the size of synaptic responses in synapses lacking the vesicular SNARE protein synaptobrevin in which synaptic responses are severely depressed. Our data suggest that binding of rabphilin to SNAP-25 regulates exocytosis of synaptic vesicles after the readily releasable pool has either been physiologically exhausted by use-dependent depression, or has been artificially depleted by deletion of synaptobrevin.
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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.