ライフサイエンスコーパス: netrin

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

2 ucture we previously published on vertebrate netrins.

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

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

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

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

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

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

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

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

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

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

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

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

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

16 Netrin-1 also induced colocalization of coexpressed full

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

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

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

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

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

22 Netrin-1 and its receptor DCC regulate melanoma progress

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 Netrin-1 binds its receptors deleted in colorectal cance

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

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

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

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

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

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

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

46 Netrin-1 downregulation occurs following axon injury and

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

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

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

50 Netrin-1 enhanced infectivity of HCV particles and promo

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

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

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

54 Netrin-1 expression was elevated in melanoma compared wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

94 Netrin-1 knockdown reduced cell proliferation and attenu

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

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

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

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

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

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

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

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

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

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

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

106 Netrin-1 promotes branching and synaptogenesis, but the

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

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

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

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

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

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

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

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

115 hological angiogenesis via interactions with netrin-1 receptors.

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

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

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

119 Netrin-1 shortened the resolution interval, decreasing e

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

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

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

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

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

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

126 Netrin-1 stimulates phosphatase 1A to dephosphorylate YA

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

128 Upon netrin-1 stimulation TRIM9 promotes DCC multimerization,

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

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

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

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

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

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

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

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

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

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

139 Although netrin-1 upregulation was initially described in cancer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

181 Netrin-1-dependent regulation of exocytotic events requi

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

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

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

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

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

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

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

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

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

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

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

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

198 ion and enhanced presynaptic release through netrin-1.

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

200 s and therapeutically administered impact of netrin-1.

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

202 gulated by chemoattractant molecules such as Netrin-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 Netrin-4 displays pathologic roles in tumorigenesis and

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

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

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

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

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

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

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

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

237 We use Netrin and its receptors as an example to analyze the co

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

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

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

241 Netrins are secreted proteins that direct cell migration

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

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

244 Structural data indicate that netrin can also mediate trans-adhesion between apposing

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

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

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

248 Netrin-dependent morphogenesis is preceded by multimeriz

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

250 Knockout of UNC5B abolishes netrin depletion-induced dopaminergic loss, whereas bloc

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

252 llistatin/kazal, immunoglobulin, Kunitz, and netrin domain-containing (WFIKKN).

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

254 Netrin expression and activity are strongly associated w

255 inated-6 (UNC-6) was the first member of the netrin family to be discovered in Caenorhabditis elegans

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

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

258 NTNG2 encodes netrin-G2, a membrane-anchored protein implicated in the

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

260 is dispensable and VZ-netrin1 sufficient for netrin guidance activity in vivo.

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 Structural studies have revealed how netrin interacts with the deleted in colorectal cancer (

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

266 Netrin is a prototypical axon guidance cue.

267 Here, we propose that netrin is involved in conditional adhesion, a reversible

268 Recently, genetic studies suggested that netrin is involved in neuronal haptotaxis, which require

269 We suggest that netrin-mediated adhesion and signaling are linked, and t

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

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 erochronic genes are components in the UNC-6/Netrin pathway of synaptic polarity of these neurons.

274 r matrix molecule MIG-6/Papilin or the UNC-6/Netrin pathway, suggesting that axon-dendrite adhesion i

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

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

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

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

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

280 roteasome system promotes degradation of the netrin receptor UNC-40 in a particular neuron only in on

281 In C. elegans the netrin receptor UNC-40/DCC controls the growth of dendri

282 ated thrombospondin type 1 repeats (TSRs) of netrin receptor UNC-5.

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

284 , which selectively binds and phosphorylates netrin receptor UNC5B on T428 residue, promoting its apo

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

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

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

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

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

290 opulations, according to their expression of 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 Upon netrin treatment, VASP is deubiquitinated, which promote

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

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

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

299 anding the p53-independent mechanisms of the netrin-UNC5B axis, such as those involving PP2A, assumes

300 tionary path of UNC-6 compared to vertebrate netrins, we decided to employ an integrated approach to