ライフサイエンスコーパス: netrin-1

1 pposes expression of the fusion plate marker netrin 1.

2 gulated by chemoattractant molecules such as Netrin-1.

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

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

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

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

7 the chemoattractant activity of full-length netrin-1.

8 cone collapse of mouse EGL cells induced by netrin-1.

9 embryos show normal outgrowth in response to Netrin-1.

10 was necessary for traction forces >30 pN on netrin-1.

11 ion and enhanced presynaptic release through netrin-1.

12 and turning response of commissural axons to Netrin-1.

13 induction of Fyn tyrosine phosphorylation by netrin-1.

14 ssion of the TNF-alpha receptor Tnfrsf1b and Netrin-1.

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

16 s and therapeutically administered impact of netrin-1.

17 Netrin-1, a bifunctional guidance cue, binds to deleted

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

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

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

21 Here we found that netrin-1, a neuroimmune guidance cue, was secreted by ma

22 s that trigger epithelial cell production of Netrin-1, a neuronal guidance molecule.

23 A candidate inhibitor is netrin-1, a secreted protein that repels migrating oligo

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

25 interacts with UNC5B, which is regulated by netrin-1-activated Akt.

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

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

28 tivation of FAK reinforces interactions with netrin-1 allowing greater forces to be exerted.

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

30 Furthermore, netrin-1 also increased albumin uptake by proximal tubul

31 Netrin-1 also induced colocalization of coexpressed full

32 Recently, we have shown that netrin-1 also interacts with the orphan transmembrane re

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

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

35 environment, our work highlights the role of Netrin-1 and a specific TNF-alpha receptor as candidate

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

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

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

39 APP interacts with DCC in the presence of netrin-1 and enhances netrin-1-mediated DCC intracellula

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

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

42 We report that netrin-1 and its receptor DCC are widely expressed by ne

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

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

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

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

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

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

49 Netrin-1 and RvD1 displayed bidirectional activation in

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

51 ly, it has been shown that DSCAM can bind to Netrin-1 and that downregulation of DSCAM expression by

52 echanotransduction during chemoattraction to netrin-1 and that mechanical activation of FAK reinforce

53 sponses to chondroitin sulfate proteoglycan, netrin-1, and fibronectin.

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

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

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

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

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

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

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

61 We have identified netrin-1 as a molecule that promotes glioblastoma invasi

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

63 These findings identify netrin-1 as a synapse-enriched protein that promotes syn

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

65 1 and FLRT3 receptors are required to induce Netrin-1 attraction by the upregulation of surface DCC t

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

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

68 Netrin-1 binds its receptors deleted in colorectal cance

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

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

71 the chemoattractant activity of full-length netrin-1, consistent with a competitive mechanism of act

72 signaling leading to increased production of Netrin-1, crypt hyperplasia, and decreased epithelial ce

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

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

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

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

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

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

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

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

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

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

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

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

85 s part of the DCC receptor complex mediating netrin-1-dependent axon guidance.

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

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

88 Netrin-1-dependent regulation of exocytotic events requi

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

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

91 Furthermore, recombinant domains VI-V of netrin-1 disrupt the chemoattractant activity of full-le

92 Netrin-1 downregulation occurs following axon injury and

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

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

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

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

97 Netrin-1 enhanced infectivity of HCV particles and promo

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

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

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

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

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

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

104 Netrin-1 expression was analyzed immunohistochemically i

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

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

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

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

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

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

111 ted full-length netrin-1 protein and shorter netrin-1 fragments in samples of normal white matter and

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

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

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

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

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

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

118 Netrin-1 has a rigid elongated structure containing two

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

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

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

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

123 Herein, we examined the distribution of netrin-1 in adult human white matter and multiple sclero

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

125 We examined the role of netrin-1 in diabetes-induced kidney inflammation and inj

126 , the role of the anti-inflammatory molecule netrin-1 in diabetic kidney disease is unknown.

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

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

129 Targeted deletion of netrin-1 in macrophages resulted in much less atheroscle

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

131 UNC5C and this interaction is stimulated by netrin-1 in primary cortical neurons and postnatal cereb

132 re we demonstrate a synaptogenic function of netrin-1 in rat and mouse cortical neurons and investiga

133 action of 5-HT on thalamic axon responses to netrin-1 in vitro.

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

135 Netrin-1 increased endogenous JNK activity in primary ne

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

137 We show that netrin-1 increases the complexity of axon and dendrite a

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

139 function manipulations, we demonstrate that netrin-1 increases the number and strength of excitatory

140 Netrin-1 increases tyrosine phosphorylation of endogenou

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

142 ect of complete genetic ablation of DSCAM on Netrin-1-induced axon guidance, we analyzed spinal commi

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

144 he specific CatB inhibitor CA-074Me inhibits netrin-1-induced cell invasion, sprouting, and Matrigel

145 Silencing of CREB suppresses netrin-1-induced glioblastoma cell invasion, sprouting,

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

147 ous knockdown of DSCAM and UNC5C also blocks netrin-1-induced growth cone collapse in EGL cells.

148 ressing dominant negative mutants suppresses netrin-1-induced growth cone collapse.

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

150 Netrin-1-induced JNK activation was inhibited either by

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

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

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

154 rence (RNAi) or the JNK inhibitor suppressed Netrin-1-induced neurite outgrowth and axon attraction.

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

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

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

158 The mechanism of netrin-1-induced suppression of inflammation was studied

159 Netrin-1-induced suppression of PGE2 production was medi

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

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

162 Netrin-1 induces axon growth cone collapse of mouse cere

163 Acting via its receptor, UNC5b, netrin-1 inhibited the migration of macrophages directed

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

165 t brain, but the biological relevance of APP/netrin-1 interaction under non-pathological conditions w

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

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

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

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

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

171 These findings suggest that netrin-1 is a major regulator of inflammation and apopto

172 onstrated that via its interaction with APP, netrin-1 is a negative regulator of amyloid-beta product

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

174 Netrin-1 is a secreted protein that directs long-range a

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

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

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

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

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

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

181 s and provide evidence that newly translated netrin-1 is selectively transported to dendrites.

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

183 Netrin-1 knockdown reduced cell proliferation and attenu

184 In our simulations, the EphA4 and Netrin-1 KO circuits switched from the left-right altern

185 In EphA4 knockout (KO) and Netrin-1 KO mice, the normal left-right alternating patt

186 In the Netrin-1 KO model, the number of contralateral CINi proj

187 he EphA4 and DCC KO circuits, but not in the Netrin-1 KO network.

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

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

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

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

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

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

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

195 DCC in the presence of netrin-1 and enhances netrin-1-mediated DCC intracellular signaling, such as M

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

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

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

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

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

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

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

203 creased staining for macrophages, TNF-alpha, netrin-1, NF-kappaB, Tnfrsf1b, and the proliferation mar

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

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

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

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

208 Neuroimmune guidance cue 1 (netrin-1 [NTN1]) plays a critical role controlling MPhi

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

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

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

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

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

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

215 Targeting netrin-1 pathways may be a promising strategy for brain

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

217 It is concluded that netrin-1 plays an important dual role in glioblastoma pr

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

219 tion of Tnfrsf1b decreased TNF-alpha-induced netrin-1 production and augmented epithelial cell apopto

220 Thus, netrin-1 promoted atherosclerosis by retaining macrophag

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

222 At sites of contact, netrin-1 promotes adhesion, while locally enriching and

223 Netrin-1 promotes branching and synaptogenesis, but the

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

225 We detected full-length netrin-1 protein and shorter netrin-1 fragments in sampl

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

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

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

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

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

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

232 -1 expression early during demyelination and netrin-1 receptors are expressed by OPCs.

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

234 hological angiogenesis via interactions with netrin-1 receptors.

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

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

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

238 Furthermore, netrin-1 regulates angiogenesis as shown in specific ang

239 Netrin-1 regulates cell survival and apoptosis by activa

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

241 onding to amino terminal domains VI and V of netrin-1 repel migrating oligodendrocyte precursor cells

242 vidence that DSCAM coordinates with UNC5C in netrin-1 repulsion.

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

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

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

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

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

248 Instead, Netrin-1 selectively triggers phosphorylation of mammali

249 9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive interaction between TRIM9 and the SNA

250 Netrin-1 shortened the resolution interval, decreasing e

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

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

253 This netrin-1 signaling pathway in glioblastoma cells include

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

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

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

257 As evidence, netrin-1 stimulates glioblastoma cell invasion directly

258 Netrin-1 stimulates phosphatase 1A to dephosphorylate YA

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

260 ore and as they crossed the floor plate, and Netrin-1 stimulation dramatically increased the level of

261 Upon netrin-1 stimulation TRIM9 promotes DCC multimerization,

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

263 y, while these myosin II-dependent forces on netrin-1 substrates or beads were needed to increase the

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

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

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

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

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

269 rylation of FAK, they were not necessary for netrin-1 to increase CAS phosphorylation.

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

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

272 in-1, we found that mechanical attachment of netrin-1 to the substrate was required for axon outgrowt

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

274 nduced using streptozotocin in wild-type and netrin-1 transgenic animals.

275 E2 (PGE2) in urine, which was suppressed in netrin-1 transgenic mice.

276 These changes were minimal in kidney of netrin-1 transgenic mice.

277 nflammation and injury using tubule-specific netrin-1 transgenic mice.

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

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

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

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

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

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

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

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

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

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

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

289 l adhesions and to generate forces >60 pN on netrin-1 was disrupted.

290 The multifunctional protein netrin-1 was initially discovered as the main attractive

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

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

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

294 spinal commissural neuron axon attraction to netrin-1, we found that mechanical attachment of netrin-

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

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

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

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

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

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