Recombinant Mouse Neuroligin-1 (Nlgn1), partial

1. 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. PMID: 30046996
2. 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. PMID: 27473321
3. Co-expression of gamma-Pcdhs inhibits the ability of Nlg1 to increase spine density and to induce presynaptic differentiation in hippocampal neurons in vitro. PMID: 28297673
4. 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. PMID: 28939043
5. 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 PMID: 28841651
6. 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. PMID: 28283575
7. Neuroligin 1 regulates spines and synaptic plasticity via LIMK1/cofilin-mediated actin reorganization. PMID: 26880202
8. 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. PMID: 26771491
9. 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 PMID: 25595979
10. the R451C mutation in the Nlgn3 gene, associated with autism spectrum disorder in humans, confers resistance to induced seizures PMID: 25592157
11. This study provided first evidence that NL1 is essential for normal excitatory transmission and long-term synaptic plasticity in the hippocampus of intact animals. PMID: 25713840
12. 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 PMID: 24860089
13. This study demonistrated that amyloid-induced neuroinflammation leads to epigenetic suppression of NLGN1 expression. PMID: 24441681
14. This study demonstrate a direct functional interaction between CaMKII and NL-1, two primary components of excitatory synapses. PMID: 24336150
15. Data indicate that absence of Neuroligin-1 (NLG1) decreases wakefulness duration. PMID: 23716671
16. Results indicate that neuroligin-1 expression selectively increases the degree, but not the onset, of excitatory synapse formation in adult-born neurons. PMID: 23110172
17. MDGA binding and suppression of synaptogenic activity was selective for neuroligin-2 and not neuroligin-1 excitatory synapse organizer. PMID: 23358245
18. Transcellular competitive processes govern synapse formation and number in developing cortex; NL1 has a central function in these processes. PMID: 23143522
19. findings suggest that the loss of Nlgn-1 is associated with some use-dependent destabilization of excitatory synapse organization, and indicate that in the absence of Nlgn-1, the tenacity of excitatory synapses might be somewhat impaired PMID: 22860111
20. This study implicated neuroligin 1 cleavage with epileptiform activity and maturation of developing neuronal circuits. PMID: 23083741
21. This study presented evidence that combined NL1 and SC1 overexpression triggers excitotoxic neurodegeneration through SC1 signaling at synaptic connections initiated by NL1. PMID: 22542674
22. these data reveal a mechanism by which membrane-diffusing AMPARs can be rapidly trapped at PSD-95 scaffolds assembled at nascent neurexin/neuroligin adhesions, in competition with existing synapses. PMID: 21940442
23. Neurexins and neuroligins, which constitute large and complex families of fundamental players in synaptic activity, are produced and processed by endothelial and vascular smooth muscle cells throughout the vasculature. PMID: 19926856
24. the clustering of synaptic vesicles triggered by neuroligin-1 overexpression required the presence of N-cadherin in neurons PMID: 20534458
25. Findings suggest that neuroligin-1 can modulate, in a pathway-specific manner, synaptic plasticity in the amygdala circuits of adult animals, likely by regulating the abundance of postsynaptic NMDA receptors. PMID: 20176955
26. These results provide for the first time evidence for an involvement of a neuroligin-neurexin protein network in core symptoms of fragile X syndrome. PMID: 19932134
27. findings demonstrate the influence of NL1 expression in vivo on synapse morphology, LTP, and acquisition of spatial learning in the water maze, and draw a link between aberrant synapse morphology, impaired synaptic plasticity, and deficits in learning PMID: 19437420
28. These data are consistent with the hypothesis that NL1 dysfunction can lead to autism- and mental retardation-related behavioral abnormalities in part via alteration of NMDA receptor (NMDAR) function. PMID: 20147539
29. Study on the expression of NLGN1 in the developing and adult olfactory bulb PMID: 12141453
30. Postsynaptic density (PSD) proteins PSD-95 and neuroligin-1 (NLG) are critical for dictating the ratio of excitatory-to-inhibitory synaptic contacts. PMID: 15358863
31. Data show that neuroligin 1 is required for proper synapse maturation and brain function, but not for the initial formation of synaptic contacts. PMID: 16982420
32. Expression of neuroligin 1 inhibits trans-binding to recombinant neurexins and reduces the density of presynaptic terminals in hippocampus. PMID: 17360903
33. Neuroligin1 is essential for presynaptic terminal maturation. PMID: 19628693

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KEGG: mmu:192167

STRING: 10090.ENSMUSP00000074565

UniGene: Mm.316080