ArticlePloS one2013
Lack of association between NLGN3, NLGN4, SHANK2 and SHANK3 gene variants and autism spectrum disorder in a Chinese population.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- The association between NLGN4 gene variants and the incidence of autism spectrum disorders in Guilan, Iran.IBRO neuroscience reports · 2025Article
- Enhanced fear limits behavioral flexibility in Shank2-deficient mice.Molecular autism · 2022Article
- Genetics of glutamate and its receptors in autism spectrum disorder.Molecular psychiatry · 2022Review
- Brain region and gene dosage-differential transcriptomic changes inFrontiers in molecular neuroscience · 2022Article
- Gene Dosage- and Age-Dependent Differential Transcriptomic Changes in the Prefrontal Cortex ofFrontiers in molecular neuroscience · 2021Article
- Early Chronic Memantine Treatment-Induced Transcriptomic Changes in Wild-Type andFrontiers in molecular neuroscience · 2021Article
- Analysis of the SNP rs3747333 and rs3747334 in NLGN4X gene in autism spectrum disorder: a meta-analysis.Annals of general psychiatry · 2019Article
- Stage 1 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: protocol for a test of the double hit hypothesis.Wellcome open research · 2018Article
- Stage 2 Registered Report: Variation in neurodevelopmental outcomes in children with sex chromosome trisomies: testing the double hit hypothesis.Wellcome open research · 2018Article
- Association Analysis of Noncoding Variants in Neuroligins 3 and 4X Genes with Autism Spectrum Disorder in an Italian Cohort.International journal of molecular sciences · 2016Article
- A Subset of Autism-Associated Genes Regulate the Structural Stability of Neurons.Frontiers in cellular neuroscience · 2016Review
- Synaptic P-Rex1 signaling regulates hippocampal long-term depression and autism-like social behavior.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Efficient strategy for the molecular diagnosis of intellectual disability using targeted high-throughput sequencing.Journal of medical genetics · 2014Article
- Microphthalmia with Linear Skin Defects (MLS) associated with Autism Spectrum Disorder (ASD) in a patient with Familial 12.9Mb Terminal Xp deletion.BMC pediatrics · 2014Article
- The role of glutamate and its receptors in autism and the use of glutamate receptor antagonists in treatment.Journal of neural transmission (Vienna, Austria : 1996) · 2014Review
- Mining the 3'UTR of autism-implicated genes for SNPs perturbing microRNA regulation.Genomics, proteomics & bioinformatics · 2014Article
- Synaptic proteins and receptors defects in autism spectrum disorders.Frontiers in cellular neuroscience · 2014Review
- Biomarkers in autism.Frontiers in psychiatry · 2014Review
- Epigenetics and autism.Autism research and treatment · 2013Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication, absence or delay in language development, and stereotyped or repetitive behaviors. Genetic studies show that neurexin-neuroligin (NRXN-NLGN) pathway genes contribute susceptibility to ASD, which include cell adhesion molecules NLGN3, NLGN4 and scaffolding proteins SHANK2 and SHANK3. Neuroligin proteins play an important role in synaptic function and trans-synaptic signaling by interacting with presynaptic neurexins. Shank proteins are scaffolding molecules of excitatory synapses, which function as central organizers of the postsynaptic density. Sequence level mutations and structural variations in these genes have been identified in ASD cases, while few studies were performed in Chinese population. In this study, we examined the copy numbers of four genes NLGN4, NLGN3, SHANK2, and SHANK3 in 285 ASD cases using multiplex fluorescence competitive polymerase chain reaction (PCR). We also screened the regulatory region including the promoter region and 5'/3' untranslated regions (UTR) and the entire coding region of NLGN4 in a cohort of 285 ASD patients and 384 controls by direct sequencing of genomic DNA using the Sanger method. DNA copy number calculation in four genes showed no deletion or duplication in our cases. No missense mutations in NLGN4 were identified in our cohort. Association analysis of 6 common SNPs in NLGN4 did not find significant difference between ASD cases and controls. These findings showed that these genes may not be major disease genes in Chinese ASD cases.
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