ライフサイエンスコーパス: DCC

1 DCC mutations result in variable dominant phenotypes wit

2 DCC receptor signaling in dopamine neurons is a molecula

3 DCC serves as a clear paradigm for addressing how conden

4 DCC subunits also participate in condensin complexes ess

5 DCC SUMOylation is triggered by the signal that initiate

6 DCC-2701 (Deciphera Pharmaceuticals, LLC), a novel c-MET

7 position by Slit/Robo repulsion and Netrin-1/DCC attraction.

8 Correction of the Netrin-1/DCC equilibrium constrains apoptosis and improves reprog

9 le for calcium-dependent retrograde netrin-1/DCC receptor signaling.

10 in and spinal cord, suggesting that Netrin-1/DCC signaling normally attracts motor neurons closer to

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

12 s of p120RasGAP to tightly regulate netrin-1/DCC-dependent axon outgrowth and guidance.

13 INA-1/PAT-3 promotes netrin receptor UNC-40 (DCC) localization to the invasive cell membrane of the A

14 We find that the netrin receptor UNC-40 (DCC) specifically enriches at the site of basement membr

15 invasion, we found that UNC-6(netrin)/UNC-40(DCC) signaling at the BM breach site directs exocytosis

16 usly to up-regulate the expression of UNC-40/DCC and MADD-2 in vm2, which in turn function together t

17 howed that the transmembrane proteins UNC-40/DCC and MIG-21, a novel thrombospondin type I repeat con

18 Ectopic expression of UNC-40/DCC in non-target vm1 muscle is sufficient to induce mus

19 migration molecules UNC-6/Netrin and UNC-40/DCC in this process, but in parallel to SAX-3/Robo.

20 echanism by which the Netrin receptor UNC-40/DCC instructs synaptic vesicle clustering in vivo.

21 previously discovered that attractive UNC-40/DCC receptor signaling stimulates growth cone filopodial

22 e that LON-2/glypican associates with UNC-40/DCC receptor-expressing cells.

23 do this through interactions with the UNC-40/DCC receptor.

24 LON-2/glypican acts as a modulator of UNC-40/DCC-mediated guidance to fine-tune axonal responses to U

25 n is dependent on the Netrin receptor UNC-40/DCC.

26 tiveness ratio of $74,255 (HCC) and $36,583 (DCC).

27 cts, deletion of an endogenous rex site at a DCC-dependent TAD boundary using CRISPR/Cas9 greatly dim

28 enriched on hermaphrodite X chromosomes in a DCC-dependent manner.

29 associates with autosomes of germ cells in a DCC-independent manner to enrich H4K20me1 and trigger ch

30 rom the X even before the 30-cell stage in a DCC-independent manner.

31 aneously bind to two DCC molecules through a DCC-specific site and through a unique generic receptor

32 d on X chromosomes several cell cycles after DCC localization to the X, suggesting that it is a late

33 ence the effects on infant development after DCC in different directions.

34 encing epigenetic marks, evidence of altered DCC, SET-1 and SET-4 activity.

35 domain 4 (FN4) and FN5, which differs among DCC and neogenin splice variants, providing a basis for

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

37 attractive signals, we examined Netrin-1 and DCC mutants, and found that motor neurons shifted dorsal

38 xon guidance molecules, such as Netrin-1 and DCC.

39 While both supramolecular chemistry and DCC operate under the regime of reversibility, DCC has t

40 rs, Unc5H2 (Unc-5 homolog B, C. elegans) and DCC (deleted in colorectal carcinoma), was found in Mull

41 shed an alternating pattern in the EphA4 and DCC KO circuits, but not in the Netrin-1 KO network.

42 lysis, when subjects with antecedent HCC and DCC were excluded, the only significant predictor of HBV

43 ries of cells coexpressing UNC5B-mCherry and DCC-EGFP revealed a netrin-1-induced increase in colocal

44 in contrast to the spinal cord, Netrin1 and DCC mutants had abundant commissural axons crossing in t

45 In Netrin1 and DCC mutants, many post-crossing axons made normal turns

46 for patients with chronic infection only and DCC were higher than the values used in many previous co

47 for patients with chronic infection only and DCC were higher than values used in many cost-effectiven

48 e show an interaction between p120RasGAP and DCC that positively regulates netrin-1-mediated axon out

49 (DUTT1, FHIT, APC, p16, FCMD, RB1, p53, and DCC genes) that are associated with GBC was tested from

50 sease progression of HCV in HCC patients and DCC patients waitlisted for LT.

51 atinib, nilotinib, dasatinib, ponatinib, and DCC-2036), we interrogated response of CML cell lines an

52 teins Syntaxin1a and PSD-95 and the TrkB and DCC receptors in Munc18-1(-/-) neurons; these defects do

53 paring chromosome structure in wild-type and DCC-defective embryos, we show that the DCC remodels her

54 kade of Netrin-1 or its receptors [Unc5b and DCC (deleted in colorectal carcinoma)] may be useful the

55 bited either by the JNK inhibitor or an anti-DCC function-blocking antibody.

56 Anti-Netrin-1 or anti-Unc5b, but not anti-DCC, antibodies significantly reduced paw inflammation (

57 hy showed bony erosions in untreated or anti-DCC-treated mice, whereas there were no erosions in anti

58 Combination of the anti-DCC function-blocking antibody with expression of DSCAM

59 interactions occurring between rex sites at DCC-dependent TAD boundaries.

60 was demonstrated in necrotic lesions of both DCC-susceptible C3H/He and B6.C3H(Dyscalc1) congenic mic

61 together positively charged patches on both DCC and netrin-1.

62 cue, binds to deleted in colorectal cancer (DCC) and DSCAM mediating axon attraction, and UNC5 media

63 its receptors deleted in colorectal cancer (DCC) and the UNC5 homologs (UNC5A-D) to activate downstr

64 d its receptor Deleted in Colorectal Cancer (DCC) are proteins enriched at paranodes that are express

65 The receptor deleted in colorectal cancer (DCC) directs dynamic polarizing activities in animals to

66 The deleted in colorectal cancer (DCC) homolog neogenin functions in both netrin- and repu

67 Deleted in colorectal cancer (DCC) is a well-established netrin-1 receptor mediating a

68 The receptor deleted in colorectal cancer (DCC) mediates the attraction of growing axons to netrin-

69 he presence of deleted in colorectal cancer (DCC) or Down syndrome cell adhesion molecule (DSCAM), an

70 d its receptor deleted in colorectal cancer (DCC) promote axon branching in developing cortical neuro

71 Frazzled (Fra)/Deleted in Colorectal Cancer (DCC) receptor promotes midline axon crossing by signalin

72 mplex with the Deleted in Colorectal Cancer (DCC) receptor.

73 Deleted in colorectal cancer (DCC), a large transmembrane receptor of netrin-1, is cri

74 axons, such as deleted in colorectal cancer (DCC), in most fiber tracts examined.

75 trin receptor, Deleted in Colorectal Cancer (DCC), is a master regulator of axonal crossing throughou

76 its receptor, deleted in colorectal cancer (DCC), on sympathetic growth cones.

77 d potentiating deleted in colorectal cancer (DCC)-mediated midline attraction to Netrin-1, but withou

78 h the receptor Deleted in Colorectal Cancer (DCC).

79 ch the UNC-40 (Deleted in Colorectal Cancer; DCC) receptor captures UNC-6 at the tips of growing dend

80 through the Deleted in Colorectal Carcinoma (DCC) family of receptors.

81 lacking the deleted in colorectal carcinoma (DCC) guidance receptor.

82 receptor 'deleted in colorectal carcinoma' (DCC), which has been implicated in congenital mirror mov

83 nct dioxobilin-type chlorophyll catabolites (DCCs) as the major breakdown products in wild-type Arabi

84 transcriptome of disseminated cancer cells (DCC) isolated from patients with nonmetastatic (UICC sta

85 ions develop from disseminated cancer cells (DCCs) that can remain dormant.

86 illated anionic dicarboxylic acid cellulose (DCC), having widths of fibres ranging from 19.0 mum to 2

87 allergen concentrations in day-care centers (DCC) with those in private homes.

88 Dynamic combinatorial chemistry (DCC) has emerged as a powerful strategy to identify liga

89 Dynamic combinatorial chemistry (DCC) is a subset of combinatorial chemistry where the li

90 Dynamic combinatorial/covalent chemistry (DCC) has been used to read structural information by sel

91 focusing on the dynamic covalent chemistry (DCC) of disulfide exchange reactions, is presented.

92 By introducing dynamic covalent chemistry (DCC), cages have become accessible in good yields from r

93 issue, known as Dynamic Covalent Chemistry (DCC), is a strategy in which reactions operate under equ

94 cipline known as dynamic covalent chemistry (DCC), which is now employed widely in the construction o

95 uses solid-state dynamic covalent chemistry (DCC).

96 cirrhosis, 12% with decompensated cirrhosis (DCC), 2% with liver cancer, 2% with a history of transpl

97 carcinoma (HCC) or decompensated cirrhosis (DCC).

98 ed (subdivided into decompensated cirrhosis [DCC] and hepatocellular carcinoma [HCC]), cancer, cardio

99 Delayed cord clamping (DCC) can prevent iron deficiency during the first 6 mont

100 ly modulated by the diurnal cycle of clouds (DCC).

101 Deep convective clouds (DCCs) play a crucial role in the general circulation, en

102 Coexpressed DCC and UNC5 homologs are proposed to form a heteromeric

103 proximity of a dosage compensation complex (DCC) binding site (rex site) is neither necessary to rep

104 abditis elegans dosage compensation complex (DCC) in the regulation of DAF-2 insulin-like signaling.

105 is elegans, the dosage compensation complex (DCC) localizes to both X chromosomes in hermaphrodites a

106 e important for dosage compensation complex (DCC) recruitment are themselves not X-specific.

107 activity of the dosage compensation complex (DCC) subunit DPY-21 define a Jumonji demethylase subfami

108 dites through a dosage compensation complex (DCC) that is homologous to condensin.

109 the ten-protein dosage compensation complex (DCC) to downregulate the expression of X-linked genes on

110 The dosage compensation complex (DCC), a condensin complex, binds to both hermaphrodite X

111 ependent on the dosage compensation complex (DCC), suggesting that the transcription and replication

112 found that the dosage compensation complex (DCC), which acetylates X chromatin in males [11], become

113 the core of the dosage compensation complex (DCC), which specifically binds to and represses transcri

114 odite-specific, dosage compensation complex (DCC)-mediated, 2-fold X chromosome downregulation.

115 the electrolyte is of the dichloro complex (DCC) solution family, Mg(AlCl2BuEt)2/THF, resulting from

116 Conditional DCC knock-out mice develop balance and coordination defi

117 alleles of dpy-21, which encodes a conserved DCC component.

118 By coupling DCC with template-directed protocols, which utilise mult

119 ompound N,N'-dicyclohexylcarbodiimide (DCCD, DCC).

120 ecific for regulation of protesome-dependent DCC degradation, resulting in accumulation of DCC.

121 We detect DCC protein distributed along the axons and dendrites of

122 dechlorination products dichlorocarbanilide (DCC) and monochlorocarbanilide (r=0.99).

123 reaction of 1 with dicyclohexylcarbodiimide (DCC) only proceeds to form the cycloaddition product [(e

124 he onset of DC is linked to differentiation, DCC localization and H4K20me1 accumulation on the X chro

125 re, we discuss recent research on C. elegans DCC in the context of canonical condensin mechanisms as

126 We show that the sole C. elegans DCC/neogenin homolog UNC-40 positively modulates a BMP-l

127 ndrocytes in vivo, we selectively eliminated DCC from mature myelinating oligodendrocytes using an in

128 r to those caused by deleting genes encoding DCC subunits.

129 ctors and condensin subunits that facilitate DCC binding beyond the low level achieved without SUMOyl

130 Fluorescent DCCs, formed by this enzyme, isomerize to the respective

131 rm FCC specificity and show that fluorescent DCCs are the products of the CYP89A9 reaction.

132 r among girls (mean [SD] score, 230 [39] for DCC vs 242 [36] for ECC), out of a maximum of 300 points

133 er among boys (mean [SD] score, 229 [43] for DCC vs 224 [39] for ECC) but 12 points lower among girls

134 ors were studied in vivo in mouse models for DCC and in vitro using luciferase reporter gene assays.

135 , APP functionally acts as a co-receptor for DCC to mediate axon guidance.

136 , we show that AKAP function is required for DCC-mediated activation of PKA and phosphorylation of cy

137 eptor pair, Netrin (Net) and Frazzled (Fra) (DCC, Deleted in Colorectal Cancer, in vertebrates), is r

138 deaths were twice as common from HCC as from DCC.

139 was collected 4 times a year from 20 German DCC (620 samples) and from the homes of children and day

140 e for dystrophic calcification of the heart (DCC) or vessels after acute injury in several strains of

141 How DCC polarizes toward netrin is poorly understood.

142 However, DCCs detected in patients before the manifestation of br

143 We identified DCC mutations in four families and five sporadic individ

144 common transcriptional criteria to identify DCCs.

145 iptional profiling to unambiguously identify DCCs for subsequent in-depth analysis.

146 Importantly, DCC-2701's anti-proliferative activity was dependent on

147 In DCC, 96% of the samples were positive for DM, 95% for Ca

148 In DCC, Can f 1 and Fel d 1 loads were higher than these th

149 This effect was absent in DCC-deficient mice.

150 Exposure to dog and cat allergens in DCC often reached levels of households with pets.

151 NA) regulation of DCC and whether changes in DCC levels in the PFC lead to vulnerability to depressio

152 rex sites engage in DCC-dependent long-range interactions, with the most fre

153 cat, and dog allergens were mostly higher in DCC than in homes.

154 Allergen loads were on average higher in DCC than in homes.

155 y rex sites and become diminished or lost in DCC-defective mutants, thereby converting the topology o

156 Aerosol particles can influence DCCs by altering cloud properties, precipitation regimes

157 The switch control inhibitor DCC-2036 was similarly inactive against FLT3 AL mutation

158 Silencing of ERM protein expression inhibits DCC-PKA interaction, DCC-mediated PKA activation, and ph

159 on is triggered by the signal that initiates DCC assembly onto X.

160 ein expression inhibits DCC-PKA interaction, DCC-mediated PKA activation, and phosphorylation of Mena

161 ia their Robo receptors, and Netrin1 via its DCC attractive receptor.

162 ning and fortuitously compensating the large DCC errors over the land.

163 ed colocalization of coexpressed full-length DCC-EGFP with DCC-T-mCherry, a putative DCC dominant neg

164 e climate projections because of the limited DCC response to global warming, it may potentially incre

165 e of netrin-1 and enhances netrin-1-mediated DCC intracellular signaling, such as MAPK activation.

166 In some models, DCC appears slightly shifted over the ocean, likely as a

167 Most DCC condensin subunits also act in other condensin compl

168 17 of which, including TCF7L2, TWIST2, MSH2, DCC, EPHB1 and EPHB2 have been previously implicated in

169 Knockdown of multiple DCC components in hermaphrodite and male animals indicat

170 everal lines of evidence suggest that netrin-DCC signaling can regulate and be regulated by the cAMP-

171 Loss of Netrin/DCC signaling components causes some OR111-7-expressing

172 ht to be major signaling effectors of Netrin/DCC.

173 ctivity to DCC is required for proper netrin/DCC-mediated signaling.

174 Our findings show that Netrin1-DCC attractive signaling, but not Slit-Robo repulsive si

175 Thus, Netrin1-DCC signaling is not required to attract pre-crossing ax

176 titution of the most abundant nonfluorescent DCC (NDCC), At-NDCC-1, was determined.

177 nsile strength of the film containing 10% of DCC was increased from 69.63 to 125.31 MPa.

178 CC degradation, resulting in accumulation of DCC.

179 epressor of DCC and detected coexpression of DCC and miR-218 in pyramidal neurons of human and mouse

180 sing and reduced commissural connectivity of DCC-dependent descending pathways or by aberrant ectopic

181 hat JNK1 is important in the coordination of DCC and DSCAM in Netrin-mediated attractive signaling.

182 a synchronized hopping gait, and the cord of DCC KO mice exhibits uncoordinated left and right oscill

183 were concerned with the whole life cycle of DCC.

184 trin-1 regulates the dynamic distribution of DCC and UNC5 homologs, we applied fluorescence confocal

185 We found that exaggerated expression of DCC and reduced levels of miR-218 in the PFC are consist

186 ere the most recent advances in the field of DCC applied to protein targets, paying particular attent

187 To identify the specific function of DCC expressed by oligodendrocytes in vivo, we selectivel

188 e a conceptual overview of how the impact of DCC on supramolecular assemblies at different levels can

189 phogenesis is preceded by multimerization of DCC, activation of FAK and Src family kinases, and incre

190 reviewed are extensions of the principles of DCC to systems that are not at equilibrium and may there

191 r results demonstrate that the production of DCC splice variants controlled by NOVA has a crucial fun

192 Mass ratios of DCC-to-TCC and of methyl-triclosan (MeTCS)-to-TCS, servi

193 Plasma membrane recruitment of DCC or UNC5B was blocked by application of the netrin-1

194 sistent with netrin-1-induced recruitment of DCC-enhanced green fluorescent protein (EGFP) from intra

195 irst demonstration of microRNA regulation of DCC and suggest that, by regulating DCC, miR-218 may be

196 , we assessed microRNA (miRNA) regulation of DCC and whether changes in DCC levels in the PFC lead to

197 ed, rapid, and feed-forward up-regulation of DCC, which is believed to sustain nitric oxide (NO) prod

198 Since the first report of DCC applied to the discovery of binders for a protein, t

199 iR-218 as a posttranscriptional repressor of DCC and detected coexpression of DCC and miR-218 in pyra

200 binding to X, suggesting that SUMOylation of DCC subunits is essential for robust association with X.

201 , which interact with the C-terminal tail of DCC, is sufficient to restore netrin-1-dependent axon ou

202 The death rate from HCC was twice that of DCC.

203 that although the widely accepted theory of DCC invigoration due to aerosol's thermodynamic effect (

204 cost-effectiveness studies, and treatment of DCC accounted for 63.9% of total Medicare's HCV expendit

205 rotein 9 (TRIM9)-dependent ubiquitination of DCC blocks the interaction with and phosphorylation of F

206 ation, but TRIM9-dependent ubiquitination of DCC is reduced, which promotes an interaction with FAK a

207 ng ice particles in the stratiform/anvils of DCCs, even when thermodynamic invigoration of convection

208 eported both invigoration and suppression of DCCs by aerosols, but few were concerned with the whole

209 viral treatment for HCV patients with HCC or DCC relative to LT is an important area of clinical and

210 or the treatment of HCV patients with HCC or DCC waitlisted for LT.

211 ion, alone and in complexes with neogenin or DCC.

212 lonal antibodies against Netrin-1, Unc5b, or DCC (10 microg/mouse) were injected weekly for 4 wk (n =

213 vivo severely disrupts binding of particular DCC subunits and causes changes in X-linked gene express

214 he closely related Fyn kinases phosphorylate DCC and form a receptor-bound signaling complex leading

215 open chromatin at a small number of primary DCC recruitment sites, whose sequence and genomic contex

216 Upon netrin-1 stimulation TRIM9 promotes DCC multimerization, but TRIM9-dependent ubiquitination

217 ngth DCC-EGFP with DCC-T-mCherry, a putative DCC dominant negative that replaces the DCC intracellula

218 tion between TRIM9 and the Netrin-1 receptor DCC as well as a Netrin-1-sensitive interaction between

219 -specific knockdown of the netrin-1 receptor DCC to determine its role in adolescent dopamine axon gr

220 ession of the Netrin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resi

221 ession of the Netrin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resi

222 gous mutations in the axon guidance receptor DCC display such mirror movements, where unilateral stim

223 We report that netrin-1 and its receptor DCC are widely expressed by neurons in the developing ma

224 ade induced by netrin-1 through its receptor DCC resulted in defective arterial innervation and sympa

225 y the secreted cue Netrin-1 and its receptor DCC, described for their respective survival/death funct

226 axon guidance by acting through its receptor DCC.

227 at the direct interaction of netrin receptor DCC and DSCAM with polymerized TUBB3, a neuron-specific

228 The Netrin receptor DCC is expressed in olfactory sensory neurons around the

229 osine phosphorylation of the Netrin receptor DCC or its Drosophila ortholog, Frazzled, is not necessa

230 filopodia tips and binds the netrin receptor DCC, interacts with and ubiquitinates the barbed-end pol

231 rin-1, acting through its principal receptor DCC (deleted in colorectal cancer), serves as an axon gu

232 e induces apoptosis mediated by the receptor DCC in a p53-independent manner.

233 activation of its main attractive receptor, DCC (deleted in colorectal cancer), axons cross the vent

234 rently normal levels of the Netrin receptors DCC (deleted in colorectal carcinoma) and Neogenin.

235 rin-1 via its interaction with the receptors DCC and UNC5s.

236 hat the expression of two Netrin1 receptors- DCC and Unc5C is under direct negative regulation by Sat

237 echanism activated by netrin-1 that recruits DCC and UNC5B to the plasma membrane.

238 recruitment site on the X results in reduced DCC binding across several megabases surrounded by topol

239 ation of DCC and suggest that, by regulating DCC, miR-218 may be a switch of susceptibility versus re

240 mutations in TP53 and the metastasis related DCC gene.

241 rmore, we demonstrate that UNC5A can replace DCC on the generic receptor binding site to switch the r

242 C operate under the regime of reversibility, DCC has the added advantage of constructing robust molec

243 ine Model for End-Stage Liver Disease score (DCC analysis only).

244 In response to netrin-1 stimulation, DCC becomes a signaling platform to recruit proteins tha

245 SUMOylated DCC subunits are enriched at recruitment sites, and SUMO

246 -1 attraction by the upregulation of surface DCC through the activation of protein kinase A.

247 c abnormalities than primary tumours or than DCCs from patients with metastases.

248 We conclude that DCC expression by oligodendrocytes is required for the m

249 We demonstrate that DCC deletion results in progressive disruption of the or

250 Importantly, we discover that DCC, a guidance cue receptor, controls the extent of thi

251 Moreover, we show that DCC and PKA physically interact and that this associatio

252 from animal models, these findings show that DCC is a master regulator of midline crossing and develo

253 Interaction analysis showed that DCC was associated with an ASQ score 5 points higher amo

254 Our data suggest for the first time that DCC-2701 may be superior to HGF antagonists that are in

255 The DCC and ECC groups did not differ in iron status (mean f

256 The DCC binds to both X chromosomes of hermaphrodites to rep

257 The DCC first localizes to hermaphrodite X chromosomes at th

258 permissive for dosage compensation, and the DCC acts via a chromosome-wide mechanism to balance tran

259 n to a synchronized hopping pattern, and the DCC KO network exhibited uncoordinated left-right activi

260 In the DCC analysis, the pre-LT treatment strategy resulted in

261 ions was significantly reduced, while in the DCC KO model, the numbers of both CINi and CINe connecti

262 antify the mean, amplitude, and phase of the DCC in climate models and compare them with satellite ob

263 Artificially induced formation of the DCC in infected females, through transgenic expression o

264 or sex-specific assembly and function of the DCC on X.

265 By performing live-cell imaging of the DCC orthologue UNC-40 during anchor cell invasion in Cae

266 expressed at the growth cone, is part of the DCC receptor complex mediating netrin-1-dependent axon g

267 be reliable, the amplitude and phase of the DCC show marked inconsistencies, inducing overestimation

268 Further dissection of the DCC via RNAi revealed that other complex members phenoco

269 emales, through transgenic expression of the DCC-specific gene msl-2, resulted in mis-localization of

270 UMOylation occurs only in the context of the DCC.

271 A secondary site can ectopically recruit the DCC when additional recruitment sites are inserted eithe

272 suggesting that TORC2 directly regulates the DCC.

273 tive DCC dominant negative that replaces the DCC intracellular domain with mCherry, consistent with n

274 We found that the DCC recruiter, SDC-2, is required to maintain open chrom

275 and DCC-defective embryos, we show that the DCC remodels hermaphrodite X chromosomes into a sex-spec

276 These results imply that the DCC reshapes the topology of X chromosomes by forming ne

277 rin-1, which mediates attraction through the DCC receptor.

278 Thus, the DCC imposes a distinct higher-order structure onto X chr

279 21 suppression of rict-1, as did RNAi to the DCC effectors set-1 and set-4, which methylate histone 4

280 wever, less research has been devoted to the DCC.

281 trin-1-dependent cardioprotection, using the DCC receptor.

282 e, providing evidence that signaling via the DCC intracellular domain triggers DCC recruitment to the

283 Three DCC subunits are SUMOylated, and SUMO depletion preferen

284 genetic evidence that Netrin signals through DCC (Deleted in Colorectal Carcinoma)/UNC-40/Frazzled (F

285 ch ERM-mediated anchoring of PKA activity to DCC is required for proper netrin/DCC-mediated signaling

286 Infants were randomized to DCC (>/=180 seconds after delivery) or ECC (</=10 second

287 onse to netrin-1, p120RasGAP is recruited to DCC in growth cones and forms a multiprotein complex wit

288 sition from a MES protein-regulated state to DCC-mediated repression.

289 ng via the DCC intracellular domain triggers DCC recruitment to the plasma membrane.

290 ound it impossible to reliably identify true DCCs.

291 ught to be epithelial-specific, whereas true DCCs may express hematopoietic transcripts.

292 in-1 molecule can simultaneously bind to two DCC molecules through a DCC-specific site and through a

293 Further, we show that the Netrin1-Unc5C/DCC interaction is involved in controlling the interhemi

294 ion of growth and reproduction by DPY-21 via DCC, SET-1 and SET-4 downstream of TORC2 in C. elegans.

295 When DCC-dependent adolescent targeting events are disrupted,

296 functional netrin-1 receptor that acts with DCC to mediate guidance in vivo.

297 Compared with DCC-resistant C57BL/6 mice, a significant increase in Op

298 ion of coexpressed full-length DCC-EGFP with DCC-T-mCherry, a putative DCC dominant negative that rep

299 APP interacts with DCC in the presence of netrin-1 and enhances netrin-1-me

300 ot bind Netrin-1 directly but interacts with DCC.