ライフサイエンスコーパス: DCC

1 DCC >=3, postoperative mortality, and POPF grade B-C wer

2 DCC mutations result in variable dominant phenotypes wit

3 DCC receptor signaling in dopamine neurons is a molecula

4 DCC serves as a clear paradigm for addressing how conden

5 DCC SUMOylation is triggered by the signal that initiate

6 DCC(+/-) mutation carriers without mirror movements migh

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

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

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

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

11 The netrin-1/DCC ligand/receptor pair has key roles in central nervou

12 ing us to investigate a role of the netrin-1/DCC pair in adult nigral neuron fate.

13 dicating an association between the Netrin-1/DCC pathway and major depressive disorder.

14 part from the dysregulation of the Netrin-1/DCC pathway by a mechanism that involves microRNA-218.

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

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

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

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

19 The participants (n = 52) included 13 DCC(+/-) mutation carriers with mirror movements, 7 DCC(

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

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

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

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

24 In C. elegans the netrin receptor UNC-40/DCC controls the growth of dendritic-like muscle cell ex

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

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

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

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

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

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

31 ) mutation carriers with mirror movements, 7 DCC(+/-) mutation carriers without mirror movements, 13

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

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

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

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

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

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

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

39 Although expression of netrin-1 and DCC is maintained in the adult brain, little is known ab

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

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

42 95% confidence interval [CI], 0.15-0.52) and DCC (HR, 0.38; 95% CI, 0.26-0.56).

43 nce of HCC (HR, 0.43; 95% CI, 0.26-0.71) and DCC (HR, 0.42; 95% CI, 0.30-0.58) in patients with nonci

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

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

46 with a decreased risk of developing HCC and DCC, resulting in decreased health care costs, especiall

47 ed to compare the risk of developing HCC and DCC, stratified by cirrhosis status.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 ic coiled-coil and a C-terminal antiparallel DCC.

64 This included genes such as DCC, which encodes the netrin-1 receptor and has an impo

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

66 few examples using disulfide-exchange-based DCC are reported for nucleic acid targets.

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

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

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

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

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

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

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

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

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

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

77 racts with the deleted in colorectal cancer (DCC) receptor, other receptors, and co-factors for signa

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

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

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

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

82 Deleted in colorectal cancer (DCC), the receptor for the multifunctional cue netrin-1,

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

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

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

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

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

88 this context, so-called internally catalysed DCC platforms have started to receive more interest in t

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

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

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

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

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

94 Dynamic combinatorial chemistry (DCC) has emerged as a promising strategy for template-dr

95 ng a biased dynamic combinatorial chemistry (DCC) library to generate a receptor mimicking the 5-side

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

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

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

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

100 ect of so-called dynamic covalent chemistry (DCC).

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

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

103 eal-world clinical (decompensated cirrhosis [DCC] and hepatocellular carcinoma [HCC]) and economic ou

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

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

106 tive bonding groups, as is done in classical DCC, is often not feasible or desirable, as it can damag

107 3 according to Dindo-Clavien Classification (DCC).

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

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

110 tein with an N-terminal dimeric coiled-coil (DCC), assembles into a hexameric array at the budding ye

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

112 specific lethal dosage compensation complex (DCC) exclusively to the male X chromosome provides an ex

113 omponent of the dosage compensation complex (DCC) in Caenorhabditis elegans and demonstrate that loop

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

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

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

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

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

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

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

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

122 via a dosage-compensation condensin complex (DCC) that binds hermaphrodite Xs and establishes megabas

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

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

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

126 ith mirror movements would exhibit decreased DCC mRNA expression, a functional ipsilateral corticospi

127 x site is necessary and sufficient to define DCC-dependent boundary locations.

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

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

130 of using internal catalysis within different DCC applications, ranging from small molecules to dynami

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

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

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

134 e initial portal release in 2013, the ENCODE DCC has updated the portal to make ENCODE data more find

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

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

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

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

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

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

141 of the axon guidance molecule receptor gene, DCC, present an opportunity to investigate, in living hu

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

143 We hypothesized that haploinsufficient DCC(+/-) mutation carriers with mirror movements would e

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

145 How DCC polarizes toward netrin is poorly understood.

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

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

148 common transcriptional criteria to identify DCCs.

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

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

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

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

153 This effect was absent in DCC-deficient mice.

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

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

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

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

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

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

160 separation of DNA nanotemplates for reuse in DCC reactions.

161 n the adult substantia nigra of mice induces DCC cleavage and a significant loss of dopamine neurons,

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

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

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

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

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

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

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

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

170 DCC is detected at GABA synapses in mammals, DCC might also tune inhibitory neurotransmission in the

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

172 Most DCC condensin subunits also act in other condensin compl

173 e domain architecture was disrupted but most DCC binding remained.

174 17 of which, including TCF7L2, TWIST2, MSH2, DCC, EPHB1 and EPHB2 have been previously implicated in

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

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

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

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

179 decades for the design and synthesis of new DCC-based polymer materials.

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

181 CC degradation, resulting in accumulation of DCC.

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

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

184 are neither the cause nor the consequence of DCC-mediated gene repression.

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

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

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

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

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

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

191 Implementation of DCC in polymers yields materials with unique combination

192 The implementation of DCC using DNA nanotemplates enables efficient identifica

193 In particular, the incorporation of DCC in polymer materials aims to find a balance between

194 MSL2 mutant resulted in an increased loss of DCC recruitment to the X chromosome.

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

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

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

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

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

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

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

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

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

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

205 Genetic silencing of DCC prodeath activity in a BRAF(V600E) mouse model incre

206 CXC domain of MSL2 binds to genomic sites of DCC recruitment in vitro Another conserved domain of MSL

207 s (8rexDelta) recapitulated TAD structure of DCC mutants, permitting analysis when chromosome-wide do

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

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

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

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

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

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

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

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

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

217 rticospinal effects and decreased peripheral DCC mRNA appeared driven by the mirror movement phenotyp

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

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

220 nce and mice lacking the Myo10 cargo protein DCC (deleted in colorectal cancer) have severe commissur

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

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

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

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

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

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

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

228 Netrin-1 and its receptor DCC regulate melanoma progression, suggesting therapeuti

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

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

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

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

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

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

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

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

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

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

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

240 irror movements were associated with reduced DCC mRNA expression, increased ipsilateral TMS-induced m

241 Reexpressing DCC in human melanoma cell lines promoted tumor cell dea

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

243 mutations in TP53 and the metastasis related DCC gene.

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

245 Ripretinib (DCC-2618) was designed to inhibit the full spectrum of m

246 as the switch-control inhibitor ripretinib (DCC-2618) and the D816V-selective inhibitor avapritinib

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

248 Since DCC is detected at GABA synapses in mammals, DCC might a

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

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

251 -1 attraction by the upregulation of surface DCC through the activation of protein kinase A.

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

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

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

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

256 Recent genomic data highlighted that DCC is the third most frequently mutated gene in melanom

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

258 We show that DCC binding at high-occupancy sites (rex sites) defines

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

260 multiway ligation events, we then show that DCC loops form a network of strong interactions that may

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

262 mice with melanoma, further supporting that DCC is a melanoma tumor suppressor.

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

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

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

266 The DCC(+/-) mutation, irrespective of mirror movements, was

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

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

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

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

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

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

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

274 ly only modestly affected recruitment of the DCC to the X chromosome in males.

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

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

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

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

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

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

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

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

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

284 21 suppression of rict-1, as did RNAi to the DCC effectors set-1 and set-4, which methylate histone 4

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

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

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

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

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

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

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

292 ound it impossible to reliably identify true DCCs.

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

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

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

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

297 When DCC-dependent adolescent targeting events are disrupted,

298 melanoma; we therefore investigated whether DCC could act as a melanoma tumor suppressor.

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

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

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