ArticleThe Journal of biological chemistry2014
O-linked β-N-acetylglucosamine (O-GlcNAc) site thr-87 regulates synapsin I localization to synapses and size of the reserve pool of synaptic vesicles.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- Role of O-GlcNAcylation in Central Nervous System Development and Injuries: A Systematic Review.Molecular neurobiology · 2024Pooled it
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Sweetening the bonds: how O-GlcNAcylation modulates cell adhesion.Acta pharmacologica Sinica · 2026Review
- Brain O-GlcNAcylation in Neurodegenerative Diseases: Context-Dependent Mechanisms and Precision Therapeutic Translation.Brain sciences · 2026Review
- Targeting O-GlcNAcylation: Novel Therapeutic Strategies for Neurological Disease.Molecular neurobiology · 2025Review
- Cross-Talk Between Tau O-GlcNAcylation and the Formation of the Early Driver of Neurodegeneration (Cis P-Thr231-Pro Tau) in Primary Cortical Neurons.Molecular neurobiology · 2025Article
- Brain O-GlcNAcylation: Bridging physiological functions, disease mechanisms, and therapeutic applications.Molecular psychiatry · 2025Review
- Characterization and chemoproteomic profiling of protein O-GlcNAcylation in SOD1-G93A mouse model.Molecular medicine (Cambridge, Mass.) · 2025Article
- The regulation of enteric neuron connectivity by semaphorin 5A is affected by the autism-associated S956G missense mutation.iScience · 2024Article
- Modulation of synaptic transmission through O-GlcNAcylation.Molecular brain · 2024Review
- Article
- Brain O-GlcNAcylation: From Molecular Mechanisms to Clinical Phenotype.Advances in neurobiology · 2023Article
- The O-GlcNAc cycling in neurodevelopment and associated diseases.Biochemical Society transactions · 2022Review
- Galnt17 loss-of-function leads to developmental delay and abnormal coordination, activity, and social interactions with cerebellar vermis pathology.Developmental biology · 2022Article
- SIRT1 deficiency increases O-GlcNAcylation of tau, mediating synaptic tauopathy.Molecular psychiatry · 2022Article
- Role ofPhysiological reviews · 2021Review
- The Dysregulation of OGT/OGA Cycle Mediates Tau and APP Neuropathology in Down Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- O-GlcNAcylation regulates dopamine neuron function, survival and degeneration in Parkinson disease.Brain : a journal of neurology · 2020Article
- Article
- O-GlcNAcylation as a Therapeutic Target for Alzheimer's Disease.Neuromolecular medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
O-GlcNAc is a carbohydrate modification found on cytosolic and nuclear proteins. Our previous findings implicated O-GlcNAc in hippocampal presynaptic plasticity. An important mechanism in presynaptic plasticity is the establishment of the reserve pool of synaptic vesicles (RPSV). Dynamic association of synapsin I with synaptic vesicles (SVs) regulates the size and release of RPSV. Disruption of synapsin I function results in reduced size of the RPSV, increased synaptic depression, memory deficits, and epilepsy. Here, we investigate whether O-GlcNAc directly regulates synapsin I function in presynaptic plasticity. We found that synapsin I is modified by O-GlcNAc during hippocampal synaptogenesis in the rat. We identified three novel O-GlcNAc sites on synapsin I, two of which are known Ca(2+)/calmodulin-dependent protein kinase II phosphorylation sites. All O-GlcNAc sites mapped within the regulatory regions on synapsin I. Expression of synapsin I where a single O-GlcNAc site Thr-87 was mutated to alanine in primary hippocampal neurons dramatically increased localization of synapsin I to synapses, increased density of SV clusters along axons, and the size of the RPSV, suggesting that O-GlcNAcylation of synapsin I at Thr-87 may be a mechanism to modulate presynaptic plasticity. Thr-87 is located within an amphipathic lipid-packing sensor (ALPS) motif, which participates in targeting of synapsin I to synapses by contributing to the binding of synapsin I to SVs. We discuss the possibility that O-GlcNAcylation of Thr-87 interferes with folding of the ALPS motif, providing a means for regulating the association of synapsin I with SVs as a mechanism contributing to synapsin I localization and RPSV generation.
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Registered trials
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