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1                                              NgR1 and FGF receptor 1 (FGFR1) are colocalized to synap
2                                              NgR1 expression by parvalbumin expressing interneurons i
3                                              NgR1 gene deletion enhances anatomical changes of inhibi
4                                              NgR1 is the founding member of the three-member NgR fami
5                                              NgR1, an axonal glycoprotein, is the founding member of
6  receptor/p75 neurotrophin receptor/LINGO-1 (NgR1/p75/LINGO-1) complex.
7 icity inhibitors Nogo-A and Nogo receptor 1 (NgR1) are differentially expressed in the SVZ-OB system,
8                 Neuronal Nogo-66 receptor 1 (NgR1) has been proposed to function as an obligatory cor
9         We examined whether Nogo Receptor 1 (NgR1) regulates the plasticity associated with fear exti
10 oke is in part mediated via Nogo receptor 1 (NgR1) signaling.
11                          Nogo-66 receptor 1 (NgR1) supports binding of the myelin inhibitors Nogo-A,
12 ted the CST in mice lacking nogo receptor 1 (NgR1), a protein implicated in limiting neural repair.
13 complex, composed of the Nogo-66 receptor 1 (NgR1), neurotrophin p75 receptor (p75), and LINGO-1, rep
14 sory cortex of mice lacking Nogo Receptor 1 (NgR1).
15 teract with the neuronal Nogo-66 receptor 1 (NgR1).
16 -dependent manner to the Nogo-66 receptor-1 (NgR1) and its homolog NgR2.
17 onal cell surface receptors Nogo receptor-1 (NgR1) and paired Ig-like receptor-B (PirB) to regulate n
18 ce (LOTUS) as an endogenous Nogo receptor-1 (NgR1) antagonist and demonstrated that LOTUS contributes
19                  Neuronal Nogo66 receptor-1 (NgR1) binds the myelin inhibitors NogoA, OMgp, and myeli
20 e sigma (RPTPsigma), and Nogo receptors 1-3 (NgR1-3).
21 harmacological experiments show that Nogo-66/NgR1 interaction reduces the proliferation of NSCs.
22 ss 3 Semaphorins, with or without additional NgR1 deletion.
23 g antibodies (Abs) against Nogo-A or against NgR1 increased long-term potentiation (LTP) induced by s
24 led that Nogo-66 and OMgp suppress LTP in an NgR1-dependent manner.
25            A Nogo signaling blockade with an NgR1 antagonist administered after stroke reduces the OP
26            A physiologic role for Nogo-A and NgR1 has been documented in the restriction of experienc
27  a new unprecedented function for Nogo-A and NgR1 in the homeostatic regulation of the pace of neurog
28 We therefore examined the role of Nogo-A and NgR1 in the regulation of neurogenesis.
29       These findings suggest that Nogo-A and NgR1 interactions may contribute to axonal branching in
30           Further analysis of the Nogo-A and NgR1 interactions revealed a novel third interaction sit
31   Reovirus virions bind to soluble JAM-A and NgR1, while infectious disassembly intermediates (ISVPs)
32         We propose that MT3-MMP activity and NgR1 shedding could stimulate circuitry remodeling in th
33 s rescued in the double mutant of LOTUS- and NgR1-KO mice.
34   PirB(-/-) and NgR1(-/-) single mutants and NgR1(-/-);PirB(-/-) double mutants show normal LTP, indi
35 h Nogo-A identifies immature neuroblasts and NgR1 germinal astrocytes.
36                                PirB(-/-) and NgR1(-/-) single mutants and NgR1(-/-);PirB(-/-) double
37 ion and detailed characterization of an anti-NgR1 monoclonal antibody, 7E11.
38                          Thus, specific anti-NgR1 antibodies may represent a useful therapeutic appro
39               Our data demonstrate that anti-NgR1 antibodies recognizing this epitope, such as 7E11,
40 ling by interfering with interaction between NgR1 and its coreceptors p75NTR or LINGO-1.
41 re, we report on a novel interaction between NgR1 and select members of the fibroblast growth factor
42 wledge of the molecular interactions between NgR1 and its ligands is imperative when assessing option
43 em-specific transmembrane protein that binds NgR1 and p75 and that is an additional functional compon
44                                     Blocking NgR1 on transfected cells or primary cortical neurons ab
45                           In postnatal brain NgR1 and NgR2 are strongly enriched in Triton X-100-inso
46        Suppression of anatomical dynamics by NgR1 is cell autonomous and is phenocopied by deletion o
47 n growth inhibition by myelin is mediated by NgR1-independent mechanisms.
48                          In the healthy CNS, NgR1 regulates dendritic spine shape and attenuates acti
49             In chronic rat spinal contusion, NgR1 decoy treatment from 4 to 6 months after injury res
50 te that four different schizophrenia-derived NgR1 variants fail to transduce myelin signals into axon
51         In primary cortical neurons, ectopic NgR1 inhibits FGF2-elicited axonal branching.
52  as dominant negatives to disrupt endogenous NgR1.
53 rface receptors of the Nogo Receptor family (NgR1, NgR2, and NgR3) restrict excitatory synapse format
54     We demonstrate the Nogo receptor family (NgR1-3) acts as Abeta receptors mediating an inhibition
55                                     Finally, NgR1(-/-) RGCs are strongly inhibited by MAG.
56 1 synapses uncovered a synaptic function for NgR1.
57 ted in primary cortical neurons derived from NgR1 null mice.
58 y were decreased in cultured OB neurons from NgR1-KO mice.
59             In the presence of VCN, however, NgR1(-/-) RGCs exhibit enhanced neurite growth.
60  evidence that certain disease-derived human NgR1 variants are dysfunctional proteins in vitro.
61 In non-neuronal cells, coexpression of human NgR1, p75 and LINGO-1 conferred responsiveness to oligod
62           Collectively, our results identify NgR1 and NgR3 as CSPG receptors, suggest that there is f
63 collapse that is significantly attenuated in NgR1-null neurons compared with wild-type controls.
64  density caudal to the injury is detected in NgR1 decoy-treated animals by immunohistology and by pos
65                     In juvenile mice, LTD in NgR1(-/-), but not PirB(-/-), slices is absent.
66 2-elicited enhancement of hippocampal LTP in NgR1 mutants.
67 GFP revealed significant CST regeneration in NgR1 knock-out mice.
68 increased in LOTUS-KO mice, whereas those in NgR1-KO mice were decreased.
69 th aged and young adult mice, stroke induces NgR1 ligands and down-regulates NgR1 inhibitors during t
70 ince this linkage was not detected in intact NgR1 or a slightly larger fragment containing Cys-335 an
71 rate pharmacological experiment, intrathecal NgR1 decoy protein administration was initiated 3 months
72                                 Mice lacking NgR1 protein exhibit reduced working memory function, co
73 lyzed the disulfide structure of full-length NgR1.
74 on beyond the injury site in either Nogo/MAG/NgR1 triple mutants or NgR1 single mutants.
75             The Nogo receptor family members NgR1 and NgR2 bind to MAIs and have been implicated in n
76 mposed of the structurally related molecules NgR1, NgR2, and NgR3.
77 ults, shRNAi-mediated knock-down of neuronal NgR1 does not result in a substantial release of L-MAG (
78      To examine the contribution of neuronal NgR1 to outgrowth inhibition, we used two different stra
79 udies with Nogo-66, we propose that neuronal NgR1 has a circumscribed role in regulating cytoskeletal
80 ndent synaptic strength and uncover neuronal NgR1 as a regulator of synaptic plasticity.
81                                   In neurons NgR1 and NgR2 support MAG binding in a sialic acid-depen
82 hat bind to a neuronal Nogo-66 receptor (NgR/NgR1) to limit axonal regeneration after central nervous
83 cap domain and stalk region of NgR2, but not NgR1, are sufficient for MAG binding, and when expressed
84        These data introduce Olfm1 as a novel NgR1 ligand that may modulate the functions of the NgR1
85 etion of disulfide loop Cys(309)-Cys(336) of NgR1 selectively increases its affinity for Nogo-66 and
86 wo different strategies, genetic ablation of NgR1 through the germline and transient short hairpin RN
87                           The LRR cluster of NgR1 supports binding of Nogo-66, OMgp, and MAG.
88                      Conditional deletion of NgR1 in the chronic state results in gradual improvement
89 neration is abolished by genetic deletion of NgR1.
90 ve when assessing options for development of NgR1-based therapeutics for central nervous system injur
91       Introduction of the shed ectodomain of NgR1 is sufficient to accelerate excitatory synapse form
92                                Expression of NgR1 confers reovirus binding and infection of nonsuscep
93 stal structures of a recombinant fragment of NgR1 had revealed a disulfide linkage between Cys-266 an
94               Olfm1 caused the inhibition of NgR1 signaling by interfering with interaction between N
95                         In addition, loss of NgR1 attenuates long-term depression of synaptic transmi
96                                  The loss of NgR1 function in adulthood eliminates spontaneous fear r
97                                      Loss of NgR1 leads to FGF2-dependent enhancement of long-term po
98                                      Loss of NgR1 leads to increased phosphorylation of extracellular
99                                      Loss of NgR1 results in altered spine morphologies along apical
100  OMgp strongly inhibits neurite outgrowth of NgR1 wild-type and mutant sensory neurons.
101 inase) pathway, without the participation of NgR1.
102 ies have shown that the entire LRR region of NgR1, including the C-terminal cap of the LRR, LRRCT, is
103 se data provide a perspective on the role of NgR1 ligand function in OPC fate in the context of a spe
104 ort a role for MT3-MMP-dependent shedding of NgR1 in regulating excitatory synapse development.SIGNIF
105                 Neural expression studies of NgR1 and NgR2 have revealed broad and overlapping, yet d
106                  Although the LRR domains on NgR1 are necessary for binding to the myelin proteins, t
107 te in either Nogo/MAG/NgR1 triple mutants or NgR1 single mutants.
108 binds to NgR1 and can replace p75 in the p75/NgR1/LINGO-1 complex to activate RhoA in the presence of
109 r, our findings establish that physiological NgR1 signaling regulates activity-dependent synaptic str
110 PlexinA4 double mutants or PlexinA3/PlexinA4/NgR1 triple mutants through a complete transection injur
111 ly of proteins named Nogo receptor proteins (NgR1 to NgR3) regulates Abeta production via interaction
112 NAQLR located in the third LRR domain of rat NgR1.
113 ligand-binding subunit (the Nogo-66 receptor NgR1) and a signal transducing subunit (the neurotrophin
114 ors, Nogo and MAG, and their common receptor NgR1 (or NgR).
115                      Nogo-A and its receptor NgR1 are present at cortical synapses.
116 emonstrate that reovirus binds Nogo receptor NgR1, a leucine-rich repeat protein expressed in the CNS
117    The expression of Nogo-A and the receptor NgR1 limits the recovery of adult mammals from central n
118 r complex comprised of the Nogo-66 receptor (NgR1) and two transmembrane co-receptors p75/TROY and LI
119 ns and in vivo We identify Nogo-66 receptor (NgR1) as an MT3-MMP substrate that is required for MT3-M
120                            Nogo-66 receptor (NgR1) is a leucine-rich repeat (LRR) protein that forms
121                        The Nogo-66 receptor (NgR1) is a promiscuous receptor for the myelin inhibitor
122  Nogo-A (Reticulon 4A) and Nogo-66 receptor (NgR1) limit adult CNS axonal growth after injury is supp
123 hrough interaction with the Nogo A receptor (NgR1) complex.
124 rived inhibitors with soluble Nogo receptor (NgR1, RTN4R) decoy protein.
125                         The Nogo66 receptor (NgR1) is a neuronal, leucine-rich repeat (LRR) protein t
126               We identify Nogo-66 receptors (NgR1) as a downstream target of MT3-MMP proteolytic acti
127                              Nogo receptors (NgR1, NgR2, and NgR3) are growth cone directive molecule
128 roke induces NgR1 ligands and down-regulates NgR1 inhibitors during the peak OPC maturation block.
129     Incubating reovirus virions with soluble NgR1 neutralizes infectivity.
130 gR1, we examined a series of Ala-substituted NgR1 mutants for ligand binding activity.
131           Furthermore, processing of surface NgR1 by MT3-MMP generates a soluble ectodomain fragment
132 ever, in reconstituted non-neuronal systems, NgR1 and p75 together are unable to activate RhoA, sugge
133 NgR2 directly and with greater affinity than NgR1.
134   Regional gene disruption demonstrates that NgR1 expression is required in both the basolateral amyg
135                                We found that NgR1 and NgR3 bind with high affinity to the glycosamino
136 ysis of synaptosomal fractions revealed that NgR1 is enriched synaptically in the hippocampus.
137                                 We show that NgR1 inhibits the formation of new synapses in the posts
138                  These findings suggest that NgR1, a receptor previously shown to restrict axon growt
139                           This suggests that NgR1 and PirB participate in ligand-dependent inhibition
140 bitors, indicating that Olfm1 attenuates the NgR1 receptor functions.
141                            We eliminated the NgR1 pathway genetically in mice by conditional gene tar
142 ion that other receptors are involved in the NgR1 complex.
143 e that AMIGO3 substitutes for LINGO-1 in the NgR1-p75/TROY inhibitory signalling complex and suggests
144 igand that may modulate the functions of the NgR1 complex in axonal growth.
145 adjacent C-terminal region (CT stalk) of the NgR1 contributes to interaction with its coreceptors.
146               We find that regardless of the NgR1 genotype, membrane-bound MAG strongly inhibits neur
147  in the middle of the concave surface of the NgR1 leucine-rich repeat domain and surrounded by differ
148 de structure in the C-terminal region of the NgR1, wherein the two Cys residues, Cys-335 and Cys-336,
149 is an additional functional component of the NgR1/p75 signaling complex.
150 ory signalling complex and suggests that the NgR1-p75/TROY-AMIGO3 receptor complex mediates myelin-in
151 endrocyte differentiation occurs through the NgR1/Lingo-1 receptor complex.
152 purified 22-kDa protein containing all three NgR1- and PirB-interacting domains (Nogo-22) is a substa
153                           Although all three NgR1-interacting domains of Nogo-A also interact with Pi
154 d share neuronal receptor mechanisms through NgR1 and PirB.
155                                        Thus, NgR1 determines the low set point for synaptic turnover
156                                        Thus, NgR1 is the predominant receptor for Nogo-22 in regenera
157                                        Thus, NgR1 robustly inhibits elimination of fear expression in
158 FGF2 bind directly and with high affinity to NgR1 but not to NgR2 or NgR3.
159 ltiple structurally distinct ligands bind to NgR1, we examined a series of Ala-substituted NgR1 mutan
160 igodendrocyte myelin glycoprotein binding to NgR1 with IC50 values of 120, 14, and 4.5 nm, respective
161 sed in postnatal and adult neurons, binds to NgR1 and can replace p75 in the p75/NgR1/LINGO-1 complex
162                  Olfm1 specifically binds to NgR1, as judged by alkaline phosphatase assay and coimmu
163     After injury to the corticospinal tract, NgR1 limits axon collateral sprouting but is not importa
164              We show here that the other two NgR1-interacting domains, Nogo-A-24 and Nogo-C39, also b
165 gp, Nogo-66, and MAG compared with wild-type NgR1 or NgR2.
166 ificant poststroke motor recovery, even when NgR1 blockade is provided during the chronic time points
167  targeting all three myelin ligands, as with NgR1 decoy receptor, provides the optimal chance for ove
168 neurite outgrowth but fail to associate with NgR1 or NgR2.
169                    Olfm1 is coexpressed with NgR1 in dorsal root ganglia and retinal ganglion cells i
170 ith MAG with a higher affinity compared with NgR1.
171          AMIGO3 interacted functionally with NgR1-p75/TROY in non-neuronal cells and in brain lysates
172 two separate domains are known interact with NgR1.
173 ggesting a trivalent Nogo-A interaction with NgR1.
174 nanomolar interactions of RTN2 and RTN3 with NgR1.
175 ing myelin-derived inhibitors signaling with NgR1 decoy augments recovery from chronic spinal cord in

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