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1 urexin 1beta are mixed with cells expressing neuroligin 1.
2 hat are similar in structure and sequence to neuroligin 1.
3 n, subtractive display identified YWK-II and neuroligin 1.
4 minants particular to the unique function of neuroligin 1.
5 TM2 without altering binding to postsynaptic neuroligin-1.
6 ation, and synaptic transmission mediated by neuroligin-1.
7 2 ligands, again rendering LRRTM2 similar to neuroligin-1.
8 synapses in transfected neurons similarly to neuroligin-1.
9                                              Neuroligins 1, 2, and 3 were active in this assay.
10 from triple neurexin-1/2/3 or from quadruple neuroligin-1/2/3/4 conditional KO mice that lacked all n
11           We identified chicken orthologs of neuroligins 1, -3, and -4, but could find no evidence of
12                                      Whereas neuroligins-1, -3, and -4 localize to glutamate postsyna
13 ces the ability of neurexin-1beta to cluster neuroligin-1/3/4 and glutamatergic postsynaptic proteins
14                                              Neuroligins 1-4 are postsynaptic transmembrane proteins
15 1 exhibit enhanced spinal cord expression of neuroligin 1, a cell-adhesion postsynaptic protein regul
16 rons and cocultured tsA 201 cells expressing neuroligin-1, a postsynaptic binding partner of neurexin
17   Beta-neurexins are candidate receptors for neuroligin-1, a postsynaptic membrane protein that can t
18       CL1 competed for neurexin binding with neuroligin-1, a well characterized neurexin ligand.
19                             An enrichment of neuroligin-1 A1 in GABAergic neuron types suggests a rol
20            Mutations in two surface loops of neuroligin 1 abolished neuroligin binding to neurexin 1b
21 downstream of mTOR effects the expression of neuroligin 1 and excitatory synaptic transmission in the
22 in (GABARAP; approximately 13%), but not for neuroligin 1 and gephyrin.
23  generated transfected cell lines expressing neuroligin 1 and neurexin 1beta.
24  excitatory and inhibitory synaptic proteins neuroligin 1 and neuroligin 2, which promote memory stre
25                              These subtypes, neuroligin 1 and neuroligin 3, have roles in synaptogene
26 r splice insertions restrict the function of neuroligin-1 and -2 to glutamatergic and GABAergic conta
27 sing an in vitro system, we demonstrate that neuroligin-1 and -2, postsynaptically localized proteins
28 that is lacking in fragile X syndrome, binds neuroligin-1 and -3 mRNA.
29 g to neurexin-1 beta, but not the folding of neuroligin-1 and confirm the validity of the binding int
30 g, whereas wild-type streptavidin aggregated neuroligin-1 and disrupted presynaptic contacts.
31 in-1beta forms a trans-synaptic complex with neuroligin-1 and neuroligin-2 and that this interaction
32                                     Although neuroligin-1 and neuroligin-2 are not directly cleaved b
33        Here, we generated neurexin-1beta and neuroligin-1 and neuroligin-2 fusion proteins containing
34 y, we found a functional distinction between neuroligins 1 and 3.
35 es the binding affinity of neurexin-1beta to neuroligins-1 and -4 but has little effect on binding to
36          We conclude that neurexin 1beta and neuroligin 1 (and, by extension, other beta-neurexins an
37  of identified PDZ3-binding proteins (CRIPT, neuroligin-1, and citron) and (2) selective mutation of
38 urexins, blocks the synaptogenic activity of neuroligin-1, and reduces the density of presynaptic ter
39 tatory synapses, the membrane confinement of neuroligin-1, and the phosphotyrosine level of neuroligi
40 vely spliced sites in neurexin-1 beta and in neuroligin-1 are positioned nearby the binding interface
41       The extracellular domain of functional neuroligin-1 associates as a dimer when analyzed by sedi
42 utes to the specificity of the neurexin-beta/neuroligin-1 association.
43                 Structure-based mutations of neuroligin-1 at the interface disrupt binding to neurexi
44 in 1 is regulated by alternative splicing of neuroligin 1 (at splice site B) and of neurexins (at spl
45 asmon resonance, we established that soluble neuroligins-1 bind neurexin-1beta, but the homologous al
46 free Ca2+, which probably acts by binding to neuroligin 1 but not to neurexin 1beta.
47           To determine if neurexin 1beta and neuroligin 1 can also interact with each other when pres
48  extremely long genes, including Neurexin-1, Neuroligin-1, Cntnap2, and GABA(A)beta3.
49 exin-independent mechanism that requires the neuroligin-1 cytoplasmic sequences.
50 nism by which interactions between MDGAs and neuroligin-1 delays the assembly of functional excitator
51  as exemplified by miR-146a, which inhibited neuroligin 1-dependent synaptogenesis.
52 ntical surfaces on the opposite faces of the neuroligin-1 dimer to form a heterotetramer.
53                                    Moreover, neuroligin-1 dimerization was not required for either th
54 evertheless, both alpha-neurexin binding and neuroligin-1 dimerization were essential for the increas
55 alpha- and beta-neurexin binding, or abolish neuroligin-1 dimerization.
56 ides chain or the terminal sialic acids from neuroligin-1 enhance its activity, whereas deglycosylati
57 ivity was selective for neuroligin-2 and not neuroligin-1 excitatory synapse organizer.
58                                              Neuroligin-1 forms a constitutive dimer, and two neurexi
59 pressed five soluble and exportable forms of neuroligin-1 from recombinant DNA sources, by truncating
60                                              Neuroligin-1 has a unique N-linked glycosylation pattern
61 d from split-GFP-modified neurexin-1beta and neuroligin-1 if and after neurexin-1beta bound to its ne
62  identify a subtype-specific role in LTP for neuroligin 1 in young CA1, which persists into adulthood
63  overexpression of AMPA receptors along with Neuroligin-1 in 293T cells is sufficient to stabilize pr
64                            Overexpression of neuroligin-1 in control or neuroligin-deficient neurons
65            Expression of a dominant-negative neuroligin-1 in cultured neurons markedly reduced the si
66   Here, we present the crystal structures of neuroligin-1 in isolation and in complex with neurexin-1
67                     Accordingly, deletion of neuroligin-1 in knockout mice selectively decreases the
68 a mechanism identical to that of the role of neuroligin-1 in NMDAR-dependent LTP.
69  in apparent synapse size that is induced by neuroligin-1 in transfected neurons.
70            Conversely, the overexpression of neuroligin-1 increased synapse numbers but not spine num
71 of the positively charged A1 insert in mouse neuroligin-1 increases its binding to heparan sulphate,
72 e deacetylase (HDAC) inhibitors that improve neuroligin-1-induced synaptogenesis by modulating class-
73                         Thus, in this assay, neuroligin-1 induces apparent synapse formation by bindi
74        cis-expression of neurexin-1beta with neuroligin-1 inhibits trans-binding to recombinant neure
75 tory proteins implicated in ASD/ID, Trio and Neuroligin 1, interact with one another to promote gluta
76 red in these neurons, confirming that PSD-95/neuroligin-1 interaction is involved in postsynaptic ass
77                                              Neuroligin 1 is a neuronal cell surface protein that bin
78 and that alpha- and beta-neurexin binding by neuroligin 1 is regulated by alternative splicing of neu
79  overexpression of neuroligin-3, which, like neuroligin-1 is also targeted to excitatory synapses, ha
80  inhibition of eIF4E or genetic reduction of neuroligin 1 levels normalizes the increased excitatory
81 tions in Trio that either inhibit or augment Neuroligin 1-mediated glutamatergic synapse formation.
82  detected in the inner retina, low levels of neuroligin 1 mRNA were also detected in the photorecepto
83 hesis, we examined the functional effects of neuroligin-1 mutations that impair only alpha-neurexin b
84                                          The neuroligin-1/neurexin-1 beta complex exhibits a nanomola
85 the validity of the binding interface of the neuroligin-1/neurexin-1 beta complex.
86                                   We deleted neuroligin-1, neuroligin-2, and neuroligin-3, the major
87     The localization and synaptic effects of neuroligin-1 (NL-1, also called NLGN1) are specific to e
88 cently, the synaptic cell adhesion molecules neuroligin 1 (NL1) and SynCAM were shown to induce presy
89 eta-neurexin association, splice insert B in neuroligin-1 (NL1) is the key element regulating the NL1
90                   The cell adhesion molecule neuroligin-1 (NL1) modifies NMDAR-dependent synaptic tra
91                                We found that neuroligin-1 (NL1), which is located at excitatory posts
92  Syt4 and the transsynaptic adhesion protein Neuroligin 1 (Nlg1).
93  synaptic adhesion molecules neurexin-1beta, neuroligin-1 (Nlg1) and leucine-rich-repeat transmembran
94               The synaptic adhesion molecule Neuroligin-1 (NLG1) controls the activity and synaptic l
95 tivity induces acute proteolytic cleavage of neuroligin-1 (NLG1), a postsynaptic adhesion molecule at
96 2 (NLGN2) limited to inhibitory synapses and neuroligin 1 (NLGN1) dominating at excitatory synapses.
97 on between Trio and the synaptogenic protein Neuroligin 1 (NLGN1) in the brain.
98 ne showed some evidence for association near neuroligin 1 (NLGN1) on chromosome 3, but did not suppor
99                                 One locus in neuroligin 1 (NLGN1) passing the genome-wide significanc
100                         The synaptic protein Neuroligin 1 (NLGN1), a cell adhesion molecule, is criti
101                                              Neuroligin 1 (NLGN1), a postsynaptic protein found in ce
102 RNA degradation of downstream targets CD144, Neuroligin 1 (NLGN1), and TNF-alpha-stimulated gene/prot
103 he hypotheses that the post-synaptic protein Neuroligin-1 (NLGN1) is affected early in the process of
104 ed heterologous synapse formation induced by neuroligin-1 or LRRTM2.
105 ioned such that binding of neurexin-1beta to neuroligin-1 or neuroligin-2 allowed GFP reconstitution
106 hey were assembled from parts of Barnase and Neuroligin-1 or of Barstar and Neurexin3beta, respective
107        We now show that in cultured neurons, neuroligin-1 overexpression increases excitatory, but no
108 , supported by assays with the autism-linked neuroligin-1-P89L mutant.
109 sion molecules, with the classical Neurexin1-Neuroligin 1 pair being the most prominent, suggesting t
110                                        Thus, neuroligin-1 performs diverse synaptic functions by mech
111 , in hippocampal CA1 pyramidal neurons, that neuroligin-1 performs two key functions in excitatory sy
112                        Our data suggest that neuroligin-1 performs two mechanistically distinct signa
113 gin-1, with ~4-6% of neurexin-1 and ~2-3% of neuroligin-1 present in the adult brain as soluble ectod
114   In this issue, Liu et al. demonstrate that neuroligin 1 promotes actin assembly associated with syn
115                          At retinal synapses neuroligin 1 protein was detected in the inner plexiform
116 urexin-beta and inhibit its interaction with neuroligin-1, raising the possibility that disruption of
117                                    Moreover, neuroligin 1 splice variants with distinct neurexin bind
118                                           In neuroligin 1, splice site B is a master switch that dete
119 ties differentially regulate synaptogenesis: neuroligin 1 that binds only beta-neurexins potently sti
120 tently stimulates synapse formation, whereas neuroligin 1 that binds to both alpha- and beta-neurexin
121 gated the interaction of neurexin 1beta with neuroligin 1 to evaluate their potential to function as
122 as essential for the ability of postsynaptic neuroligin-1 to dramatically increase synapse density, s
123  mice targeting all three major neuroligins [neuroligin-1 to neuroligin-3 (NL123)] with parvalbumin-C
124 uires trans-synaptic binding of postsynaptic neuroligin-1 to presynaptic beta-neurexins but not the c
125  with monovalent streptavidin allowed stable neuroligin-1 tracking without cross-linking, whereas wil
126 , the AMPA-type glutamate receptor GluA1 and neuroligin 1 undergo spatially restricted entry into the
127  suppresses the synapse-boosting activity of neuroligin-1, whereas chronic inhibition of general syna
128 eurexins are decreased, whereas the level of neuroligin 1 (which binds to neurexins that in turn bind
129   Labeling of site-specifically biotinylated neuroligin-1 with monovalent streptavidin allowed stable
130 ally cleaved by ADAM10 similar to its ligand neuroligin-1, with ~4-6% of neurexin-1 and ~2-3% of neur

 
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