No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human Neuroligin 1 Antibodies:
anti-Mouse (Murine) Neuroligin 1 Antibodies:
anti-Rat (Rattus) Neuroligin 1 Antibodies:
Go to our pre-filtered search.
Mammalian Monoclonal Neuroligin 1 Primary Antibody for ISt, IHC - ABIN1304856
Zou, McSweeney, Sebastian, Reynolds, Dong, Zhou, Deng, Wang, Liu, Zhu, Zou, Shi, Albert, Mao: A critical role of RBM8a in proliferation and differentiation of embryonic neural progenitors. in Neural development 2015
Show all 8 Pubmed References
Dog (Canine) Polyclonal Neuroligin 1 Primary Antibody for ELISA - ABIN547490
Chih, Engelman, Scheiffele: Control of excitatory and inhibitory synapse formation by neuroligins. in Science (New York, N.Y.) 2005
Rat (Rattus) Polyclonal Neuroligin 1 Primary Antibody for WB - ABIN1742286
Dahlhaus, Hines, Eadie, Kannangara, Hines, Brown, Christie, El-Husseini: Overexpression of the cell adhesion protein neuroligin-1 induces learning deficits and impairs synaptic plasticity by altering the ratio of excitation to inhibition in the hippocampus. in Hippocampus 2010
Coinjection of low doses of morpholinos for beta-neurexin 1a and neuroligin 1 together or in combination with morpholinos targeting the -heparin--binding isoforms of vascular endothelial growth factor A recapitulates the observed abnormalities
Findings support a contribution of the NLGN1 gene pathway to the neurobiological underpinnings of PTSD.
We show that a novel NLGN1 Pro89Leu (P89L) missense variant found in two autism spectrum disorder (ASD) siblings leads to changes in cellular localization, protein degradation, and to the impairment of spine formation. Furthermore, we generated the knock-in P89L mice, and we show that the P89L heterozygote mice display abnormal social behavior, a core feature of ASD
the expression of NL1 and its binding partner neurexin-1beta was increased in temporal lobe epileptic foci in patients and lithium-pilocarpine-treated epileptic rats.
Neuroligin 1 (NL1) promotes the formation of glutamatergic synapses and mediates long-term potentiation.
NLGN1 was associated with schizophrenia in Chinese Han Populations
Increasing expression of TGF-beta1 protein, decreasing expressions of Ghrelin, Neurexin, and Neuroligin proteins can induce the loss or dysfunction of ganglion cells in distal intestinal canal
Neuroligin-1 and Glu may represent new markers of ganglion cells, whose expression may correlate with the pathogenesis, diagnosis, differential diagnosis or classification of Hirschsprung's disease.
Results indicate that the neurexin and neuroligin synaptic complex is intrinsically involved in the regulation of DISC1 function, thus contributing to a better understanding of the pathology of schizophrenia.
Monitoring the attachment and detachment of neurexin (Nrx)-coated quantum dots measures the rates of neurexin (Nrx)/neuroligin interaction in the hippocampus.
We identified a cluster of single nucleotide polymorphisms at the NLGN1 locus showing significant association with BP variability. Follow-up analyses did not support an association with risk of ischemic stroke and its subtypes
Expression levels of neurexin and neuroligin in ENS are significantly down-regulated in HSCR, which may be involved in the pathogenesis of HSCR.
these manipulations of NL1 function illuminate the significance of NL1 intracellular signaling in vivo, and enhance our understanding of the factors that gate the maturation of glutamatergic synapses and complex behavior
Amyloid beta-peptide binds to the extracellular domain of neuroligin-1 with a K(d) in the nanomolar range.
glycosylation processing of neuroligin, in addition to mRNA splicing and gene selection, contributes to the specificity of the neurexin-beta/neuroligin-1 association
the neurexin 1beta/neuroligin 1 complex has a role in synapse formation
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.
Our discoveries provide insight into the specific interaction of the GOPC PDZ domain with the C-terminal peptide of Nlg and also provide a general insight about the possible binding mode of the interaction of Nlg with other PDZ domain-containing proteins.
Neuroligin-1 performs diverse synaptic functions by mechanisms that include as essential components of alpha-neurexin binding and neuroligin dimerization, but extend beyond these activities.
This study provides a novel approach to understand the molecular basis of Fragile X syndrome by linking the dysregulated synaptic expression of NLGNs with FMRP
To characterize the possible contribution of NLGN1 to inflammatory pain, the present study analyzed the changes of NLGN1 expression after intraplantar injection of complete Freund's adjuvant (CFA). Our data revealed an activity-dependent recruitment of NLGN1 into synapses, which was essential for NMDAR hyperfunction and pain hypersensitivity.
Results demonstrate that NLG1 regulates hippocampal long-term depression (LTD) in a gene dosage-dependent manner. Thus, NLG1+/-, but not NLG1-/- mice, show impaired NMDAR-LTD and elevated mGluR-LTD. In addition, NLG1+/- mice exhibit autistic-like behavior including increased grooming and impairments in social recognition and contextual fear memory.
This review propose that shifts in NLGN1 and NLGN2 expression in specific excitatory and inhibitory neuronal subpopulations in response to experience regulate the dynamic processes of memory consolidation and strengthening.
Replacing endogenous neuroligin-1 (Nlg1) with either Nlg1-Y782A or -Y782F in CA1 hippocampal neurons impaired long-term potentiation (LTP).
Study generated a knock-in mouse line in which an hemagglutinin (HA) epitope was inserted into the Nlgn1 gene. Using HA-Nlgn1 mice, study demonstrated the cellular and subcellular localization of endogenous Nlgn1 in cerebellar circuits, providing insights into cell- and synapse-specific roles of Nlgn1.
SynCAM1, Neuroligin-1B and Neuroligin-2A were overexpressed in newborn neurons in the dentate gyrus of 7- to 9-week-old mice. SynCAM1 increased the morphological maturation of dendritic spines and mossy fiber terminals while Neuroligin-1B increased spine density. In contrast, Neuroligin-2A increased both spine density and size as well as GABAergic innervation and resulted in a drastic increase of neuronal survival.
Co-expression of gamma-Pcdhs inhibits the ability of Nlg1 to increase spine density and to induce presynaptic differentiation in hippocampal neurons in vitro.
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 results indicate that Nrx2alpha and NL1 are targets of Abeta oligomers and that prevention of this interaction reduces the deleterious impact of Abeta oligomers on synapses and cognition.
Neuroligin 1 regulates spines and synaptic plasticity via LIMK1/cofilin-mediated actin reorganization.
Study shows that astrocyte-secreted hevin is a trans-synaptic linker that bridges presynaptic NRX1alpha with postsynaptic NL1B. This way, hevin organizes both pre- and postsynaptic specializations and aligns them across the synapse.
Results are indicative of an altered immediate response of the brain to peripheral stimulation in Nlgn1 KO mice, and suggest a role for NLGN1 in the regulation of cerebrovascular responses
the R451C mutation in the Nlgn3 gene, associated with autism spectrum disorder in humans, confers resistance to induced seizures
This study provided first evidence that NL1 is essential for normal excitatory transmission and long-term synaptic plasticity in the hippocampus of intact animals.
NLGN1 and alpha6 integrin preferentially colocalize in the mature retinal vessels, whereas NLGN1 deletion causes an aberrant VE-cadherin, laminin and alpha6 integrin distribution in vessels
This study demonistrated that amyloid-induced neuroinflammation leads to epigenetic suppression of NLGN1 expression.
This study demonstrate a direct functional interaction between CaMKII and NL-1, two primary components of excitatory synapses.
Data indicate that absence of Neuroligin-1 (NLG1) decreases wakefulness duration.
transmembrane ligand for neurexins\; involved in development and maturation of synaptic connections
, neuroligin I
, neuroligin 1 isoform A1A2B