ArticleFrontiers in cellular neuroscience2019
Neuroligin 3 Regulates Dendritic Outgrowth by Modulating Akt/mTOR Signaling.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Comparing the Gut Microbiome in Autism and Preclinical Models: A Systematic Review.Frontiers in cellular and infection microbiology · 2022Pooled it
- Neuroligin-2 is ubiquitinated by Nedd4l to control developmental astrocyte morphogenesis.The Journal of cell biology · 2026Article
- NLGN3 contributes to angiogenesis in myocardial infarction via activation of the Gαi1/3-Akt pathway.Basic research in cardiology · 2026Article
- Targeting the mTOR Pathway with Natural Products: A Potential Therapeutic Approach for Autism Spectrum Disorders.Current neuropharmacology · 2026Review
- Neuroligin-2 is ubiquitinated by Nedd4l to control developmental astrocyte morphogenesis.bioRxiv : the preprint server for biology · 2025Article
- PRRG4 Brain-Specific Conditional Knockout Mice Display Autism Spectrum Disorder-Like Behaviors.Biological procedures online · 2025Article
- Neuroligin-3 R451C induces gain-of-function gene expression in astroglia in an astroglia-enriched brain organoid model.Cell regeneration (London, England) · 2025Article
- Assessing the Neurodevelopmental Impact of Fluoxetine, Citalopram, and Paroxetine on Neural Stem Cell-Derived Neurons.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Astrocytic neuroligin 3 regulates social memory and synaptic plasticity through adenosine signaling in male mice.Nature communications · 2024Article
- Cell Adhesion Molecule Signaling at the Synapse: Beyond the Scaffold.Cold Spring Harbor perspectives in biology · 2024Review
- Article
- Microglial- neuronal crosstalk in chronic viral infection through mTOR, SPP1/OPN and inflammasome pathway signaling.Frontiers in immunology · 2024Review
- Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Article
- Autism-linked NLGN3 is a key regulator of gonadotropin-releasing hormone deficiency.Disease models & mechanisms · 2023Article
- mTOR Signaling Disruption and Its Association with the Development of Autism Spectrum Disorder.Molecules (Basel, Switzerland) · 2023Review
- Neuroligins in neurodevelopmental conditions: how mouse models ofNeuronal signaling · 2022Article
- Neuroligin-3: A Circuit-Specific Synapse Organizer That Shapes Normal Function and Autism Spectrum Disorder-Associated Dysfunction.Frontiers in molecular neuroscience · 2021Review
- Deletion of Kv10.2 Causes Abnormal Dendritic Arborization and Epilepsy Susceptibility.Neurochemical research · 2020Article
- [Proteolytic cleavage of neuroligins and functions of their cleavage products].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroligins (NLs) are a group of postsynaptic cell adhesion molecules that function in synaptogenesis and synaptic transmission. Genetic defects in neuroligin 3 (NL3), a member of the NL protein family, are associated with autism. Studies in rodents have revealed that mutations of NL3 gene lead to increased growth and complexity in dendrites in the central nervous system. However, the detailed mechanism is still unclear. In our study, we found that deficiency of NL3 led to morphological changes of the pyramidal neurons in layer II/III somatosensory cortex in mice, including enlarged somata, elongated dendritic length, and increased dendritic complexity. Knockdown of NL3 in cultured rat neurons upregulated Akt/mTOR signaling, resulting in both increased protein synthesis and dendritic growth. Treating neurons with either rapamycin to inhibit the mTOR or LY294002 to inhibit the PI3K/Akt activity rescued the morphological abnormalities resulting from either NL3 knockdown or knockout (KO). In addition, we found that the hyperactivated Akt/mTOR signaling associated with NL3 defects was mediated by a reduction in phosphatase and tensin (PTEN) expression, and that MAGI-2, a scaffold protein, interacted with both NL3 and PTEN and could be a linker between NL3 and Akt/mTOR signaling pathway. In conclusion, our results suggest that NL3 regulates neuronal morphology, especially dendritic outgrowth, by modulating the PTEN/Akt/mTOR signaling pathway, probably
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