ArticleProceedings of the National Academy of Sciences of the United States of America2016
nArgBP2 regulates excitatory synapse formation by controlling dendritic spine morphology.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Epigenetic signatures in antidepressant treatment response: a methylome-wide association study in the EMC trial.Translational psychiatry · 2022Trial
- SORBS2: A Molecular Nexus in Multisystem Diseases Through Scaffold-Mediated Regulation.Journal of cellular and molecular medicine · 2026Review
- Human brain and organoid transcriptomes reveal key receptor tyrosine kinase pathways and genetic signatures in Alzheimer's disease.Experimental & molecular medicine · 2026Article
- Mesenchymal stem cells reverse disease-specific abnormalities in nociceptive regions of the brain.Brain communications · 2026Article
- Article
- LUZP1 Regulates Dendritic Spine Maturation and Synaptic Plasticity in the Hippocampal Dentate Gyrus of Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- A Novel Missense Variant in SORBS2 Is Causative With Familial Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- Hippocampal tau-induced GRIN3A deficiency in Alzheimer's disease.FEBS open bio · 2024Article
- nArgBP2 together with GKAP and SHANK3 forms a dynamic layered structure.Frontiers in cellular neuroscience · 2024Article
- Microglia-synapse engulfment via PtdSer-TREM2 ameliorates neuronal hyperactivity in Alzheimer's disease models.The EMBO journal · 2023Article
- Biomolecular condensate assembly of nArgBP2 tunes its functionality to manifest the structural plasticity of dendritic spines.Experimental & molecular medicine · 2023Article
- Review
- Article
- SCAMP5 mediates activity-dependent enhancement of NHE6 recruitment to synaptic vesicles during synaptic plasticity.Molecular brain · 2021Article
- Molecular architecture of postsynaptic Interactomes.Cellular signalling · 2020Review
- TSPAN5 Enriched Microdomains Provide a Platform for Dendritic Spine Maturation through Neuroligin-1 Clustering.Cell reports · 2019Article
- Myosin XVI Regulates Actin Cytoskeleton Dynamics in Dendritic Spines of Purkinje Cells and Affects Presynaptic Organization.Frontiers in cellular neuroscience · 2019Article
- Neuroprotective Effects of Ginsenoside-Rg1 Against Depression-Like Behaviors via Suppressing Glial Activation, Synaptic Deficits, and Neuronal Apoptosis in Rats.Frontiers in immunology · 2018Article
- Peptide regulation of cofilin activity in the CNS: A novel therapeutic approach for treatment of multiple neurological disorders.Pharmacology & therapeutics · 2017Review
- Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural Abelson-related gene-binding protein 2 (nArgBP2) was originally identified as a protein that directly interacts with synapse-associated protein 90/postsynaptic density protein 95-associated protein 3 (SAPAP3), a postsynaptic scaffolding protein critical for the assembly of glutamatergic synapses. Although genetic deletion of nArgBP2 in mice leads to manic/bipolar-like behaviors resembling many aspects of symptoms in patients with bipolar disorder, the actual function of nArgBP2 at the synapse is completely unknown. Here, we found that the knockdown (KD) of nArgBP2 by specific small hairpin RNAs (shRNAs) resulted in a dramatic change in dendritic spine morphology. Reintroducing shRNA-resistant nArgBP2 reversed these defects. In particular, nArgBP2 KD impaired spine-synapse formation such that excitatory synapses terminated mostly at dendritic shafts instead of spine heads in spiny neurons, although inhibitory synapse formation was not affected. nArgBP2 KD further caused a marked increase of actin cytoskeleton dynamics in spines, which was associated with increased Wiskott-Aldrich syndrome protein-family verprolin homologous protein 1 (WAVE1)/p21-activated kinase (PAK) phosphorylation and reduced activity of cofilin. These effects of nArgBP2 KD in spines were rescued by inhibiting PAK or activating cofilin combined with sequestration of WAVE. Together, our results suggest that nArgBP2 functions to regulate spine morphogenesis and subsequent spine-synapse formation at glutamatergic synapses. They also raise the possibility that the aberrant regulation of synaptic actin filaments caused by reduced nArgBP2 expression may contribute to the manifestation of the synaptic dysfunction observed in manic/bipolar disorder.
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