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Our data suggest that these four previously described neuroligin mutations are not primary risk factors for autism.
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NLGN4X might represent novel biomarkers and therapeutic targets for breast cancer. Inhibition of NLGN4X may be a new target for the prevention and treatment of breast cancer
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Noncoding polymorphisms on NLGN4X may be associated to autism suggesting the key role of NLGN4X in autism pathophysiology and in its male prevalence.
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Endogenous NLGN4X is intensely phosphorylated on T707 upon PKC stimulation in human neurons.
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Our data provided a further evidence for the involvement of NLGN3 and NLGN4X gene in the pathogenesis of autism in Chinese population.
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The present study explores, for the first time, the contribution of NLGN3 and NLGN4X genetic variants in Greek patients with autistic disorder.
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In vitro models show NLGN4X knockdown directly impacts neurodevelopmental process during the formation of neurons and their connections.
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Lack of association between NLGN3, NLGN4, SHANK2 and SHANK3 gene variants and autism spectrum disorder in a Chinese population.
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Neuroligins are adhesion proteins that bind to beta-neurexin to form functional synapses.
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Five genes have been directly disrupted in Tourette Syndrome by independent genomic rearrangements and copy number variations with unique breakpoints.
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The autism-associated DeltaE4 mutation in NLGN4 compromises the ability of NLGN4 to localize correctly to the cell surface when overexpressed and to induce synaptic differentiation.
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results indicate that the genetic variants located in NLGN4 can affect the cognitive abilities of boys.
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Results suggest that unique conformational reshaping of the neuroligin 4 surface is required to permit neurexin 1beta association.
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finding further contributes to consideration of neuroligins as probable candidate genes for future molecular genetic studies, suggesting that a defect of synaptogenesis may predispose to autism
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report mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 in siblings with autism-spectrum disorders
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Scanning and sequencing of 2.5Mb of the NLGN4 genes reveals an association of NLGN4 structural variants at highly conserved amino acids with an estimated attributable risk for autism of about 3% in the cohorts studies.
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Neuroligin mutations most probably represent rare causes of autism; it is unlikely that the allelic variants in any of these genes would be major risk factors for autism.
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Data indicate that coding mutations in neuroligin 4 are very rarely associated to autism spectrum disorders.
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Splice variants of the NLGN4 gene are associated with autism.
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Syntrophin-gamma2 (SNTG2) is a de novo binding partner of X-linked neuroligin 4, which correlates with autism-related mutations.
