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Human Polyclonal NLGN4X Primary Antibody for ELISA, WB - ABIN4338786
Zhang, Gao, Qi, Li, Zheng, Zhang: Gender differences in cognitive ability associated with genetic variants of NLGN4. in Neuropsychobiology 2010
Our data suggest that these four previously described neuroligin mutations are not primary risk factors for autism.
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
Noncoding polymorphisms on NLGN4X may be associated to autism suggesting the key role of NLGN4X in autism pathophysiology and in its male prevalence.
Endogenous NLGN4X is intensely phosphorylated on T707 upon PKC stimulation in human neurons.
Our data provided a further evidence for the involvement of NLGN3 and NLGN4X gene in the pathogenesis of autism in Chinese population.
The present study explores, for the first time, the contribution of NLGN3 and NLGN4X genetic variants in Greek patients with autistic disorder.
In vitro models show NLGN4X knockdown directly impacts neurodevelopmental process during the formation of neurons and their connections.
Lack of association between NLGN3, NLGN4, SHANK2 and SHANK3 gene variants and autism spectrum disorder in a Chinese population.
Neuroligins are adhesion proteins that bind to beta-neurexin to form functional synapses.
Five genes have been directly disrupted in Tourette Syndrome by independent genomic rearrangements and copy number variations with unique breakpoints.
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.
results indicate that the genetic variants located in NLGN4 can affect the cognitive abilities of boys.
Results suggest that unique conformational reshaping of the neuroligin 4 surface is required to permit neurexin 1beta association.
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
report mutations in two X-linked genes encoding neuroligins NLGN3 and NLGN4 in siblings with autism-spectrum disorders
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.
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.
Data indicate that coding mutations in neuroligin 4 are very rarely associated to autism spectrum disorders.
Splice variants of the NLGN4 gene are associated with autism.
Syntrophin-gamma2 (SNTG2) is a de novo binding partner of X-linked neuroligin 4, which correlates with autism-related mutations.
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. The encoded protein interacts with discs, large (Drosophila) homolog 4 (DLG4). Mutations in this gene have been associated with autism and Asperger syndrome. Two transcript variants encoding the same protein have been identified for this gene.
, X-linked neuroligin 4
, neuroligin 4, X-linked
, neuroligin-4, X-linked-like
, neuroligin 4
, Neuroligin-4, X-linked