ライフサイエンスコーパス: netrin

1 d generates F-actin in the absence of UNC-6 (netrin).

2 t and adaptable mechanism to polarize toward netrin.

3 s in animals toward its extracellular ligand netrin.

4 membranes towards a polarity cue provided by netrin.

5 etrin-1, but without binding either Slits or Netrins.

6 Netrin 1 (Ntn1) is a multifunctional guidance cue expres

7 mice, fusion depends on the secreted protein netrin 1 (Ntn1), which is necessary for basement membran

8 zone (DZ) protoglomerulus in the absence of Netrin 1/Dcc signaling.

9 Netrin-1 (Ntn1) emanating from the ventral midline has b

10 , which overlap with an obesity related gene Netrin-1 (Ntn1), were consistent with Ntn1 RNA expressio

11 demonstrated that the neuronal guidance cue netrin-1 activates a program of reparative angiogenesis

12 Here, we demonstrate that netrin-1 also impacts the resolution of inflammation and

13 Netrin-1 also induced colocalization of coexpressed full

14 These findings indicate that netrin-1 and DCC are critical for the control of arteria

15 ting ventral attractive signals, we examined Netrin-1 and DCC mutants, and found that motor neurons s

16 ntrolled by axon guidance molecules, such as Netrin-1 and DCC.

17 e TRIM9 as a critical catalytic link between Netrin-1 and exocytic SNARE machinery in murine cortical

18 Netrin-1 and HCV are, therefore, reciprocal inducers in

19 Here we identify the secreted cue Netrin-1 and its receptor DCC, described for their respe

20 Netrin-1 and its receptor Deleted in Colorectal Cancer (

21 Extracellular netrin-1 and its receptor deleted in colorectal cancer (

22 Netrin-1 and its receptor Unc5b are novel targets for th

23 al studies, we investigated the induction of netrin-1 and its receptors in murine liver tissues after

24 indicate that the vagus nerve regulates both netrin-1 and pro-resolving lipid mediators, which act in

25 Netrin-1 and RvD1 displayed bidirectional activation in

26 Combination of netrin-1 and SIAH RNAi may prove to be a substantially e

27 n occurs following axon injury and exogenous netrin-1 applied after injury normalizes spine density,

28 ciation involving a cancer-related virus and Netrin-1 argues for evaluating the implication of UNC5 r

29 Collectively, these findings identify netrin-1 as a macrophage retention signal in adipose tis

30 odendrocyte precursor migration, identifying netrin-1 as a potential target for therapies that promot

31 Here, we identified the axon guidance cue netrin-1 as an essential factor required for development

32 1 and FLRT3 receptors are required to induce Netrin-1 attraction by the upregulation of surface DCC t

33 hat acts as a context-dependent modulator of Netrin-1 attraction in thalamocortical axons.

34 We first demonstrate that Netrin-1 attracts and repels distinct motor axon populat

35 Netrin-1 binds its receptors deleted in colorectal cance

36 d by secretion of the axon guidance molecule netrin-1 by arterial VSMCs.

37 interacted with polymerized TUBB3 in MTs and netrin-1 decreased this interaction.

38 was performed in mice with a partial genetic netrin-1 deficiency (Ntn1(+/-) ) or wild-type C57BL/6 tr

39 This study reveals that netrin-1 degradation products are capable of modulating

40 ary external granule layer cells showed that netrin-1 differentially increased MT dynamics in the GC

41 Robo3 does not bind Netrin-1 directly but interacts with DCC.

42 Netrin-1 downregulation occurs following axon injury and

43 mediates the attraction of growing axons to netrin-1 during brain development.

44 s knockdown of DSCAM partially inhibited the Netrin-1 effect.

45 kdown of either UNC5C or TUBB3 abolished the netrin-1 effect.

46 We also demonstrate that the chemoattractant Netrin-1 elicits increases in the frequency and slopes o

47 Netrin-1 enhanced infectivity of HCV particles and promo

48 Hence, our findings support that netrin-1 exerts oncogenic activity through YAP signaling

49 Conversely, mice treated with exogenous netrin-1 exhibited increased liver protection and repair

50 ow that in MS lesions, astrocytes upregulate netrin-1 expression early during demyelination and netri

51 hin model of demyelination (astrocyte-free), netrin-1 expression is absent during early phases and de

52 We show that Netrin-1 expression is significantly elevated in HCV+ li

53 Conversely, lentiviral-mediated induction of netrin-1 expression prior to OPC recruitment reduced the

54 Netrin-1 expression was analyzed immunohistochemically i

55 Our findings support the conclusion that netrin-1 expression within demyelinating MS plaques bloc

56 osis and HCV contributed to the induction of Netrin-1 expression, whereas anti-HCV treatment resulted

57 nti-HCV treatment resulted in a reduction of Netrin-1 expression.

58 Netrin-1 fails to attract pontine neurons lacking Robo3,

59 Thus, MMP-9 may release netrin-1 fragments from the extracellular matrix and fac

60 use lesions, antibody-mediated disruption of netrin-1 function at the peak phase of recruitment incre

61 ic survival factors represented by decreased Netrin-1 gene expression were associated with delayed ki

62 CKGROUD: Variations in the expression of the Netrin-1 guidance cue receptor DCC (deleted in colorecta

63 Variations in the expression of the Netrin-1 guidance cue receptor DCC (deleted in colorecta

64 n the emergent cooperation between Slit1 and Netrin-1 guidance cues presented by intermediate cellula

65 Here, we provide evidence suggested that Netrin-1 has a critical role in glioma growth.

66 Netrin-1 has a rigid elongated structure containing two

67 Netrin-1 has recently been found to modulate the immune

68 Mechanistically, Netrin-1 imbalance induces apoptosis mediated by the rec

69 nd shows that the treatment with recombinant Netrin-1 improves the generation of mouse and human iPS

70 , HCV increased the level and translation of Netrin-1 in a NS5A-La-related protein 1 (LARP1)-dependen

71 Here we present the crystal structure of netrin-1 in complex with the Deleted in Colorectal Cance

72 However, the role of netrin-1 in glioma remains largely unknown.

73 indicates a previously unrecognized role for netrin-1 in liver protection and its contribution to tis

74 vestigated the role of the guidance molecule netrin-1 in OPC recruitment and central nervous system (

75 Netrin-1 increased endogenous JNK activity in primary ne

76 Netrin-1 increased JNK1, not JNK2 or JNK3, activity in t

77 hole-cell patch-clamp electrophysiology that netrin-1 increases the frequency and amplitude of mEPSCs

78 Further studies found that netrin-1 induced NF-kappaB p65(ser536) phosphorylation a

79 stigations of the mechanism of ephrin-B2 and Netrin-1 integration demonstrate that the Netrin recepto

80 the humanized SCID mouse, local injection of Netrin-1 into skin enhanced inflammation and the number

81 betic macular edema, was capable of cleaving netrin-1 into the VI-V fragment.

82 In vitro migration assays demonstrated that netrin-1 is a chemorepellent for migrating adult OPCs.

83 Since netrin-1 is a diffusible extracellular cue, the pathophy

84 Netrin-1 is a guidance cue that can trigger either attra

85 Netrin-1 is a neuronal guidance cue that regulates cellu

86 Netrin-1 is a secreted protein that was first identified

87 During development, netrin-1 is both an attractive and repulsive axon guidan

88 the attractive response to the guidance cue Netrin-1 is controlled by Slit/Robo1 signaling and by FL

89 -independently show that floor plate-derived netrin-1 is dispensable for commissural neuron axon guid

90 re we show that the neuroimmune guidance cue netrin-1 is highly expressed in obese but not lean adipo

91 in retina of a murine model of diabetes that netrin-1 is metabolized into a bioactive fragment corres

92 Netrin-1 knockdown reduced cell proliferation and attenu

93 Netrin-1 may be a novel therapeutic target for treatment

94 by activating NF-kappaB signaling via UNC5A, netrin-1 may be a potential therapeutic target for the t

95 by a transient transcriptional repression of Netrin-1 mediated by an Mbd3/Mta1/Chd4-containing NuRD c

96 res (ct) together with a lower expression of Netrin-1 might predict DGF development (training area un

97 We show that one netrin-1 molecule can simultaneously bind to two DCC mol

98 Netrin-4, but not netrin-1 mRNA expression, increased in response to relat

99 The influence of netrin-1 on CNS remyelination was examined using gain an

100 ast to the protective effects of full-length netrin-1 on retinal microvasculature, the VI-V fragment

101 we observed that the promigratory effects of Netrin-1 on T effectors is dependent on its interactions

102 Anti-Netrin-1 or anti-Unc5b, but not anti-DCC, antibodies sig

103 We asked whether blockade of Netrin-1 or its receptors [Unc5b and DCC (deleted in col

104 Our findings indicate that endogenous netrin-1 plays a role in NG2(+) glial cell homeostasis t

105 Human monocytes incubated with netrin-1 produced proresolving mediators, including reso

106 Netrin-1 promotes branching and synaptogenesis, but the

107 Taken together, these results suggested netrin-1 promotes glioma cell proliferation by activatin

108 n HEK293 or stable HeLa cells, the 3 mutated netrin-1 proteins were almost exclusively detected in th

109 d a direct interaction between TRIM9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive in

110 bination with cell-specific knockdown of the netrin-1 receptor DCC to determine its role in adolescen

111 olorectal cancer (DCC) is a well-established netrin-1 receptor mediating attractive responses.

112 close relative neogenin is also a functional netrin-1 receptor that acts with DCC to mediate guidance

113 Taken together, these results show that the netrin-1 receptor UNC5B plays a critical role in cell su

114 -1 expression early during demyelination and netrin-1 receptors are expressed by OPCs.

115 led the mRNA and protein expression of known Netrin-1 receptors on human CD4(+) T cells.

116 hological angiogenesis via interactions with netrin-1 receptors.

117 t does not bind directly to any of the known netrin-1 receptors.

118 Netrin-1 reduced this interaction as well as the colocal

119 We determined the structures of a functional netrin-1 region, alone and in complexes with neogenin or

120 Netrin-1 regulates cell survival and apoptosis by activa

121 To investigate how netrin-1 regulates the dynamic distribution of DCC and U

122 ic axons containing FLRT3 can modulate their Netrin-1 responsiveness in a context-dependent manner.

123 Instead, Netrin-1 selectively triggers phosphorylation of mammali

124 Netrin-1 shortened the resolution interval, decreasing e

125 d receptor-5 (UNC5A) as an antagonist of the Netrin-1 signal, though it did not affect the death of H

126 We reveal that netrin-1 signaling is involved in the NG2(+) glial cell

127 s regulates synaptic remodeling and involves netrin-1 signaling.Spinal cord injury can induce synapti

128 cally integrate both attractive or repulsive Netrin-1 signals together with repulsive ephrin signals.

129 ng a novel microfluidic assay, we found that Netrin-1 stimulated bidirectional migration and enhanced

130 Netrin-1 stimulates phosphatase 1A to dephosphorylate YA

131 d synaptogenesis, but the mechanism by which Netrin-1 stimulates plasma membrane expansion is unknown

132 Upon netrin-1 stimulation TRIM9 promotes DCC multimerization,

133 In response to netrin-1 stimulation, DCC becomes a signaling platform t

134 Our findings reveal a mechanism activated by netrin-1 that recruits DCC and UNC5B to the plasma membr

135 sruption of the signaling cascade induced by netrin-1 through its receptor DCC resulted in defective

136 or wild-type C57BL/6 treated with exogenous netrin-1 to examine the endogenous and therapeutically a

137 However, the ability of Netrin-1 to interact with lymphocytes and its in-depth e

138 UNC5B expressed alone was also recruited by netrin-1 to the plasma membrane.

139 s associated with a significant reduction of netrin-1 transcript and protein in murine liver tissue.

140 We report that Netrin-1 triggers a burst of beta-actin synthesis at mul

141 types II/X downregulated, deiodinase II and netrin-1 upregulated.

142 C or UNC5B was blocked by application of the netrin-1 VI-V peptide, which fails to activate chemoattr

143 This was clearly demonstrated for netrin-1 via its interaction with the receptors DCC and

144 Here we show that netrin-1 via its transmembrane receptors, deleted in col

145 Interestingly, activation of NF-kappaB by netrin-1 was dependent on UNC5A receptor, because suppre

146 Netrin-1 was produced by arterial smooth muscle cells (S

147 We found that netrin-1 was significantly increased in glioma samples a

148 Furthermore, Netrin-1 was upregulated in all histological stages of H

149 matory properties of the axonal guidance cue netrin-1 were reported.

150 rial innervation required the interaction of netrin-1 with its receptor, deleted in colorectal cancer

151 eptor of netrin-1, is critical for mediating netrin-1's cardioprotective function.

152 RNAi inhibition of SIAH1/2 further augmented netrin-1's cardioprotective function.

153 Our work also sheds light on Netrin-1's function in protecting embryonic stem cells f

154 In netrin-1(+/-) mice, resolvin D1 (RvD1) was less effectiv

155 Netrin-1, a chemorepulsant, laminin-like matrix protein,

156 Netrin-1, a laminin-related secreted protein, displays p

157 the possible link between HCV infection and Netrin-1, a ligand for dependence receptors that sustain

158 Netrin-1, acting through its principal receptor DCC (del

159 he vagus nerve regulates local expression of netrin-1, an axonal guidance molecule that activates res

160 Netrin-1, an extracellular guidance cue critical for neu

161 ich shows unique features in comparison with netrin-1, and show that it does not bind directly to any

162 cancer (DCC)-mediated midline attraction to Netrin-1, but without binding either Slits or Netrins.

163 Inactivating netrin-1, deleted in colorectal cancer, or uncoordinated

164 ate that full-length and fragmented forms of netrin-1, found in multiple sclerosis lesions, have the

165 the spatial regulation of axon branching by Netrin-1, in which localized plasma membrane expansion o

166 cer (DCC), a large transmembrane receptor of netrin-1, is critical for mediating netrin-1's cardiopro

167 ever, mainly based on shared homologies with netrin-1, netrin-4 was also proposed to play a role in n

168 In response to netrin-1, p120RasGAP is recruited to DCC in growth cones

169 lamic axons lacking FLRT3 are insensitive to Netrin-1, thalamic axons containing FLRT3 can modulate t

170 Given the diverse roles of netrin-1, the absence of manifestations other than CMM i

171 Murine monoclonal antibodies against Netrin-1, Unc5b, or DCC (10 microg/mouse) were injected

172 evels, abrogating cancer cell progression by netrin-1, whereas knockdown of mammalian STE20-like prot

173 he intracellular compartment, contrary to WT netrin-1, which is detected in both intracellular and ex

174 ligands for roundabout (Robo) receptors, and Netrin-1, which mediates attraction through the DCC rece

175 Netrin-1, whose expression is induced in macrophages by

176 nsistent with receptor recruitment requiring netrin-1-activated signaling.

177 Subsequent studies in netrin-1-deficient mice revealed lower efficacies in red

178 rminal tail of DCC, is sufficient to restore netrin-1-dependent axon outgrowth in p120RasGAP-deficien

179 herapeutic target of SIAH in facilitating NO/netrin-1-dependent cardioprotection, using the DCC recep

180 Netrin-1-dependent regulation of exocytotic events requi

181 exchange factor (GEF) Trio is essential for netrin-1-induced axon outgrowth and guidance.

182 A novel finding is that netrin-1-induced glioblastoma invasiveness and angiogene

183 essing UNC5B-mCherry and DCC-EGFP revealed a netrin-1-induced increase in colocalization, with both r

184 M shRNA in primary neurons totally abolished Netrin-1-induced JNK activation, whereas knockdown of DS

185 m of MKK4, a JNK upstream activator, blocked Netrin-1-induced JNK1 activation in HEK293 cells.

186 expression of both of them further enhanced Netrin-1-induced JNK1 activity in vitro.

187 (D10N) abrogated Trio Rac1 GEF activity and netrin-1-induced Rac1 activation.

188 ellular domain with mCherry, consistent with netrin-1-induced receptor oligomerization, but with no c

189 eceptor aggregation that are consistent with netrin-1-induced recruitment of DCC-enhanced green fluor

190 the Hippo pathway, has no effect in blocking netrin-1-induced up-regulation of YAP.

191 we investigated novel mechanisms underlying netrin-1-induced, rapid, and feed-forward up-regulation

192 Hsc70 was required for netrin-1-mediated axon growth and attraction in vitro, w

193 p120RasGAP and DCC that positively regulates netrin-1-mediated axon outgrowth and guidance in embryon

194 fic MT subunit in the brain, is required for netrin-1-mediated axon outgrowth, branching, and attract

195 in-1-repulsive receptor UNC5C is involved in netrin-1-mediated axonal repulsion.

196 ies implicated the A2B adenosine receptor in netrin-1-mediated protection during hepatic I/R injury.

197 Knockdown of either TUBB3 or UNC5C blocked netrin-1-promoted axon repulsion in vitro and caused def

198 ow that uncoupling of polymerized TUBB3 with netrin-1-repulsive receptor UNC5C is involved in netrin-

199 9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive interaction between TRIM9 and the SNA

200 s and therapeutically administered impact of netrin-1.

201 gulated by chemoattractant molecules such as Netrin-1.

202 because of a decrease in the sensitivity to netrin-1.

203 capacity, which can be restored by blocking netrin-1.

204 r positively charged patches on both DCC and netrin-1.

205 cytosis and axon branching in the absence of Netrin-1.

206 ion and enhanced presynaptic release through netrin-1.

207 with mutations in NTN1, the gene coding for netrin-1.

208 in cathepsin K(+) and CD68(+) cells in anti-Netrin-1/anti-Unc5b-treated animals.

209 ted a marked decrease in osteoclasts in anti-Netrin-1/anti-Unc5b-treated animals.

210 mice, whereas there were no erosions in anti-Netrin-1/anti-Unc5b-treated-animals.

211 a static position by Slit/Robo repulsion and Netrin-1/DCC attraction.

212 Correction of the Netrin-1/DCC equilibrium constrains apoptosis and improv

213 aled a role for calcium-dependent retrograde netrin-1/DCC receptor signaling.

214 e hindbrain and spinal cord, suggesting that Netrin-1/DCC signaling normally attracts motor neurons c

215 tivation by Trio and this function underlies netrin-1/DCC-dependent axon outgrowth and guidance.

216 N terminus of p120RasGAP to tightly regulate netrin-1/DCC-dependent axon outgrowth and guidance.

217 Collectively, our findings demonstrate that Netrin-1/neogenin interactions augment CD4(+) T cell che

218 afish development and acts downstream of the Netrin-1/Unc5-homolog B (Unc5B) signaling cascade.

219 Blockade of Netrin-1/Unc5b by monoclonal antibodies prevents bone de

220 polymerized TUBB3 plays an essential role in netrin-1/UNC5C-mediated axon repulsion.SIGNIFICANCE STAT

221 tubulin isoform in neurons, is essential for netrin-1/UNC5C-promoted axon repulsion.

222 Among the variation, we observed changes in netrin 4, fibroblast growth factor 2, tenascin C, collag

223 To answer the question whether netrin-4 acts either pro- or anti-angiogenic, angiogenes

224 Our study unveils netrin-4 as a non-enzymatic extracellular matrix protein

225 Our results indicate a role for netrin-4 as an angiogenesis modulating factor in O2-depe

226 Netrin-4 displays pathologic roles in tumorigenesis and

227 We show that netrin-4 disrupts laminin networks and basement membrane

228 ly based on shared homologies with netrin-1, netrin-4 was also proposed to play a role in neuronal ou

229 The basement membrane protein netrin-4 was found to be localised to mature retinal blo

230 Netrin-4, but not netrin-1 mRNA expression, increased in

231 we present the high-resolution structure of netrin-4, which shows unique features in comparison with

232 ived neurotrophic factors (BDNFs) [6], UNC-6/Netrin [7], and the conserved MNR-1/Menorin-SAX-7/L1CAM

233 Netrins, a family of laminin-related molecules, have bee

234 crossing by signaling locally in response to Netrin and by inducing transcription of commissureless (

235 These data are the first to show that Netrin and Frazzled regulate the placement of gap juncti

236 Netrin and its receptor, Frazzled, dictate the strength

237 However, the mechanisms regulating netrin and its receptors in the extracellular milieu are

238 it this bottleneck to define roles for glial Netrin and Semaphorin in pioneer- and follower-axon guid

239 situ hybridization assays revealed that both netrin and slit mRNAs are expressed along the midline fa

240 cer (DCC) homolog neogenin functions in both netrin- and repulsive guidance molecule (RGM)-mediated a

241 Netrins are a family of matrix-binding proteins that fun

242 Netrins are secreted proteins that direct cell migration

243 Netrins are secreted proteins that regulate axon guidanc

244 of differential sensitivity to the conserved Netrin attractants and Slit repellents is insufficient t

245 on, inhibits Slit repulsion, and facilitates Netrin attraction to achieve a common guidance purpose.

246 both silences Slit repulsion and potentiates Netrin attraction.

247 Several lines of evidence suggest that netrin-DCC signaling can regulate and be regulated by th

248 f PKA activity to DCC is required for proper netrin/DCC-mediated signaling.

249 VASP to modulate filopodial stability during netrin-dependent axon guidance.

250 iated vesicle fusion and axon branching in a Netrin-dependent manner.

251 Netrin-dependent morphogenesis is preceded by multimeriz

252 Together these studies define a netrin-dependent pathway that builds an invasive protrus

253 Together, our data suggest that UNC-6 (netrin) directs polarized responses by stabilizing UNC-4

254 omplex in a ligand-dependent manner and that Netrin-ephrin synergistic growth cones responses involve

255 Netrin expression and activity are strongly associated w

256 The phylogenetically conserved Netrin family of chemoattractants signal outgrowth and a

257 tic approaches in mice to selectively remove netrin from different regions of the spinal cord.

258 terns in mouse sSC: cadherin 7, contactin 3, netrin G2, cadherin 6, protocadherin 20, retinoid-relate

259 n form transsynaptic adhesion complexes with netrin-G2, which we show to be expressed by photorecepto

260 till cross the midline in the absence of the Netrin genes (NetA and NetB) or their receptor frazzled.

261 ed growth cone morphology and tropism toward netrin in ERM-knockdown cells, expression of an AKAP-def

262 ver, the mechanism by which the guidance cue netrin increases filopodia density is unknown.

263 MA and LIN-5, is an essential component of a Netrin-independent pathway that acts in parallel to prom

264 UNC-6/Netrin is a conserved axon guidance cue that can mediate

265 Netrin is a key axon guidance cue that orients axon grow

266 How DCC polarizes toward netrin is poorly understood.

267 e NCX-9 in a LON-2/heparan sulfate and UNC-6/netrin-mediated, RAC-dependent signaling pathway to guid

268 In Netrin mutant animals, the synaptic coupling between a g

269 In cases in which Netrin mutants displayed apparently normal synaptic anat

270 ing that gap junctions were disrupted in the Netrin mutants.

271 The ligand-receptor pair, Netrin (Net) and Frazzled (Fra) (DCC, Deleted in Colorec

272 (mud) dramatically enhances the phenotype of Netrin or frazzled mutants, resulting in many more axons

273 s in both the attractive and repulsive UNC-6/netrin pathways.

274 es have shown that the direct interaction of netrin receptor DCC and DSCAM with polymerized TUBB3, a

275 at localizes to filopodia tips and binds the netrin receptor DCC, interacts with and ubiquitinates th

276 tractant and Unc5 contributes as a repellant Netrin receptor for glia migration.

277 t the timely and threshold expression of the Netrin receptor Frazzled triggers the initiation of glia

278 mutation, T835M (rs137875858), in the UNC5C netrin receptor gene that segregated with disease in an

279 in receptor heterodimer INA-1/PAT-3 promotes netrin receptor UNC-40 (DCC) localization to the invasiv

280 he C. elegans NSM neuron is dependent on the Netrin receptor UNC-40/DCC.

281 The two extracellular TSRs of the netrin receptor UNC5A contain WxxWxxWxxC motifs that can

282 nd Netrin-1 integration demonstrate that the Netrin receptor Unc5c and the ephrin receptor EphB2 can

283 y this year provide evidence that in humans, Netrin receptor, Deleted in Colorectal Cancer (DCC), is

284 homologs are proposed to form a heteromeric netrin-receptor complex to mediate a chemorepellent resp

285 binding allows for the association of other netrin receptors at the generic binding site, eliciting

286 nteraction fractions of fluorescently tagged netrin receptors expressed in HEK293T cells.

287 e proteins, including protocadherins, ROBOs, netrin receptors, neuroligins, GPCRs, and channels.

288 Expression of netrin receptors, Unc5H2 (Unc-5 homolog B, C. elegans) a

289 opulations, according to their expression of Netrin receptors.

290 nd as heterophilic repulsive ligands of Unc5/Netrin receptors.

291 eparan sulfate proteoglycan, modulates UNC-6/netrin signaling and may do this through interactions wi

292 opmental and pathological processes, but how netrin signaling is coordinated with other pathways duri

293 CCGs are enriched in Wnt, PI3K, MAPK and netrin signaling pathway components and are more highly

294 dance to fine-tune axonal responses to UNC-6/netrin signals during migration.

295 eak symmetry and oscillate in the absence of netrin, suggesting the presence of interlinked positive

296 Upon netrin treatment, VASP is deubiquitinated, which promote

297 y rescue growth cone morphology and switched netrin tropism from attraction to repulsion.

298 UNC-6 (netrin)/UNC-40 interactions generate an invasive protrus

299 chor cell (AC) invasion, we found that UNC-6(netrin)/UNC-40(DCC) signaling at the BM breach site dire

300 L3 axons then produce Netrin, which regulates the layer-specific targeting of