ライフサイエンスコーパス: growth cone collapse

1 quired for dendrite elaboration but not axon growth cone collapse.

2 use frontal cortex through ephrin-A5-induced growth cone collapse.

3 t signaling pathways that converge to induce growth cone collapse.

4 ary neurons interferes with ephrin-A-induced growth cone collapse.

5 or (2) electrical stimulation, which causes growth cone collapse.

6 ement of Sema3A receptors and F-actin during growth cone collapse.

7 is may be a general principle of physiologic growth cone collapse.

8 nst a universal signaling pathway underlying growth cone collapse.

9 x 1 in sensory neurons blocks Sema3A-induced growth cone collapse.

10 n growth cones and inhibits thrombin-induced growth cone collapse.

11 rowth cones and oligodendrocytes resulted in growth cone collapse.

12 tive rac1 remain sensitive to myelin-induced growth cone collapse.

13 ganglia neurons by inhibiting Sema3A-induced growth cone collapse.

14 dation of RhoA, a mediator of Sema3A-induced growth cone collapse.

15 ein-synthesis requirement for Sema3A-induced growth cone collapse.

16 lomotor neurons abrogates Sema3A/C-dependent growth cone collapse.

17 negative mutants suppresses netrin-1-induced growth cone collapse.

18 activated mTOR and inhibited ephrin-induced growth cone collapse.

19 blocked its axonal distribution and induced growth cone collapse.

20 ons lacking heparan sulfate exhibit impaired growth cone collapse.

21 domain that was required for Sema3A-induced growth cone collapse.

22 te application of soluble inhibitor to assay growth cone collapse.

23 ), the transmembrane receptor p75NTR signals growth cone collapse.

24 axonal RhoA mRNA abolishes Sema3A-dependent growth cone collapse.

25 pecifically tailored to control Eph-mediated growth cone collapse.

26 s cytoskeletal rearrangements that result in growth cone collapse.

27 necessary and sufficient for Sema3A-mediated growth cone collapse.

28 d this phosphorylation event is required for growth cone collapse.

29 rotein kinase C substrate phosphorylation in growth cone collapse.

30 activation is necessary for thrombin-induced growth cone collapse.

31 cytosis of the plasma membrane, resulting in growth cone collapse.

32 target binding, and inhibits Sema3A-induced growth-cone collapse.

33 nce of the floor plate, but without inducing growth-cone collapse.

34 of BDNF-mediated protection from NO-induced growth-cone collapse.

35 ts thus provide unexpected evidence that the growth cone-collapsing activities and substrate growth-i

36 Sema 3A growth cone collapse activity is inhibited by hanatoxin,

37 In addition, cPTPRO had potent growth cone collapsing activity in vitro, and locally ap

38 We report that >90% of axonal growth cones collapsed after contact with oligodendrocyt

39 protein retains biological activity as a DRG growth cone collapsing agent and saturably binds to DRG

40 r neurotrophin-3 (NT-3) prevented NO-induced growth cone collapse and axon retraction.

41 ling destabilizes microtubules to facilitate growth cone collapse and axon termination.

42 Mastoparan treatment produced rapid growth cone collapse and axonal retraction which persist

43 creted protein that in vitro causes neuronal growth cone collapse and chemorepulsion of neurites, and

44 e effects of Shh on axonal growth, including growth cone collapse and chemorepulsive axon turning but

45 s on two populations of embryonic neurons in growth cone collapse and collagen matrix chemorepulsion

46 axons to netrin-1, preventing UNC5A-mediated growth cone collapse and converting netrin-1-stimulated

47 athfinding, presynaptic differentiation, and growth cone collapse and extension.

48 In acute SCI, macrophages induce growth cone collapse and facilitate axon retraction away

49 idic devices and stripe assays, we show that growth cone collapse and guidance at low concentrations

50 Sema3A, and are required for Sema3A-mediated growth cone collapse and guidance.

51 ic acid (poly I:C) or by mRNA rapidly causes growth cone collapse and irreversibly inhibits neurite e

52 n-A2, slit-3, and semaphorin3A still induced growth cone collapse and loss of actin filaments, nerve

53 rowth inhibitory action of central myelin in growth cone collapse and neurite outgrowth in vitro assa

54 It has been implicated in growth cone collapse and neurite outgrowth inhibition by

55 Ephrin-A5 induces EphB2-mediated growth cone collapse and neurite retraction in a model s

56 ved neurotrophic factor (BDNF) induces rapid growth cone collapse and neurite retraction of embryonic

57 Growth cone collapse and pathway selection assays demons

58 ve rac1 or cdc42 negated collapsin-1-induced growth cone collapse and promoted neurite outgrowth on a

59 es macropinocytosis in the axons and elicits growth cone collapse and repulsive axon turning.

60 in assembly led to filopodial retraction and growth cone collapse and resulted in the bifurcation of

61 This study showed that NO induced growth cone collapse and retraction of developing retina

62 retinal ganglion cell growth cones, causing growth cone collapse and retraction.

63 3A gradients can be divided into two steps: growth cone collapse and retraction.

64 results in inhibition of RGMA-NEO1-mediated growth cone collapse and RGMA- or NET1-NEO1-mediated neu

65 s a local synthesis of proteins that mediate growth cone collapse and turning in response to guidance

66 EphB2-4/5 mutant, restored ephrin-B1-induced growth cone collapse and withdrawal in EphB-deficient ne

67 from PAK, but not that from N-WASP, inhibits growth-cone collapse and that the inhibitory activity co

68 tutively active, producing cell contraction, growth cone collapse, and inhibition of neurite outgrowt

69 expression of the Type I PIP kinase inhibits growth cone collapse, and that regulation of PIP(2) leve

70 In vitro, semaphorin III causes growth-cone collapse, and repels cutaneous sensory axons

71 l actin bundle loss coincided with localized growth cone collapse, as well as asymmetrical lamellipod

72 nd the basis of this discrepancy we used the growth cone collapse assay on chick dorsal root ganglion

73 Using a growth cone collapse assay, we demonstrate that mouse em

74 ence microscopy, and cell-based and neuronal growth cone collapse assays.

75 The small GTPase Rac1 is involved in growth cone collapse, but the nature of its role is not

76 to signaling of F-actin depolymerization and growth cone collapse by molecules such as the myelin-ass

77 l development, including neuronal migration, growth cone collapse, dendrite branching, and spine grow

78 a-axonal translation of RhoA is required for growth cone collapse elicited by Semaphorin 3A (Sema3A),

79 cribe the biochemical purification of an RGC growth cone collapsing factor from bovine brain membrane

80 Sema3A/Plexin-A1-induced growth cone collapse, for example, requires Rac activity

81 These proteins also induced growth cone collapse from newborn DRG neurons when added

82 presence of laminin, which triggers typical growth cone collapse, growth cones co-stimulated by L1 d

83 finding that the NG2 molecule itself induces growth cone collapse, have led to a widely held speculat

84 Ephrin-induced growth cone collapse, however, correlated with resumptio

85 of EphA3 was essential for ephrin-A5-induced growth cone collapse in cortical GABAergic interneurons,

86 ted EphA4 and is required for ephrin-induced growth cone collapse in cortical neurons.

87 -HETE mimics the thrombin effect and induces growth cone collapse in culture.

88 , we first showed that semaphorin 3A-induced growth cone collapse in cultured hippocampal neurons was

89 etinal axons in vivo, only the latter causes growth cone collapse in cultured retinal axons, suggesti

90 rotein that is essential for proBDNF-induced growth cone collapse in developing dopaminergic processe

91 DSCAM and UNC5C also blocks netrin-1-induced growth cone collapse in EGL cells.

92 not Rap2, is critical for ephrin-A-dependent growth cone collapse in hippocampal neurons and decrease

93 e myelin glycoprotein), and is important for growth cone collapse in response to acutely presented in

94 t for the depolymerization of F-actin during growth cone collapse in response to ephrin-A2 and semaph

95 In contrast, cell rounding and growth cone collapse in response to ephrin-A5, which doe

96 ibits RGC neurite outgrowth and enhances RGC growth cone collapse in response to exogenous ephrinA5 l

97 activity and mediates neurite retraction and growth cone collapse in response to repulsive guidance c

98 ermore, the compounds inhibit EphA4-mediated growth cone collapse in retinal explants and EphA2-depen

99 eral other EphA receptors as well and causes growth cone collapse in retinal explants, demonstrating

100 l cells, and was required for Sema3F-induced growth cone collapse in thalamic neuron cultures, consis

101 ndocytosis is blocked, leading to defects in growth cone collapse in vitro and significant defects in

102 cue Semaphorin3a (Sema3a), leading to axonal growth cone collapse in vitro.

103 e neuronally expressed receptor Robo mediate growth cone collapse in vivo.

104 ry sensory, trigeminal, and jugular ganglion growth cones collapse in the presence of soluble collaps

105 eing able to block Sema3A chemorepulsion and growth-cone collapse in axons at the extracellular level

106 re able to inhibit endogenous EphA4-mediated growth-cone collapse induced by ephrin-B3.

107 Axonal growth cone collapse is accompanied by a reduction in fi

108 Because growth cone collapse is associated with actin depolymeri

109 We suggest that growth cone collapse is mediated by both actin filament

110 results indicate that semaphorin 3A-mediated growth cone collapse is mediated in part by m-calpain ac

111 traenoic acid (HETE), whereas Sema3A-induced growth cone collapse is prevented when 12(S)-HETE synthe

112 , we demonstrate that semaphorin 3A-mediated growth cone collapse is reduced in hippocampal neurons f

113 These findings provide insight into how growth cone collapse is regulated during axon terminatio

114 Our results suggest that Sema3A-induced growth-cone collapse is mediated by Rac1 amino acids 17-

115 by triggering a reduction of p-Cofilin-S3, a growth cone collapse marker, through decreasing a novel

116 ins (Nogo-22) is a substantially more potent growth cone-collapsing molecule than Nogo-66 for chick d

117 observations indicate that thrombin-induced growth cone collapse occurs by a mechanism that involves

118 Thus, we observe that complete growth cone collapse occurs in vivo and not just in cult

119 resent, relatively little is known about how growth cone collapse occurs prior to axon termination in

120 The addition of Olfm1 inhibited the growth cone collapse of dorsal root ganglia neurons indu

121 2 nM) concentration was necessary to induce growth cone collapse of dorsal root ganglion neurons.

122 Netrin-1 induces axon growth cone collapse of mouse cerebellum external granul

123 phosphorylation of these proteins as well as growth cone collapse of mouse EGL cells induced by netri

124 the developing extraocular muscles and cause growth cone collapse of oculomotor neurons in vitro.

125 Sema6A was observed to induce growth cone collapse of sympathetic neurons with an EC50

126 We show that the dependence of growth cone collapse on protein synthesis varies accordi

127 wed that exposure to soluble EphB-ECD led to growth cone collapse or other inhibitory responses.

128 Growth cone collapse prior to termination is facilitated

129 ing effects on the growth cone: EphAs direct growth cone collapse/repulsion and ephrin-As signal moto

130 al ganglion cells, we show that semD-induced growth cone collapse requires two segments of the ectodo

131 logical processes, including modulating axon growth cone collapse response and regulating cell surfac

132 l, SB-216763, and SB-415286) can inhibit the growth cone collapse response induced by Sema 3A.

133 Rac1 has recently been shown to inhibit the 'growth-cone collapse' response induced by chick Sema3A,

134 Growth cone collapse results from concomitant cytoskelet

135 In growth cone collapse, substratum choice and neurite outg

136 MAG-Fc and OMgp-Fc induce a modest degree of growth cone collapse that is significantly attenuated in

137 overexpression of wild-type MARCKS inhibits growth cone collapse triggered by PKC activation.

138 Retinal growth cone collapse triggered by Slit D2 requires cell

139 phin receptor (p75(NTR)) or TROY to initiate growth cone collapse via a Rho-A inhibitory signaling pa

140 esults indicate that semaphorin 3A initiates growth cone collapse via activation of calpain that in t

141 onstrated for collapsin-1, CNS myelin-evoked growth cone collapse was accompanied by a reduction of r

142 BDNF-induced growth cone collapse was only observed in 6 hr cultures

143 p53 inhibition-induced axonal growth cone collapse was significantly reduced by the Rh

144 Given the prominence of the cytoskeleton in growth cone collapse, we assessed the relationship betwe

145 emaphorin 3A-mediated calpain activation and growth cone collapse were associated with m-calpain phos

146 r by dominant-negative forms, induced axonal growth cone collapse, whereas p53 overexpression led to