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