ArticleJournal of molecular neuroscience : MN2015
Novel interactive partners of neuroligin 3: new aspects for pathogenesis of autism.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Analysis of neuronal activity impairment in iPSC-derived neurons from idiopathic autism patients.iScience · 2025Article
- Establishing a Mouse Model of NL3R617W-Associated Autism Spectrum Disorder for a Functional Study.Actas espanolas de psiquiatria · 2025Article
- Astrocytic Neuroligin-3 influences gene expression and social behavior, but is dispensable for synapse number.Molecular psychiatry · 2025Article
- Deriving comprehensive literature trends on multi-omics analysis studies in autism spectrum disorder using literature mining pipeline.Frontiers in neuroscience · 2024Article
- Understanding copy number variations through their genes: a molecular view on 16p11.2 deletion and duplication syndromes.Frontiers in pharmacology · 2024Review
- Decoding microRNAs in autism spectrum disorder.Molecular therapy. Nucleic acids · 2022Review
- Colonic dilation and altered ex vivo gastrointestinal motility in the neuroligin-3 knockout mouse.Autism research : official journal of the International Society for Autism Research · 2020Article
- Downregulation of an Evolutionary Young miR-1290 in an iPSC-Derived Neural Stem Cell Model of Autism Spectrum Disorder.Stem cells international · 2019Article
- Triclosan Impairs Hippocampal Synaptic Plasticity and Spatial Memory in Male Rats.Frontiers in molecular neuroscience · 2018Article
- Loss of the Chr16p11.2 ASD candidate geneMolecular autism · 2018Article
- Article
- Filamin, a synaptic organizer ineLife · 2016Article
- The cellular and molecular landscape of neuroligins.Trends in neurosciences · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism is a neurodevelopmental disorder with a strong genetic predisposition. Neurolign 3 (NLGN3) as a postsynaptic transmembrane protein, functions in both neuron synaptogenesis and glia-neuron communications. Previously, a gain of function mutation (R451C) in NLGN3 was identified in autistic patients, which illustrates the involvement of NLGN3 in autism pathogenesis. As proper synaptic targeting and functioning are controlled by intracellular protein interactions, in the current study, we tried to discover the intracellular regulation network in which NLGN3 might be involved by a yeast two-hybrid-based interactor identification. Fifty-one protein candidate partners were identified after screening a human fetal complementary DNA (cDNA) library with an intracellular fragment of NLGN3. The interactions of NLGN3 with a subset of candidates, including EEF1A1, FLNA, ITPRIP, CYP11A1, MT-CO2, GPR175, ACOT2, and QPRT, were further validated in human neuroblastoma cells or brain tissues. Furthermore, our study suggested that NLGN3 was functioning in cytosolic calcium balance and participating in calcium-regulated cellular processes. Our findings of novel NLGN3 binding partners provide evidences of involvement of NLGN3 in multiple biological pathways, especially calcium regulating and mitochondrial function, thus suggesting further significance. This new data not only leads to a better understanding of the physiological functions of NLGN3, but also provide new aspects for pathogenesis of autism.
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