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e found that NLGN3 function at inhibitory synapses in rat CA1 (zeige CA1 ELISA Kits) depends on the presence of NLGN2 (zeige NLGN2 ELISA Kits) and identified a domain in the extracellular region that accounted for this functional difference between NLGN2 (zeige NLGN2 ELISA Kits) and 3 specifically at inhibitory synapses.
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 (zeige 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 (zeige NLGN4X ELISA Kits) genetic variants in Greek patients with autistic disorder.
Lack of association between NLGN3, NLGN4 (zeige NLGN4X ELISA Kits), SHANK2 (zeige SHANK2 ELISA Kits) and SHANK3 (zeige SHANK3 ELISA Kits) gene variants and autism spectrum disorder in a Chinese population.
Neuroligins are adhesion proteins that bind to beta-neurexin (zeige 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 (zeige NLGN1 ELISA Kits)/3 heteromers; autism-associated neuroligin mutant (neuroligin 3 R471C) forms heterodimers with neuroligin 1 (zeige 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
Data suggest an unanticipated mechanism of developmental compensation whereby cerebellin-1 (zeige CBLN1 ELISA Kits) and neuroligin-3 functionally occlude each other during development of calyx synapses.
Nlgn3(R451C) knock-in mice, an established genetic model for autism spectrum disorders, exhibited normal duration and distribution of sleep/wake states but significantly altered electroencephalography (EEG) power spectral profiles for wake and sleep.
The alternatively spliced segment 4 (AS4) of NRX genes (Nrxn) is a critical element in selective trans-synaptic interactions. This study evaluated the synaptogenic receptor activity of NL1/2/3 isoforms in a neuron-fibroblast co-culture system, in which the Nrxn AS4 segments are manipulated using SLM2, a selective and dominant regulator of AS4 splicing.
The NL3 deletion-mutant mouse was a dramatic reduction of the number of GABAAalpha2-subunit containing GABAA (zeige GABRg1 ELISA Kits) receptor clusters at the retinal inner plexiform layer.
that neuroligin-3 specifies the properties of excitatory synapses on parvalbumin (zeige PVALB ELISA Kits)-containing interneurons by a retrograde trans-synaptic mechanism and suggest a molecular pathway whereby neuroligin-3 mutations contribute to neuropsychiatric disorders
Study shows altered mating behavior in the Neuroligin-3(R451C mutation) mouse and has provides new insights into the aggressive phenotype in this model.
Nlgn3 and Nrxn1 (zeige 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 (zeige DST ELISA Kits) impairs spatial memory through upregulation of expression of synaptic proteins Nrxn1 (zeige 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.
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