Associated Papers
Alternative splicing in autism spectrum disorder: Recent insights from mechanisms to therapy.
Zheng M et al.
Asian Journal of Psychiatry, 2025
Analyses of Human Genetic Data to Identify Clinically Relevant Domains of Neuroligins.
Lehr AW et al.
Genes, 2024
Downregulation of mGluR1-mediated signaling underlying autistic-like core symptoms in Shank1 P1812L-knock-in mice.
Qin Y et al.
Translational Psychiatry, 2023
Association between Neuroligin-1 polymorphism and plasma glutamine levels in individuals with autism spectrum disorder.
Lee IH et al.
Ebiomedicine, 2023
Synaptic genes and neurodevelopmental disorders: From molecular mechanisms to developmental strategies of behavioral testing.
Michetti C et al.
Neurobiology of Disease, 2022
A recurrent SHANK1 mutation implicated in autism spectrum disorder causes autistic-like core behaviors in mice via downregulation of mGluR1-IP3R1-calcium signaling.
Qin Y et al.
Molecular Psychiatry, 2022
35388181 (PubMed )
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Imaging neural circuit pathology of autism spectrum disorders: autism-associated genes, animal models and the application of in vivo two-photon imaging.
Terashima H et al.
Microscopy (oxford, England), 2022
The neuroligins and the synaptic pathway in Autism Spectrum Disorder.
Trobiani L et al.
Neuroscience and Biobehavioral Reviews, 2020
Alternative splicing at neuroligin site A regulates glycan interaction and synaptogenic activity.
Oku S et al.
Elife, 2020
Autism-associated variants of neuroligin 4X impair synaptogenic activity by various molecular mechanisms.
Yumoto T et al.
Molecular Autism, 2020
Polymorphisms of Ionotropic Glutamate Receptor-Related Genes and the Risk of Autism Spectrum Disorder in a Chinese Population.
Xie X et al.
Psychiatry Investigation, 2019
Neurodevelopmental synaptopathies: Insights from behaviour in rodent models of synapse gene mutations.
Luo J et al.
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2018
Functional significance of rare neuroligin 1 variants found in autism.
Nakanishi M et al.
Plos Genetics, 2017
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