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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Neuroligin 3

NL3, NLGN3, neuroligin 3
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. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: neuroligin-1, NLGN4, ANGPTL4, CAN, ACID
Papers on NL3
Developmental expression of the neuroligins and neurexins in fragile X mice.
New
Foster et al., Hamilton, Canada. In J Comp Neurol, Apr 2016
Sex differences in hippocampal expression of NLGN2, NRXN1, NRXN2, and NRXN3 mRNAs and in S1 cortex expression of NRXN3 mRNAs were observed WT mice, whereas sex differences in NLGN3, NRXN1, NRXN2, and NRXN3 mRNA expression in the hippocampus and in NLGN1, NRXN2 and NRXN3 mRNA expression in S1 cortex were detected in FMR1-KO mice.
Developmental neurogenetics and multimodal neuroimaging of sex differences in autism.
New
GENDAAR Research Consortium et al., Los Angeles, United States. In Brain Imaging Behav, Feb 2016
DRD1, NLGN3, MAOA, and SHANK1 deletion have been discovered in ASD.
A frightening thought: Neuronal activity enhances tumor growth.
New
Sontheimer et al., Birmingham, United States. In Cell Res, Aug 2015
A recent study by Venkatesh et al. published in Cell has identified Neuroligin-3 (NLGN3) as a mitogen promoting high-grade glioma growth.
Axo-glial communication through neurexin-neuroligin signaling regulates myelination and oligodendrocyte differentiation.
New
Colicos et al., Calgary, Canada. In Glia, Jul 2015
Here, we demonstrate the existence of a parallel axo-glial signaling pathway between axonal NX and oligodendritic (OL) NL3.
Shedding light on glioma growth.
New
Impact
Stevens et al., Boston, United States. In Cell, Jun 2015
In this issue of Cell, Venkatesh et al. demonstrate that this also occurs in the brain, identifying neuronal activity-induced secretion of neuroligin-3 as a novel mechanism promoting glioma proliferation.
Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion.
New
Impact
Monje et al., Stanford, United States. In Cell, Jun 2015
The synaptic protein neuroligin-3 (NLGN3) was identified as the leading candidate mitogen, and soluble NLGN3 was sufficient and necessary to promote robust HGG cell proliferation.
The interplay between synaptic activity and neuroligin function in the CNS.
Review
Xu et al., Hangzhou, China. In Biomed Res Int, 2014
Consistent with their localization, NL1 and NL3 selectively affect excitatory synapses, whereas NL2 specifically affects inhibitory synapses.
A neuroligin-3 mutation implicated in autism causes abnormal aggression and increases repetitive behavior in mice.
Hannan et al., Melbourne, Australia. In Mol Autism, 2014
METHODS: We investigated aggression in mice containing the ASD-associated R451C (arginine to cysteine residue 451 substitution) mutation in neuroligin-3 (NL3).
Neuroligins, synapse balance and neuropsychiatric disorders.
Review
Wędzony et al., Kraków, Poland. In Pharmacol Rep, 2014
Neuroligin 3 and 4 are present on both types of synapses.
Autism-associated neuroligin-3 mutations commonly impair striatal circuits to boost repetitive behaviors.
Impact
Südhof et al., Stanford, United States. In Cell, 2014
In humans, neuroligin-3 mutations are associated with autism, whereas in mice, the corresponding mutations produce robust synaptic and behavioral changes.
How far can mice carry autism research?
Impact
Hyman, Cambridge, United States. In Cell, 2014
In the face of growing controversy about the utility of genetic mouse models of human disease, Rothwell et al. report on a shared mechanism by which two different neuroligin-3 mutations, associated with autism spectrum disorders in humans, produce an enhancement in motor learning.
A review on the current neuroligin mouse models.
Review
Xia et al., Hangzhou, China. In Sheng Li Xue Bao, 2012
In most of the models, including the human autism-linked NL3 and NL4 mutation mice, there are social interaction defects, memory impairment and repetitive behaviors.
Shared synaptic pathophysiology in syndromic and nonsyndromic rodent models of autism.
Impact
Scheiffele et al., Basel, Switzerland. In Science, 2012
Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor-dependent synaptic plasticity, a hallmark of fragile X.
Homodimerization and isoform-specific heterodimerization of neuroligins.
GeneRIF
Brose et al., Göttingen, Germany. In Biochem J, 2012
Data from studies using cross-linking reagents suggest that neuroligins form dimers, including homodimers and, most notably, neuroligin 1/3 heteromers; autism-associated neuroligin mutant (neuroligin 3 R471C) forms heterodimers with neuroligin 1.
Autism-linked neuroligin-3 R451C mutation differentially alters hippocampal and cortical synaptic function.
GeneRIF
Südhof et al., Stanford, United States. In Proc Natl Acad Sci U S A, 2011
in NL3(R451C) mutant mice, a single point mutation in a synaptic cell adhesion molecule causes context-dependent changes in synaptic transmission
Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons.
GeneRIF
Südhof et al., Stanford, United States. In J Cell Biol, 2011
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+)/CaM-dependent signaling pathway.
An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus.
GeneRIF
Südhof et al., Palo Alto, United States. In Embo J, 2011
An autism-associated point mutation in the neuroligin cytoplasmic tail selectively impairs AMPA receptor-mediated synaptic transmission in hippocampus.
A sex-specific association of common variants of neuroligin genes (NLGN3 and NLGN4X) with autism spectrum disorders in a Chinese Han cohort.
GeneRIF
Zhao et al., Hangzhou, China. In Behav Brain Funct, 2010
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.
A synaptic trek to autism.
Review
Bourgeron, Paris, France. In Curr Opin Neurobiol, 2009
Mutations in NLGN3/4, SHANK3, or NRXN1 alter synaptic function and lead to mental retardation, typical autism, or Asperger syndrome.
Multiple rare variants in the etiology of autism spectrum disorders.
Review
Buxbaum, New York City, United States. In Dialogues Clin Neurosci, 2008
Of particular recent interest are the synaptic cell adhesion and associated molecules, including neurexin 1, neuroligin 3 and 4, and SHANK3, which implicate glutamatergic synapse abnormalities in ASDs.
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