ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Shank3-Rich2 interaction regulates AMPA receptor recycling and synaptic long-term potentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 63 citations in OpenAlex.
- Endosomal system genetics and autism spectrum disorders: A literature review.Neuroscience and biobehavioral reviews · 2016Pooled it
- Glutamatergic candidate genes in autism spectrum disorder: an overview.Journal of neural transmission (Vienna, Austria : 1996) · 2014Pooled it
- The Molecular Machinery of Synaptic Plasticity and Its Potential Role in the Aetiology of Schizophrenia.Molecular neurobiology · 2026Review
- Article
- DeSUMOylation of Spastin Enhances AMPA Receptor Recycling and Synaptic Plasticity via IST1-Dependent Endosomal Sorting.Molecular neurobiology · 2025Article
- Comparative Single-Cell Transcriptome Analysis of c-Met Receptor Expressing and Non-Expressing Projection Neurons in the Developing Frontal and Visual Cortices.Developmental neuroscience · 2025Article
- Learning-Associated Flexibility of Cortical Taste Coding Is Impaired in Shank3 Knockout Mice.bioRxiv : the preprint server for biology · 2025Article
- KLF5 Shapes Developing Respiratory Tubules by Inhibiting Actin Asymmetry in Epithelial Cells.American journal of respiratory cell and molecular biology · 2025Article
- Roles of AMPA receptors in social behaviors.Frontiers in synaptic neuroscience · 2024Review
- Understanding the role of AMPA receptors in autism: insights from circuit and synapse dysfunction.Frontiers in psychiatry · 2024Review
- Neurodevelopmental Consequences of Dietary Zinc Deficiency: A Status Report.Biological trace element research · 2023Review
- The Evaluation of Rac1 Signaling as a Potential Therapeutic Target of Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Postsynaptic Protein Shank3a Deficiency Synergizes with Alzheimer's Disease Neuropathology to Impair Cognitive Performance in the 3xTg-AD Murine Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Caveolin-1-Mediated Cholesterol Accumulation Contributes to Exaggerated mGluR-Dependent Long-Term Depression and Impaired Cognition in Fmr1 Knockout Mice.Molecular neurobiology · 2023Article
- Pathogenic TRIO variants associated with neurodevelopmental disorders perturb the molecular regulation of TRIO and axon pathfinding in vivo.Molecular psychiatry · 2023Article
- Expression Analyses of Rich2/Arhgap44, a Rho Family GTPase-Activating Protein, during Mouse Brain Development.Developmental neuroscience · 2023Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
- Dietary zinc supplementation rescues fear-based learning and synaptic function in the Tbr1Molecular autism · 2022Article
- Utilizing Genomically Targeted Molecular Data to Improve Patient-Specific Outcomes in Autism Spectrum Disorder.International journal of molecular sciences · 2022Article
- S100B dysregulation during brain development affects synaptic SHANK protein networks via alteration of zinc homeostasis.Translational psychiatry · 2021Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic long-term potentiation (LTP) is a key mechanism involved in learning and memory, and its alteration is associated with mental disorders. Shank3 is a major postsynaptic scaffolding protein that orchestrates dendritic spine morphogenesis, and mutations of this protein lead to mental retardation and autism spectrum disorders. In the present study we investigated the role of a new Shank3-associated protein in LTP. We identified the Rho-GAP interacting CIP4 homolog 2 (Rich2) as a new Shank3 partner by proteomic screen. Using single-cell bioluminescence resonance energy transfer microscopy, we found that Rich2-Shank3 interaction is increased in dendritic spines of mouse cultured hippocampal neurons during LTP. We further characterized Rich2 as an endosomal recycling protein that controls AMPA receptor GluA1 subunit exocytosis and spine morphology. Knock-down of Rich2 with siRNA, or disruption of the Rich2-Shank3 complex using an interfering mimetic peptide, inhibited the dendritic spine enlargement and the increase in GluA1 subunit exocytosis typical of LTP. These results identify Rich2-Shank3 as a new postsynaptic protein complex involved in synaptic plasticity.
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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.