ライフサイエンスコーパス: Sema3A

1 Sema3A alone did not cause injury in normal brains.

2 Sema3A also reduced tumor hypoxia and halted cancer diss

3 Sema3A depletion also reduces dispersal, which is recove

4 Sema3A expression is higher in non-innervated vessels.

5 Sema3A increased the intracellular concentration of guan

6 Sema3A induces intra-axonal translation of RhoA mRNA, an

7 Sema3A interacts with glycosaminoglycans (GAGs), presuma

8 Sema3A is not retrogradely transported in older, surviva

9 Sema3A is therefore a candidate for a PNN effector in co

10 Sema3A mRNA transcripts are expressed at significantly h

11 Sema3A receptor and Syb2 colocalize in endosomal membran

12 Sema3A repelled trigeminal axons in vitro regardless of

13 Sema3A(K108N) mutant mice phenocopy Sema3A-null mice, an

14 Sema3A-mediated apoptosis utilizes the extrinsic pathway

15 Sema3A-mediated VP was inhibited either in adult mice ex

16 Sema3A/C are expressed in and around the developing extr

17 Sema3A/Plexin-A1-induced growth cone collapse, for examp

18 ating the endocytosis of the L1/neuropilin 1 Sema3A receptor complex.

19 d we investigated the role of semaphorin 3A (Sema3A) and neuropilin-1 (Nrp-1) in lymphatic vessel mat

20 Npn-1) is a receptor for both semaphorin 3A (Sema3A) and vascular endothelial growth factor 165 (VEGF

21 Semaphorin 3A (Sema3A) binds to neuropilin-1 (NP1) and activates the tr

22 Here, we show that semaphorin 3A (Sema3A) expression overcomes the proinvasive and prometa

23 We demonstrate here that semaphorin 3A (Sema3A) induces a coordinated rearrangement of Sema3A re

24 Semaphorin 3A (Sema3A) is a membrane-associated secreted protein that h

25 Semaphorin 3A (Sema3A) is a secreted factor known to guide axon/dendrit

26 has shown that VEGF-A165 and semaphorin 3A (Sema3A) promote vessel maturation through the recruitmen

27 homolog of L1 (CHL1) and the semaphorin 3A (Sema3A) receptor, neuropilin 1 (Npn1), important for est

28 ll type-specific responses to Semaphorin 3A (Sema3A), a guidance cue that would be presented similarl

29 Semaphorin 3A (Sema3A), a known inhibitor of axonal sprouting, also alt

30 , an angiogenesis factor, and semaphorin 3A (Sema3A), a mediator of axonal guidance.

31 Semaphorin 3A (Sema3A), a secreted guidance cue that primarily function

32 wth cone collapse elicited by Semaphorin 3A (Sema3A), an axonal guidance cue.

33 Semaphorin 3A (Sema3A), in addition to its function as a chemorepulsive

34 Semaphorin 3A (Sema3A), which lies adjacent to this turn, stimulates ra

35 ed branching by >50%, whereas semaphorin 3A (Sema3A), which repels cortical axons, inhibited branchin

36 nds the secreted guidance cue Semaphorin 3A (Sema3A).

37 responses to the guidance cue Semaphorin 3A (Sema3A).

38 ensitive to the repellent cue Semaphorin 3A (Sema3A).

39 ion of repulsive guidance cue semaphorin 3A (Sema3A).

40 Semaphorin-3A (Sema3A) is a major guidance cue in the developing nervou

41 of a secreted 65 kDa form of Semaphorin-3A (Sema3A), containing the full semaphorin domain.

42 We have demonstrated that semaphorin-3A (Sema3A)-induced growth cone detachment and collapse requ

43 in GBMs was previously shown, its role as a Sema3A receptor remained elusive.

44 fy the endocytosis effector flotillin-1 as a Sema3A signaling candidate.

45 todomain of PlexinA1 associate with NP1 in a Sema3A-independent fashion.

46 lized cultures of rat sympathetic neurons, a Sema3A-initiated apoptosis signal is retrogradely transp

47 Taken together, a Sema3A-initiated apoptotic signaling complex regulates t

48 To determine whether a Sema3A-dependent damage pathway is activated following i

49 Administration of a ligand of plexin-A4, Sema3A (semaphorin 3A), exacerbates the cytokine storm c

50 ive knock-down of axonal RhoA mRNA abolishes Sema3A-dependent growth cone collapse.

51 or PlexinAs in oculomotor neurons abrogates Sema3A/C-dependent growth cone collapse.

52 Furthermore, CRMP accelerates Sema3A-induced cell contraction.

53 ganize to vacuoles and membrane ridges after Sema3A treatment.

54 s to TLR signaling and suggest plexin-A4 and Sema3A as new intervention points for treating sepsis.

55 A1 is autoinhibited by its sema domain, and Sema3A/NP1 releases this inhibition.

56 ulated sequentially IL-1 receptor type I and Sema3A expression through Erk/Jnk-dependent processes.

57 epress sequentially IL-1 receptor type I and Sema3A expression.

58 mutant mice phenocopy Sema3A-null mice, and Sema3A(K108N) protein fails to repel or collapse DRG axo

59 tic arborization of hippocampal neurons, and Sema3A regulates dendritic F-actin distribution via Farp

60 imposes either attraction or repulsion, and Sema3A achieves this through cGMP signaling.

61 Here we show that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via

62 The distribution of mRNAs for Sema3F and Sema3A makes them candidates for triggering the pruning.

63 ows that plexin-A3 contributes to Sema3F and Sema3A signaling and that plexin-A3 regulates the develo

64 ere exposed to two NRP1 ligands, VEGF165 and Sema3A.

65 ecules are capable of binding to VEGF165 and Sema3A.

66 he biologically relevant interaction between Sema3A and GAGs, thus revealing SICHI as a new, to our k

67 eurons express an Nrp1 mutant unable to bind Sema3A.

68 express Nrp1 receptors incapable of binding Sema3A.

69 entified by our group as being able to block Sema3A chemorepulsion and growth-cone collapse in axons

70 domains (a1a2) of NRP1 and completely blocks Sema3A induced neuron collapse; antibody (YW107.4.87) bi

71 A truncated RanBPM protein blocks Sema3A responsiveness in non-neuronal and neuronal cells

72 o (E12.5-E16.5) with an antibody that blocks Sema3A binding to Nrp-1 but not with an antibody that bl

73 oke in mice, immunohistochemistry shows both Sema3A and 12/15-LOX are increased in the cortex up to 2

74 While both Sema3A- and VEGF-induced VP was Nrp-1 dependent, they us

75 But when injected into postischemic brains, Sema3A increased cortical damage by 79%, and again, this

76 ays after a unilateral olfactory bulbectomy, Sema3A transcript levels increased in regenerating neuro

77 by FGF-2 and the inhibition of branching by Sema3A were mediated by opposing effects on the growth c

78 ltured Xenopus spinal neuron growth cones by Sema3A, which triggers the production of the cGMP that a

79 is reduced in amount by NP1 but enhanced by Sema3A/NP1.

80 , are rapidly and transiently inactivated by Sema3A, and are required for Sema3A-mediated growth cone

81 inal axon outgrowth, and this is mediated by Sema3A.

82 sident monocytes, distinctively recruited by Sema3A.

83 rowth of the apical dendrite is regulated by Sema3A, which acts as a dendritic chemoattractant.

84 , in vitro, trigeminal axons are repelled by Sema3A when they would be penetrating the Sema3A-mRNA ri

85 rom which they would normally be repelled by Sema3A.

86 Functionally, Farp1 is required by Sema3A to promote dendritic arborization of hippocampal

87 a constitutively active protein that causes Sema3A-independent COS-7 contraction.

88 selective neutralization of endothelial-cell Sema3A signaling in adult Sema3aloxP/loxP mice by the in

89 loss of responsiveness to the chemorepellant Sema3A.

90 In conclusion, Sema3A binding to CS-E in the PNNs may be a mechanism wh

91 deletion of Nrp1 in GnRH neurons counteract Sema3A-induced axonal sprouting.

92 Here we show that the extracellular cue Sema3A induces an initial burst in local translation tha

93 ural view of CRMP function in Plex-dependent Sema3A signaling.

94 These results demonstrate that lens-derived Sema3A mediates initial repulsion of trigeminal sensory

95 In contrast, a distinct Sema3A-Npn-1/PlexA4 signalling cascade controls basal de

96 with the operation of at least two distinct Sema3A signaling pathways: one that is PS-dependent, inv

97 Downregulating Sema3A signaling in rat embryonic cortical progenitors v

98 extran by the growth cone is enhanced during Sema3A treatment, and sites of dextran accumulation colo

99 on, we investigate the release of endogenous Sema3A from rat brain by biochemical and enzymatic extra

100 implantation, we demonstrate that exogenous Sema3A protein inhibits Vegf-induced vascularization of

101 repulsion by E14 and older tongue explants, Sema3A mRNA persists throughout the dorsal epithelium th

102 n the caudal OB, avoiding regions expressing Sema3A.

103 Finally, Sema3A and TAOK2 modulate the formation of basal dendrit

104 h that L1 is lost from the complex following Sema3A binding.

105 V/VIII domain (CF V/VIII) are essential for Sema3A binding, but only the amino-terminal Npn-1 CF V/V

106 new insights into therapeutic potential for Sema3A in neovascular diseases.

107 ion of Neuropilin-1 (Nrp1), the receptor for Sema3A, in sensory axons.

108 e defined a domain of Plexin-A1 required for Sema3A signaling in a reconstituted environment and then

109 Here we show that Syb2 is required for Sema3A-dependent repulsion but not Sema3C-dependent attr

110 in the CHL1 Ig1 domain that was required for Sema3A-induced growth cone collapse.

111 he PlxnA4 cytoplasmic domain is required for Sema3A-mediated cortical neuron dendritic elaboration bu

112 inactivated by Sema3A, and are required for Sema3A-mediated growth cone collapse and guidance.

113 remove the protein-synthesis requirement for Sema3A-induced growth cone collapse.

114 These findings define a novel role for Sema3A both as a selective inhibitor of VEGF-mediated an

115 tion of RhoA is necessary and sufficient for Sema3A-mediated growth cone collapse.

116 a1 CUB domain were generated and tested for Sema3A and VEGF(165) binding.

117 isolated either from the bone marrow or from Sema3A-expressing muscles, exerted antitumor activity de

118 Furthermore, Sema3A inhibits periocular neural crest migration in vit

119 cephalon, an intermediate target with graded Sema3A expression, VB axons were caudally shifted in CHL

120 Using this assay, we identified Sema3A(K108N), a novel loss-of-function allele of Sema3A

121 Together, these findings implicate Sema3A as an autocrine signal for neuropilin-1 to promot

122 In Sema3A homozygous mutant mice, many npn-1(+) axons are m

123 In Sema3A knockout mice, geniculate and trigeminal afferent

124 timing of target contact by sensory axons in Sema3A-/minus; and +/+ mice.

125 target the ventral OB are also misrouted in Sema3A mutants.

126 tact of the epithelium occurs prematurely in Sema3A-/minus; mice, but not penetration.

127 hat 12/15-LO activity is a necessary step in Sema3A collapse signaling in growth cones and suggest a

128 Class 3 semaphorins, which include Sema3A, are structurally conserved secreted proteins tha

129 TLR engagement can induce Sema3A expression, thus completing an autocrine loop.

130 Introduction of a peptide that inhibits Sema3A/Npn-1 signaling results in premature entry of neu

131 ify a previously unknown function for 65 kDa Sema3A-Nrp1 signaling in the induction of axonal growth,

132 ecapitulated in mice lacking the Nrp1 ligand Sema3A and in mice whose sensory neurons express an Nrp1

133 The authors localized Sema3A mRNA expression in the primary olfactory pathway

134 of the undifferentiated neurite to localized Sema3A suppressed its differentiation into axon and prom

135 utgrowth and vascular innervation; while low Sema3A expressing vessels favor Nrp1-VEGFR2 signaling pr

136 s and signaling, and show that raft-mediated Sema3A endocytosis is defined by and depends on the recr

137 lied product of 12/15-LO, 12(S)-HETE, mimics Sema3A-induced collapse.

138 at signaling from the axon guidance molecule Sema3A via eicosanoid second messengers can contribute t

139 We found that the axonal guidance molecules Sema3A and Sema3D were highly expressed by lymphatic ves

140 from neurons lacking Satb2 internalize more Sema3A, and they do so via a raft-mediated endocytic pat

141 nct downstream effectors since VEGF- but not Sema3A-induced VP required Src kinase signaling.

142 This work identifies a novel Sema3A-Nrp1/PlxnA4/FARP2/Rac1 signaling pathway that spe

143 Later, Nrp1/Sema3A signaling is essential for segmental dorsal root

144 tcomes dependent on the timing at which Nrp1/Sema3A signaling is altered.

145 and guidance are impaired in the absence of Sema3A-Npn-1 signaling.

146 screen we have identified a novel allele of Sema3A that provides structural insight into the mechani

147 A(K108N), a novel loss-of-function allele of Sema3A.

148 Extracellular application of Sema3A decreases cell-substrate adhesion in a neuropilin

149 m the Sema3A source, and bath application of Sema3A to polarized neurons promoted dendrite growth but

150 mpaired expression, secretion, or binding of Sema3A to its high-affinity receptor Neuropilin-1 (Npn-1

151 is interaction is involved in the binding of Sema3A to rat brain-derived PNN glycosaminoglycans, as d

152 Blockade of Sema3A signaling via lens removal or injection of a synt

153 We also demonstrate that the combination of Sema3A and PNN GAGs is a potent inhibitor of axon growth

154 ation and operative at all concentrations of Sema3A examined.

155 eral diseases; therefore, the development of Sema3A inhibitors is of therapeutic interest.

156 RNA interference-mediated downregulation of Sema3A inhibits migration and alters cell morphology tha

157 by abolishing the growth-promoting effect of Sema3A but inducing a branching response in the presence

158 sly shown to mediate the repulsive effect of Sema3A on axons and to participate in axonal specificati

159 DRG neurite outgrowth-inhibiting effects of Sema3A and reduces Sema3A-induced axonal repulsion.

160 ere unresponsive to the repellent effects of Sema3A in vitro, which might account, at least in part,

161 demonstrate an essential direct function of Sema3A-Nrp1-PlexinA1 signaling in lymphatic valve format

162 ents underlying these disparate functions of Sema3A signaling are unclear.

163 Spatial gradients of Sema3A and VEGF-A may promote differential Nrp1 binding.

164 Inhibition of Sema3A signaling abrogates axon repulsion by the lens an

165 Both the inhibition of Sema3A/Nrp1 signaling and the conditional deletion of Nr

166 Here, we characterize the interaction of Sema3A with CS of the PNNs.

167 Our results confirm the interaction of Sema3A with CS-E containing glycosaminoglycans in the de

168 that the expression of the 65 kDa isoform of Sema3A, the ligand of Nrp1, by adult vascular endothelia

169 ate axon outgrowth, but the minimum level of Sema3A required to repel depended on the neurotrophic fa

170 R-223-KO exosomes contained higher levels of Sema3A and Stat3, two known targets of miR-223 (5p &3p),

171 Vessels expressing high levels of Sema3A favor Nrp1-PlexinA1 signaling, producing chemorep

172 pulations of axons express similar levels of Sema3A receptors (neuropilin-1, cell adhesion molecule L

173 High levels of Sema3A transcript were found at 1 week postbulbectomy, p

174 iant, Npn-1(2ABC), exhibits complete loss of Sema3A binding while retaining normal VEGF(165) binding.

175 des structural insight into the mechanism of Sema3A/Npn-1/PlexinA signaling.

176 Thus, RanBPM is a mediator of Sema3A signaling through Plexin-A.

177 ation and degradation of RhoA, a mediator of Sema3A-induced growth cone collapse.

178 are atypically located in the ventral OB of Sema3A(-/-) mice, indicating that aberrant axon trajecto

179 Loss of miR-124 delayed the onset of Sema3A sensitivity and concomitant neuropilin-1 (NRP1) r

180 ma3A) induces a coordinated rearrangement of Sema3A receptors and F-actin during growth cone collapse

181 Reconstitution of Sema3A receptor in nonneuronal cells revealed that Sema3

182 diomyocytes, resulting in down-regulation of Sema3A and Stat3.

183 red detachment and collapse, and reversal of Sema3A-induced repulsion into attraction.

184 ability (VP) factor, we examined the role of Sema3A on VEGF-mediated VP in mice.

185 hese results reveal an unanticipated role of Sema3A-Nrp-1 signaling in the maturation of the lymphati

186 ur data reveal a novel and essential role of Sema3A/Npn-1 signaling in coordinating periocular neural

187 ntrast microscopy reveals that some sites of Sema3A-induced F-actin reorganization correlate with dis

188 localized intracerebral infusion of Nrp1- or Sema3A-neutralizing antibodies in vivo disrupts the ovar

189 Sema3A(K108N) mutant mice phenocopy Sema3A-null mice, and Sema3A(K108N) protein fails to rep

190 -1 cells and tested for alkaline phosphatase-Sema3A as well as alkaline phosphatase-VEGF(165) binding

191 one potential at the resting state prevented Sema3A-induced repulsion; depolarizing potentials conver

192 he downstream signaling molecules to promote Sema3A-mediated cortical neuron dendritic elaboration, b

193 Recombinant Sema3A interacts with CS type E (CS-E), and this interac

194 following ischemia, we injected recombinant Sema3A into the striatum.

195 Either 90 nM recombinant Sema3A, or the 12/15-lipoxygenase (12/15-LOX) metabolite

196 assay for CRMP, we exploited a reconstituted Sema3A signaling system in COS-7 cells expressing the re

197 ation of NRP1 by NRSF overexpression reduced Sema3A activity.

198 wth-inhibiting effects of Sema3A and reduces Sema3A-induced axonal repulsion.

199 Suppression of RanBPM expression reduces Sema3A responsiveness.

200 As a result, reexpressing Sema3A in cancer cells converts metastatic PNETs and cer

201 The repellents Sema3A and Slit2 caused hyperpolarization, and the attra

202 xCNGCs is required to mediate the repulsive Sema3A signal.

203 Altogether, our results reveal Sema3A signaling as an important cue during the establis

204 We also showed that GBM cells secrete Sema3A endogenously, and RNA interference-mediated downr

205 protein-protein interaction between secreted Sema3A and the Nrp1 receptor.

206 ilin1, the obligate receptor to the secreted Sema3A.

207 ing control of sensitivity to the semaphorin Sema3A in Xenopus laevis retinal ganglion cell (RGC) gro

208 The secreted semaphorin, Sema3A, mediates repulsive effects on axons from various

209 Semaphorin3A (Sema3A) is a vertebrate-secreted protein that was initia

210 ial growth factor (VEGF-A) and Semaphorin3A (Sema3A) which both signal via neuropilin-1 (Nrp1).

211 Neuropilin-1 is a receptor for semaphorin3A (Sema3A), a secreted chemorepellent that facilitates axon

212 pulsive axon guidance molecule Semaphorin3A (Sema3A) plays a role in lymphatic valve formation.

213 dy, we investigate the role of Semaphorin3A (Sema3A), a cell guidance chemorepellent, on angioblast m

214 Secreted Semaphorin3A (Sema3A) proteins are known to act as diffusible and repe

215 We show that Semaphorin3A (Sema3A) is expressed in the lens epithelium and its rece

216 ying this effect, we find that semaphorin3A (Sema3A) is expressed in the lens placode and epithelium

217 Recently, we have shown that semaphorin3A (Sema3A), a repulsive axon guidance molecule, localizes t

218 afficking of components of the semaphorin3A (Sema3A) receptor complex into distinct endosomal compart

219 n mediates axonal responses to Semaphorin3A (Sema3A) and other guidance cues.

220 The class 3 Semaphorins Sema3A and Sema3F are potent axonal repellents that caus

221 gly, in contrast to canonical UPR signaling, Sema3A-induced eIF2alpha phosphorylation bypasses global

222 ing, specifically through binding of soluble Sema3A to Neuropilin/PlexinA coreceptors.

223 s dispersal, which is recovered by supplying Sema3A exogenously.

224 Surprisingly, Sema3A not only stimulated VEGF-mediated VP but also pot

225 e G (PKG)-mediated depolarization, switching Sema3A-induced repulsion to attraction.

226 via lens removal or injection of a synthetic Sema3A inhibitor causes ectopic migration of angioblasts

227 ubstrate adhesion and suggest that targeting Sema3A-neuropilin-1 signaling may limit GBM infiltration

228 A is expressed in lymphatic vessels and that Sema3A protein binds to lymphatic valves expressing the

229 We find that Sema3A activates the small GTPase Rac1, and that Rac1 ac

230 dorsal root ganglion neurons, we found that Sema3A treatment stimulates the synthesis of the eicosan

231 We show here that Sema3A-induced collapse of COS-7 cells expressing Plexin

232 We investigated the hypothesis that Sema3A continues to act as a repellent and that subpopul

233 tes, supporting our previous hypothesis that Sema3A-based repulsion mediates the early restriction of

234 Taken together, our data imply that Sema3A acts as a short-range repellent that regulates th

235 These observations indicate that Sema3A expression by ensheathing cells plays an importan

236 r semaphorin family members, we predict that Sema3A(K108N) interacts poorly with the Npn-1/PlexA holo

237 receptor in nonneuronal cells revealed that Sema3A further inhibited the exocytosis of Syb2.

238 Using mouse knockout models, we show that Sema3A is selectively required for lymphatic valve forma

239 We show that Sema3A mRNA is expressed in lymphatic vessels and that S

240 Here we show that Sema3A selectively interferes with VEGF- but not bFGF-in

241 We show that Sema3A, Vegf, and Nrp1 are expressed in the anterior eye

242 e energy transfer (FRET) imaging showed that Sema3A elevated the cGMP but reduced cAMP and protein ki

243 Using immunohistochemistry, we showed that Sema3A is overexpressed in a subset of human GBMs compar

244 ns enter the limb precociously, showing that Sema3A controls the timing of motor axon in-growth to th

245 These findings suggest that Sema3A and perhaps other semaphorins play a role in dire

246 The Sema3A effect is reversed by inhibiting 12/15-LOX, and n

247 The Sema3A-Nrp1/PlxnA4 signaling pathway promotes cortical n

248 utero electroporation of siRNAs against the Sema3A receptor neuropilin-1 also resulted in polarizati

249 r proteins, neuropilin-1 and plexin, and the Sema3A signaling molecule, rac1, also reorganize to vacu

250 s NRP1 expression and thereby diminishes the Sema3A mediated inhibition of HaCaT keratinocyte migrati

251 n, resulting in axon formation away from the Sema3A source, and bath application of Sema3A to polariz

252 Furthermore, the Sema3A receptor proteins, neuropilin-1 and plexin, and t

253 routing, and mice carrying a mutation in the Sema3A binding site of Nrp1, or deficient for Plxna1, de

254 g a change in its association with L1 in the Sema3A response such that L1 is lost from the complex fo

255 the reported SICHI inhibitory effect in the Sema3A signaling pathway, we looked first to the protein

256 Although mice lacking the Sema3A protein display skeletal abnormalities and heart

257 s was found to regulate axonal levels of the Sema3A receptor neuropilin 1.

258 active ERMs regulates internalization of the Sema3A receptor, Npn1, and its coreceptor, L1CAM, while

259 d Plexin A1, two essential components of the Sema3A receptor, via its juxtatransmembrane domain.

260 Analysis of the Sema3A structure and structure-based mutagenesis data id

261 by Sema3A when they would be penetrating the Sema3A-mRNA rich epithelium in vivo.

262 SICHI binds to GAGs, thereby perturbing the Sema3A-GAG interaction.

263 how that SICHI does not bind directly to the Sema3A sema domain or to Nrp1 extracellular domains.

264 proteins translationally controlled via the Sema3A-p-eIF2alpha pathway.

265 Therefore, Sema3A-mediated signaling and axonal repulsion require S

266 Consistent with this, Sema3A disrupted VEGF- but not bFGF-mediated endothelial

267 Thus, Sema3A regulates the earliest step of neuronal morphogen

268 Thus, Sema3A-Npn-1 and Sema3F-Npn-2 signaling control distinct

269 e tested the contributions of flotillin-1 to Sema3A endocytosis and signaling, and show that raft-med

270 pse on protein synthesis varies according to Sema3A concentration, from near-total at low concentrati

271 ral features of Npn-1 that confer binding to Sema3A or VEGF(165).

272 n neurons reverses axonal desensitization to Sema3A, but this is hampered in a mutant Nrp1 with high

273 ns from the double mutant are insensitive to Sema3A and Sema3F in vitro, and defects in axonal projec

274 m 12/15-LOX-knockout mice are insensitive to Sema3A.

275 mutants, in which axons are nonresponsive to Sema3A.

276 is explained in part by loss of response to Sema3A.

277 e membrane and actin dynamics in response to Sema3A.

278 cone repulsion to attraction in response to Sema3A.

279 hat are consistent with enhanced response to Sema3A.

280 orrelated with gain of repulsive response to Sema3A.

281 s have revealed a dependence of responses to Sema3A on local protein synthesis (PS) in axonal growth

282 ivation and regulates axon responsiveness to Sema3A in presumptive corticofugal axons.

283 g Ctip2 or Tbr1 respond far more robustly to Sema3A than those from presumptive callosal neurons expr

284 t evidence that TAG-1 affects sensitivity to Sema3A by binding to L1 and modulating the endocytosis o

285 etrate the epithelium become unresponsive to Sema3A.

286 t the identity of the Plexins that transduce Sema3A and Sema3F responses in vivo is uncertain.

287 troscopy) to characterize the binding of two Sema3A C-terminus-derived basic peptides (FS2 and NFS3)

288 Unexpectedly, Sema3A also requires neuronal activity to promote dendri

289 Moreover, upon Sema3A treatment, Syb2-deficient neurons failed to colla

290 isting prior to the origin of the vertebrate Sema3A-G and Sema4A-G subfamilies.

291 hydroxyeicosatetraenoic acid (HETE), whereas Sema3A-induced growth cone collapse is prevented when 12

292 ops in growth cones over many hours, whereas Sema3A depolymerized actin filaments, attenuated microtu

293 ther had an effect on proliferation, whereas Sema3A, but not VEGF165, inhibited cell migration.

294 These data support a model whereby Sema3A stimulates endocytosis by focal and coordinated r

295 These results delineate a pathway whereby Sema3A and Nrp1 transduce signals through TAOK2 and JNK

296 To determine whether Sema3A prevents premature target penetration in vivo, we

297 sensory neurons in vitro The extent to which Sema3A regulates developmental cell death in vivo, howev

298 tion and extending the normalization window, Sema3A counteracted sunitinib-induced activation of HIF-

299 d that SICHI binds to GAGs and competes with Sema3A C-terminus-derived basic peptides for binding to

300 toskeleton because growth cones treated with Sema3A and 12/15-LO inhibitor remain spread despite acti