ライフサイエンスコーパス: netrin-1

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

2 s and therapeutically administered impact of netrin-1.

3 axon turning in response to the guidance cue netrin-1.

4 gulated by chemoattractant molecules such as Netrin-1.

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

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

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

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

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

10 quired for axon turning toward a gradient of netrin-1.

11 idelitous responses to the axon guidance cue netrin-1.

12 ion and enhanced presynaptic release through netrin-1.

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

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

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

16 Netrin-1, a navigation cue during embryonic development,

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

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

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

20 C), the receptor for the multifunctional cue netrin-1, acts as a tumor suppressor in intestinal cance

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

22 Netrin-1 also induced colocalization of coexpressed full

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

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

25 r TCA navigation and that the molecular cues netrin 1 and semaphorin 3a are likely to be involved.

26 We demonstrate that both overexpression of netrin-1 and brain administration of recombinant netrin-

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

28 Although expression of netrin-1 and DCC is maintained in the adult brain, littl

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

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

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

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

33 regulator of the neuroimmune retention cues, Netrin-1 and its coreceptor UNC5B.

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

35 Netrin-1 and its receptor DCC regulate melanoma progress

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

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

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

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

40 olorectal cancer database, the expression of netrin-1 and its receptor UNC5B correlates with a cancer

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

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

43 Netrin-1 and RvD1 displayed bidirectional activation in

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

45 Mechanistically, we reveal how Netrin-1 and the balance of its receptors Neo1 and Unc5B

46 Netrin-1 and UNC5B are deregulated in multiple cancers,

47 tains a similar head-to-stalk arrangement as netrins -1 and -4.

48 gulated KLF4 and STAT6, reduced secretion of Netrin-1, and increased migration toward the lymph node

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

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

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

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

53 Anticancer strategies utilizing anti-netrin-1 antibody treatment are already in clinical tria

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

55 so requires PP2A.IMPORTANCE UNC5B, PP2A, and netrin-1 are deregulated in a variety of cancers.

56 in-1 and brain administration of recombinant netrin-1 are neuroprotective and neurorestorative in mou

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

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

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

60 Collectively, this work identifies Netrin-1 as a regulator of pluripotency and reveals that

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

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

63 1 and FLRT3 receptors are required to induce Netrin-1 attraction by the upregulation of surface DCC t

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

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

66 Netrin-1 binds its receptors deleted in colorectal cance

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

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

69 Furthermore, we demonstrate that Netrin-1 can substitute for blockade of Gsk3alpha/beta a

70 Therapeutic antibody blockade of netrin-1 combined with dacarbazine increased overall sur

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

72 er, these data support that interfering with netrin-1 could be a viable therapeutic approach in patie

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 The Netrin-1/DCC guidance cue pathway plays a critical role

77 The netrin-1/DCC ligand/receptor pair has key roles in centr

78 gra, leading us to investigate a role of the netrin-1/DCC pair in adult nigral neuron fate.

79 tudies indicating an association between the Netrin-1/DCC pathway and major depressive disorder.

80 ginate in part from the dysregulation of the Netrin-1/DCC pathway by a mechanism that involves microR

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

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

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

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

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

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

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

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

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

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

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

92 elated E3 ubiquitin ligases are required for netrin-1-dependent filopodial responses, axon turning an

93 nd axonal branching patterns in a TRIM9- and netrin-1-dependent manner.

94 Netrin-1-dependent regulation of exocytotic events requi

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

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

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

98 Netrin-1 downregulation occurs following axon injury and

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

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

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

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

103 Netrin-1 enhanced infectivity of HCV particles and promo

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

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

106 viable therapeutic approach in patients with netrin-1-expressing melanoma.

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

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

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

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

111 Netrin-1 expression was analyzed immunohistochemically i

112 Netrin-1 expression was elevated in melanoma compared wi

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

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

115 We also show that netrin-1 expression, which is known to inhibit UNC5B apo

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

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

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

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

120 show that Netrin-1 from distinct sources controls neuronal migrati

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

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

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

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

125 and depression in adulthood by targeting the netrin-1 guidance cue receptor gene Dcc in the medial pr

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

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

128 Netrin-1 has a rigid elongated structure containing two

129 ce in chick, humans, mice and zebrafish that Netrin-1 has an evolutionarily conserved and essential r

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

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

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

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

134 These results highlight the key role of netrin-1 in adult dopamine neuron fate, and the therapeu

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

136 ase (PD), we studied the potential impact of netrin-1 in different animal models of PD.

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

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

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

140 Knockout of Netrin-1 in osteoclasts abrogates sensory innervation in

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

142 Here, we show that silencing netrin-1 in the adult substantia nigra of mice induces D

143 Upregulation of netrin-1 in the skin cells of a BRAF(V600E)-mutated muri

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

145 Netrin-1 increased endogenous JNK activity in primary ne

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 Netrin-1 induces Fak kinase to inactivate Gsk3alpha/beta

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

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

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

167 Remarkably, one source of Netrin -1 is forebrain axons traversing the midbrain, an

168 Thus, reciprocal inhibition between Bmp2 and netrin 1 is involved in canal formation of the vestibule

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

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

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

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

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

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

175 In multiple animal models, interference with netrin-1 is associated with inhibition of tumor growth a

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 Notably, netrin-1 is highly expressed in the adult substantia nig

181 astasis by triggering cancer cell death when netrin-1 is lowly expressed.

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

183 Netrin-1 is upregulated in a large fraction of human neo

184 Together these data demonstrate that netrin-1 is upregulated not only in cancer cells but als

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

186 With homology to human netrin-1, it is a key signaling molecule involved in dir

187 Netrin-1 knockdown reduced cell proliferation and attenu

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

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

190 Of interest, we observed that netrin-1 levels are significantly reduced in PD patient

191 Pharmacologic inhibition of netrin-1 with a netrin-1-mAb (Net1-mAb) abrogated the CAF-mediated incre

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

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

194 rect activity on cancer cells, inhibition of netrin-1 may reduce proneoplastic CAF-cancer cell cross-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

210 ntary transcriptomic profiling and show that Netrin-1 (NTN1) is precisely expressed in the chick fiss

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

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

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

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

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

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

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

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

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

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

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

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

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

224 Netrin-1 promotes branching and synaptogenesis, but the

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

226 Here we show that the axon guidance cue Netrin-1 promotes naive pluripotency by triggering profo

227 In contrast, netrin-1 promotes survival by inhibiting dependence rece

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

229 ncluded genes such as DCC, which encodes the netrin-1 receptor and has an important role in the devel

230 validated cancer associated genes EPHA7, DCC netrin-1 receptor and zinc-finger protein ZNF479.

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

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

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

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

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

236 -1 expression early during demyelination and netrin-1 receptors are expressed by OPCs.

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

238 hological angiogenesis via interactions with netrin-1 receptors.

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

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

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

242 Netrin-1 regulates cell survival and apoptosis by activa

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

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

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

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

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

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

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

250 Instead, Netrin-1 selectively triggers phosphorylation of mammali

251 9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive interaction between TRIM9 and the SNA

252 Netrin-1 shortened the resolution interval, decreasing e

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

254 , and the therapeutic potential of targeting netrin-1 signaling in PD.

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

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

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

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

259 Netrin-1 stimulates phosphatase 1A to dephosphorylate YA

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

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

262 Upon netrin-1 stimulation TRIM9 promotes DCC multimerization,

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

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 ventional drugs leads to the upregulation of netrin-1 through activated p53, which is counterintuitiv

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

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

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

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

274 Similar to netrin-1, UNC-6 interacts with multiple receptors (UNC-5

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

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

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

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

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

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

281 cocultured with respective cancer cells, and netrin-1 upregulation in CAF was associated with increas

282 Although netrin-1 upregulation was initially described in cancer

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

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

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

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

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

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

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

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

291 Both colon and lung CAF secreted netrin-1 when cocultured with respective cancer cells, a

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

293 The lack of Bmp2 causes Ntn1 (which encodes netrin 1), which is required for canal resorption, to be

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

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

296 t mode to transiently suppress attraction to Netrin-1 while motor axons exit the spinal cord.

297 otes survival in the presence of its ligand, netrin-1, while inducing cell death in its absence.

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

299 Pharmacologic inhibition of netrin-1 with a netrin-1-mAb (Net1-mAb) abrogated the CA

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