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1 or (2) electrical stimulation, which causes growth cone collapse.
2 ement of Sema3A receptors and F-actin during growth cone collapse.
3 is may be a general principle of physiologic growth cone collapse.
4 nst a universal signaling pathway underlying growth cone collapse.
5 x 1 in sensory neurons blocks Sema3A-induced growth cone collapse.
6 n growth cones and inhibits thrombin-induced growth cone collapse.
7 dation of RhoA, a mediator of Sema3A-induced growth cone collapse.
8 rowth cones and oligodendrocytes resulted in growth cone collapse.
9 ein-synthesis requirement for Sema3A-induced growth cone collapse.
10 tive rac1 remain sensitive to myelin-induced growth cone collapse.
11 lomotor neurons abrogates Sema3A/C-dependent growth cone collapse.
12 negative mutants suppresses netrin-1-induced growth cone collapse.
13 activated mTOR and inhibited ephrin-induced growth cone collapse.
14 blocked its axonal distribution and induced growth cone collapse.
15 ons lacking heparan sulfate exhibit impaired growth cone collapse.
16 domain that was required for Sema3A-induced growth cone collapse.
17 te application of soluble inhibitor to assay growth cone collapse.
18 ), the transmembrane receptor p75NTR signals growth cone collapse.
19 axonal RhoA mRNA abolishes Sema3A-dependent growth cone collapse.
20 use frontal cortex through ephrin-A5-induced growth cone collapse.
21 pecifically tailored to control Eph-mediated growth cone collapse.
22 s cytoskeletal rearrangements that result in growth cone collapse.
23 necessary and sufficient for Sema3A-mediated growth cone collapse.
24 d this phosphorylation event is required for growth cone collapse.
25 rotein kinase C substrate phosphorylation in growth cone collapse.
26 activation is necessary for thrombin-induced growth cone collapse.
27 cytosis of the plasma membrane, resulting in growth cone collapse.
28 t signaling pathways that converge to induce growth cone collapse.
29 ary neurons interferes with ephrin-A-induced growth cone collapse.
30 target binding, and inhibits Sema3A-induced growth-cone collapse.
31 nce of the floor plate, but without inducing growth-cone collapse.
32 of BDNF-mediated protection from NO-induced growth-cone collapse.
33 ts thus provide unexpected evidence that the growth cone-collapsing activities and substrate growth-i
37 protein retains biological activity as a DRG growth cone collapsing agent and saturably binds to DRG
41 creted protein that in vitro causes neuronal growth cone collapse and chemorepulsion of neurites, and
42 e effects of Shh on axonal growth, including growth cone collapse and chemorepulsive axon turning but
43 s on two populations of embryonic neurons in growth cone collapse and collagen matrix chemorepulsion
44 axons to netrin-1, preventing UNC5A-mediated growth cone collapse and converting netrin-1-stimulated
46 idic devices and stripe assays, we show that growth cone collapse and guidance at low concentrations
48 ic acid (poly I:C) or by mRNA rapidly causes growth cone collapse and irreversibly inhibits neurite e
49 n-A2, slit-3, and semaphorin3A still induced growth cone collapse and loss of actin filaments, nerve
50 rowth inhibitory action of central myelin in growth cone collapse and neurite outgrowth in vitro assa
53 ved neurotrophic factor (BDNF) induces rapid growth cone collapse and neurite retraction of embryonic
55 ve rac1 or cdc42 negated collapsin-1-induced growth cone collapse and promoted neurite outgrowth on a
57 in assembly led to filopodial retraction and growth cone collapse and resulted in the bifurcation of
61 s a local synthesis of proteins that mediate growth cone collapse and turning in response to guidance
62 EphB2-4/5 mutant, restored ephrin-B1-induced growth cone collapse and withdrawal in EphB-deficient ne
63 from PAK, but not that from N-WASP, inhibits growth-cone collapse and that the inhibitory activity co
64 tutively active, producing cell contraction, growth cone collapse, and inhibition of neurite outgrowt
65 expression of the Type I PIP kinase inhibits growth cone collapse, and that regulation of PIP(2) leve
67 l actin bundle loss coincided with localized growth cone collapse, as well as asymmetrical lamellipod
68 nd the basis of this discrepancy we used the growth cone collapse assay on chick dorsal root ganglion
72 to signaling of F-actin depolymerization and growth cone collapse by molecules such as the myelin-ass
73 l development, including neuronal migration, growth cone collapse, dendrite branching, and spine grow
74 a-axonal translation of RhoA is required for growth cone collapse elicited by Semaphorin 3A (Sema3A),
75 cribe the biochemical purification of an RGC growth cone collapsing factor from bovine brain membrane
78 presence of laminin, which triggers typical growth cone collapse, growth cones co-stimulated by L1 d
79 finding that the NG2 molecule itself induces growth cone collapse, have led to a widely held speculat
81 of EphA3 was essential for ephrin-A5-induced growth cone collapse in cortical GABAergic interneurons,
84 , we first showed that semaphorin 3A-induced growth cone collapse in cultured hippocampal neurons was
85 etinal axons in vivo, only the latter causes growth cone collapse in cultured retinal axons, suggesti
86 rotein that is essential for proBDNF-induced growth cone collapse in developing dopaminergic processe
88 not Rap2, is critical for ephrin-A-dependent growth cone collapse in hippocampal neurons and decrease
89 e myelin glycoprotein), and is important for growth cone collapse in response to acutely presented in
90 t for the depolymerization of F-actin during growth cone collapse in response to ephrin-A2 and semaph
92 ibits RGC neurite outgrowth and enhances RGC growth cone collapse in response to exogenous ephrinA5 l
93 activity and mediates neurite retraction and growth cone collapse in response to repulsive guidance c
94 ermore, the compounds inhibit EphA4-mediated growth cone collapse in retinal explants and EphA2-depen
95 eral other EphA receptors as well and causes growth cone collapse in retinal explants, demonstrating
96 l cells, and was required for Sema3F-induced growth cone collapse in thalamic neuron cultures, consis
97 ndocytosis is blocked, leading to defects in growth cone collapse in vitro and significant defects in
99 ry sensory, trigeminal, and jugular ganglion growth cones collapse in the presence of soluble collaps
100 eing able to block Sema3A chemorepulsion and growth-cone collapse in axons at the extracellular level
105 results indicate that semaphorin 3A-mediated growth cone collapse is mediated in part by m-calpain ac
106 traenoic acid (HETE), whereas Sema3A-induced growth cone collapse is prevented when 12(S)-HETE synthe
107 , we demonstrate that semaphorin 3A-mediated growth cone collapse is reduced in hippocampal neurons f
108 These findings provide insight into how growth cone collapse is regulated during axon terminatio
109 Our results suggest that Sema3A-induced growth-cone collapse is mediated by Rac1 amino acids 17-
110 ins (Nogo-22) is a substantially more potent growth cone-collapsing molecule than Nogo-66 for chick d
111 observations indicate that thrombin-induced growth cone collapse occurs by a mechanism that involves
113 resent, relatively little is known about how growth cone collapse occurs prior to axon termination in
115 2 nM) concentration was necessary to induce growth cone collapse of dorsal root ganglion neurons.
117 phosphorylation of these proteins as well as growth cone collapse of mouse EGL cells induced by netri
118 the developing extraocular muscles and cause growth cone collapse of oculomotor neurons in vitro.
121 wed that exposure to soluble EphB-ECD led to growth cone collapse or other inhibitory responses.
123 ing effects on the growth cone: EphAs direct growth cone collapse/repulsion and ephrin-As signal moto
124 al ganglion cells, we show that semD-induced growth cone collapse requires two segments of the ectodo
125 logical processes, including modulating axon growth cone collapse response and regulating cell surfac
127 Rac1 has recently been shown to inhibit the 'growth-cone collapse' response induced by chick Sema3A,
130 MAG-Fc and OMgp-Fc induce a modest degree of growth cone collapse that is significantly attenuated in
133 phin receptor (p75(NTR)) or TROY to initiate growth cone collapse via a Rho-A inhibitory signaling pa
134 esults indicate that semaphorin 3A initiates growth cone collapse via activation of calpain that in t
135 onstrated for collapsin-1, CNS myelin-evoked growth cone collapse was accompanied by a reduction of r
138 Given the prominence of the cytoskeleton in growth cone collapse, we assessed the relationship betwe
139 emaphorin 3A-mediated calpain activation and growth cone collapse were associated with m-calpain phos
140 r by dominant-negative forms, induced axonal growth cone collapse, whereas p53 overexpression led to
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