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NLGN3 encodes a member of a family of neuronal cell surface proteins. Additionally we are shipping Neuroligin 3 Antibodies (94) and Neuroligin 3 Proteins (13) and many more products for this protein.
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No statistically significant haplotypes have been found associated to autism in the NLGN3 after logistic regression and permutation analysis.
The synaptic protein neuroligin-3 (NLGN3) was identified as the leading candidate mitogen, and soluble NLGN3 was sufficient and necessary to promote robust high-grade glioma cell proliferation.
Our data provided a further evidence for the involvement of NLGN3 and NLGN4X (show NLGN4X ELISA Kits) gene in the pathogenesis of autism in Chinese population.
The present study explores, for the first time, the contribution of NLGN3 and NLGN4X (show NLGN4X ELISA Kits) genetic variants in Greek patients with autistic disorder.
Lack of association between NLGN3, NLGN4 (show NLGN4X ELISA Kits), SHANK2 (show SHANK2 ELISA Kits) and SHANK3 (show SHANK3 ELISA Kits) gene variants and autism spectrum disorder in a Chinese population.
Neuroligins are adhesion proteins that bind to beta-neurexin (show NRXN1 ELISA Kits) to form functional synapses.
Data from studies using cross-linking reagents suggest that neuroligins form dimers, including homodimers and, most notably, neuroligin 1 (show NLGN1 ELISA Kits)/3 heteromers; autism-associated neuroligin mutant (neuroligin 3 R471C) forms heterodimers with neuroligin 1 (show NLGN1 ELISA Kits).
study provides initial evidence that a common variant in NLGN3 gene may play a role in the etiology of ASDs among affected males in Chinese Han population.
further characterization of the R451C mutation in NLGN3;role in protein folding
report mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 (show NLGN4X ELISA Kits) in siblings with autism-spectrum disorders
Nlgn3 and Nrxn1 (show NRXN1 ELISA Kits) are differentially expressed in cerebral cortex and hippocampus which might be responsible for alternations in synaptic plasticity during aging.
These findings suggest that structural changes in the brain of NL-3 mice are induced by the mutation in the NL-3 gene
Thus our data suggest that perinatal exposure to BPA (show DST ELISA Kits) impairs spatial memory through upregulation of expression of synaptic proteins Nrxn1 (show NRXN1 ELISA Kits) and Nlgn3 and increased dendritic spine density in cerebral cortex and hippocampus of postnatal male mice.
Therefore, we sought to replicate our findings in the neuroligin-3 R451C point mutant knock-in mouse model (NL3R451C) in a different genetic background.
We used MRI (show C7ORF49 ELISA Kits) to image three genetic mouse models with single mutations implicated in autism: Neuroligin-3 R451C knock-in, Methyl-CpG binding protein-2 (MECP2 (show MECP2 ELISA Kits)) 308-truncation and integrin beta3 homozygous knockout.
Results indicate that autism spectrum disorders (ASD (show GUSB ELISA Kits))-associated NL3 mutations commonly disrupt striatal circuits in a subregion-, cell-type-, and synapse-specific fashion and suggest that this disruption may shape repetitive and stereotypic behaviors associated with ASD (show GUSB ELISA Kits).
Neuroligin-3 R704C-mutant induced neurons exhibit a large and selective decrease in AMPA (show GRIA3 ELISA Kits)-type glutamate (show GRIN1 ELISA Kits) receptor-mediated synaptic transmission without changes in NMDA-type glutamate (show GRIN1 ELISA Kits) receptor- or in GABAA (show GABRg1 ELISA Kits) receptor-mediated synaptic transmission.
Our data thus suggest that neuroligin-3 is specifically required for tonic endocannabinoid signaling
in NL3(R451C) mutant mice, a single point mutation in a synaptic cell adhesion molecule (show CADM1 ELISA Kits) causes context-dependent changes in synaptic transmission
The NL-3 acts redundantly to maintain excitatory synapses and that synapse elimination caused by the absence of NL-3 is promoted by synaptic activity and mediated by a postsynaptic Ca(2 (show CA2 ELISA Kits)+)/CaM-dependent signaling pathway.
This gene encodes a member of a family of neuronal cell surface proteins. Members of this family may act as splice site-specific ligands for beta-neurexins and may be involved in the formation and remodeling of central nervous system synapses. Mutations in this gene may be associated with autism and Asperger syndrome. Multiple transcript variants encoding distinct isoforms have been identified for this gene.
, neuroligin 3 isoform A1A2
, carboxylesterase clade L, member 3
, gliotactin homolog
, neuroligin 3 protein