ライフサイエンスコーパス: VPC

1 VPC could be safely administered to patients with NSCLC,

2 VPC events corresponded to decreases in measures of neur

3 VPC may be beneficial to reduce post-operative neuroinfl

4 VPC-13789 is a potent, selective, and orally bioavailabl

5 Among five subclones of LTKOSN.2 VPC, the vector copy number ranged from 1 to approximate

6 ried in a population of established LTKOSN.2 VPC.

7 In addition, VPCs on both sides of the axis of symmetry possess a uni

8 showed that the Wnts most strongly affecting VPC fate were expressed predominantly in the posterior,

9 degrees cell fate choice, but must act after VPC S phase to influence a 3 degrees versus 2 degrees ce

10 es that used induction both before and after VPC division and serves to maximize the probability that

11 r(s) acting through VPCact is present in all VPCs but is not modulated by the inductive signal, and t

12 at causes ectopic expression of MAB-5 in all VPCs reduces the sensitivity of all VPCs to inductive si

13 nt, VPCrep, which mediates repression in all VPCs when the inductive signal is absent, and another pr

14 5 in all VPCs reduces the sensitivity of all VPCs to inductive signal.

15 VPCs are competent to respond to LIN-3, and VPC daughters lose competence after fusing with the hypo

16 Anterior VPCs were more strongly affected by loss of Wnt function

17 several months with progenitor cells such as VPCs in developmental arrest.

18 egulation of lin-14, activity delay or block VPC division and prevent vulval differentiation.

19 Both VPC and PTFE had significantly more regression than PC.

20 n LIN-3-deficient animals, we find that both VPCs and the daughters of VPCs are competent to respond

21 LPA-mediated proliferation was blocked by VPC-32179, a competitive antagonist of LPA(1) and LPA(3)

22 ge-dependent changes in plasticity caused by VPC suggest that VPC may be adaptive.

23 t this difference in plasticity is caused by VPC using mutant lines.

24 vandetanib with paclitaxel and carboplatin (VPC) was compared with paclitaxel and carboplatin (PC) i

25 uoro-1H-Indol-3-yl)-quinoline-5-carboxamide (VPC-13789), a potent AR BF3 antagonist with markedly imp

26 tion of Wnt signaling is sufficient to cause VPCs to adopt induced fates and that a canonical Wnt pat

27 ants of the 1 degrees vulval precursor cell (VPC) establish a fixed spatial pattern of two different

28 During vulval precursor cell (VPC) fate determination, six equipotential cells uniform

29 enorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch a

30 aenorhabditis elegans vulval precursor cell (VPC) fate patterning.

31 Specification of vulval precursor cell (VPC) fates in C. elegans has served as an important sign

32 ligand is the primary vulval precursor cell (VPC) P6.p, which controls the orientation of the neighbo

33 resident coronary vascular progenitor cell (VPC) from human myocardial samples.

34 Retroviral vector producer cells (VPC) have been considered genetically stable.

35 on of helper virus in vector producer cells (VPC) in up to 2% of the population per day.

36 enorhabditis elegans vulval precursor cells (VPCs) adopt one of the final vulA, B1, B2, C, D, E, and

37 ate specification by vulval precursor cells (VPCs) and migration of the Q(L) neuroblast progeny.

38 signaling pathway in vulval precursor cells (VPCs) and thereby inducing and patterning VPCs.

39 Vulval precursor cells (VPCs) are induced to adopt vulval fates in the third lar

40 Six vulval precursor cells (VPCs) are initially equivalent but adopt different fates

41 The vulval precursor cells (VPCs) are spatially patterned by a LET-23/EGF receptor-m

42 The vulval precursor cells (VPCs) are spatially patterned during the L3 stage by the

43 f the six multipotent vulva precursor cells (VPCs) are specified by extracellular signals.

44 s of the multipotent vulval precursor cells (VPCs) are specified by intercellular signals.

45 as-MAPK signaling in vulval precursor cells (VPCs) by LIN-3/EGF from the gonad induces vulval develop

46 enorhabditis elegans vulval precursor cells (VPCs) choose among three fates (1 degrees, 2 degrees, an

47 the six multipotent vulval precursor cells (VPCs) commits to one of three fates (primary, secondary,

48 n orientation of the vulval precursor cells (VPCs) flanking the axis of symmetry.

49 duces the equipotent vulval precursor cells (VPCs) in Caenorhabditis elegans to assume the 3 -3 -2 -1

50 tterning of a row of vulval precursor cells (VPCs) in Caenorhabditis elegans: activation of the EGFR-

51 the progeny of three vulval precursor cells (VPCs) induced to divide and differentiate by a signal fr

52 The vulval precursor cells (VPCs) of Caenorhabditis elegans are polarized epithelial

53 rning of multipotent vulval precursor cells (VPCs) of Caenorhabditis elegans We have previously shown

54 uclear region of the vulval precursor cells (VPCs) of living hermaphrodites, consistent with a locali

55 enorhabditis elegans vulval precursor cells (VPCs) offer a paradigm for investigating how multipotenc

56 in the percentage of vulval precursor cells (VPCs) that adopt vulval cell fates, indicating that cell

57 enorhabditis elegans vulval precursor cells (VPCs) to adopt a spatial pattern: a central "1 degrees "

58 athways causes three vulval precursor cells (VPCs) to adopt induced cell fates.

59 mutations cause the vulval precursor cells (VPCs) to enter S phase and to divide one larval stage ea

60 enorhabditis elegans vulval precursor cells (VPCs) to respond to the inductive signal from the anchor

61 In vulva precursor cells (VPCs), a pathway of heterochronic genes acts via cki-1 t

62 the multipotency of vulval precursor cells (VPCs), allowing vulval development to reinitiate if cond

63 se to the vulva, the vulval precursor cells (VPCs), remain quiescent for two larval stages before res

64 ental origins to the vulval precursor cells (VPCs), which generate the vulva in the hermaphrodite.

65 d neurons (VCNs) and vulval precursor cells (VPCs).

66 berrant induction of vulval precursor cells (VPCs): in wild-type animals, three VPCs are induced to f

67 nstrated survival of vector-producing cells (VPCs) at 7 days but indicated limited gene transfer to t

68 LIN-12 downregulation in the central VPC is a prerequisite for the activity of the lateral si

69 of the EGFR-Ras-MAPK pathway in the central VPC promotes endocytosis and degradation of LIN-12 prote

70 evelopment known as vegetative phase change (VPC) contributes to age-dependent changes in phenotypic

71 elopment reflecting vegetative phase change (VPC) in Arabidopsis.

72 pmental transition, vegetative phase change (VPC), on morphological and photosynthetic changes.

73 a process known as vegetative phase change (VPC).

74 losures (PTFE), and 130 vein patch closures (VPC).

75 ioned using variance partition coefficients (VPCs).

76 val processes, the visual paired comparison (VPC) task measures spontaneous eye movements made toward

77 e adult monkeys to visual paired comparison (VPC) with mixed delays (10-120 sec), followed by three c

78 t increase in ventricular premature complex (VPC) runs (sertraline: 13.1%; placebo: 12.9%), QTc inter

79 ustering of ventricular premature complexes (VPCs), on entry Holter recording as a predictor of futur

80 here termed vacant, perturbed consciousness (VPC).

81 89.1%), treatment (VPC, 85.9%), and control (VPC, 95.6%) were within states, not between states.

82 ition by utilizing voltage phase-controlled (VPC) method and negative dielectrophoresis (nDEP) theory

83 e (RTK)/Ras/MAP kinase cascade that controls VPC cell fate, disrupts the temporary VPC quiescence.

84 Although the ventral premotor cortex (VPC) is known for its role in complex temporal processes

85 Valley Hall photonic crystals (VPCs) offer the potential for creating topological waveg

86 The current VPC regime induced local skin inflammatory reaction limi

87 In wild-type dauers, VPCs undergo a phenomenon reminiscent of natural direct

88 chip, all-silicon implementation of deformed VPCs that enable robust transmission along arbitrary sha

89 in the asymmetric divisions of the 1 degrees VPC daughters and the proper orientation of the outcome.

90 well as intrinsic polarity of the 1 degrees VPC daughters, is involved in the asymmetric divisions o

91 naling between the inner and outer 1 degrees VPC descendants, as well as intrinsic polarity of the 1

92 naling between the inner and outer 1 degrees VPC descendants.

93 respond to LIN-3, indicating that 2 degrees VPCs are not irreversibly committed.

94 lin-12 activity in the presumptive 2 degrees VPCs.

95 pt a spatial pattern: a central "1 degrees " VPC, in which epidermal growth factor receptor (EGFR)-mi

96 activity is low, flanked by two "2 degrees " VPCs, in which LIN-12/Notch activity is high and EGFR-MA

97 auer development, these otherwise determined VPC progeny become reprogrammed back to the multipotent,

98 st of the variability in diabetes diagnosis (VPC, 89.1%), treatment (VPC, 85.9%), and control (VPC, 9

99 tively and positively on lin-39 in different VPCs.

100 During VPC patterning, there is reciprocal modulation of endocy

101 During VPC, power spectral density and coherence at low frequen

102 ral control of LIN-45/Raf degradation during VPC patterning.

103 e EGF receptor-Ras-MAP kinase pathway during VPC specification.

104 rict control of cell-cycle quiescence during VPC development involves transcriptional induction of CK

105 Each VPC subnetwork contains 20 components.

106 ulva, but, in fog; fbf mutants, four or five VPCs are typically induced, resulting in ectopic vulvae.

107 veral consequences of dauer life history for VPC specification.

108 This study establishes a role for VPC in leaf composition and photosynthetic performance a

109 Specifically, we propose that, for VPC, because of passive (incidental) encoding, the anima

110 ene, the Scr homolog lin-39, is required for VPCs in wild-type animals to respond to activation of in

111 Fractal D was greater (VPCs less clustered) in those patients free of arrhythmi

112 d in immunosuppressed dogs, and tagged human VPCs were injected in proximity to the constricted arter

113 We previously identified VPC-00628 as a potent and selective type-II inhibitor of

114 n PC, 6/13 (46%) in PTFE, and 10/28 (36%) in VPC.

115 t a specific subset of its components act in VPC quiescence.

116 20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally red

117 m-3/mig-14, egl-18, and sem-4 play a role in VPC fate specification; (3) lin-26 is required for prope

118 ignaling in specifying HCG fates, whereas in VPC specification EGF signaling is the major inductive s

119 tion and increased accumulation of LIN-12 in VPCs in which LET-23 is not active, and to impaired down

120 ired downregulation of basolateral LET-23 in VPCs in which LIN-12 is active.

121 The pattern of LIN-12::GFP accumulation in VPCs and in the VPC lineages is dynamic and does not alw

122 in VPCs, and functions cell autonomously in VPCs.

123 , suggesting its activity is constitutive in VPCs.

124 nt biomarker of 3 cell fate, is expressed in VPCs, and functions cell autonomously in VPCs.

125 the ETS factor LIN-1 mediates repression in VPCs other than P6.p; however, loss of LIN-1 decreases e

126 l three genes is initiated or upregulated in VPCs in response to inductive signaling, suggesting that

127 actor, and lateral signaling between induced VPCs.

128 ingly, we found that all five Wnts influence VPC fate.

129 ey limitation for terahertz-scale integrated VPC-based devices has been the absence of arbitrary bend

130 er stage features rather than features of L3 VPCs in continuous development.

131 terochronic genes acts via cki-1 to maintain VPCs in G1 during the L2 stage.

132 g neurons and muscles, promotes or maintains VPC competence before vulval induction.

133 DBS modulated VPC likelihood in a frequency-specific manner.

134 R-Ras-ERK signal transduction in the nearest VPC, P6.p.

135 ignal, which activates LIN-12 in neighboring VPCs.

136 we analyzed the chemical building blocks of VPC-00628 that played a key role in achieving potency an

137 ave partially developed vulvae consisting of VPC progeny.

138 with VPC reversed the protective effects of VPC against neuroinflammation.

139 e phase: lin-12 must act prior to the end of VPC S phase to influence a 1 degrees versus 2 degrees ce

140 l for population-level adaptive evolution of VPC.

141 Overall, the features of VPC and implicated networks were similar to those of abs

142 cise primary-secondary-tertiary formation of VPC fates is controlled by a network of intercellular si

143 NA methylation in the genetic instability of VPC.

144 We propose that maintenance of VPC competence after the first cell cycle and the priori

145 er findings pertaining to the maintenance of VPC competence and quiescence in dauer larvae.

146 and contributes to the invariant pattern of VPC fates.

147 in generating the precise spatial pattern of VPC fates.

148 with levels of miR156, a major regulator of VPC in plants, and corresponding changes in wall ingrowt

149 sion of microRNA156, the master regulator of VPC, to modulate the timing of VPC in Populus tremula x

150 d miR156 expression, the master regulator of VPC.

151 ctive and lateral signaling is the relief of VPC-wide lag-2 repression in P6.p.

152 tributing to the precision and robustness of VPC fate patterning.

153 undation for further research on the role of VPC in the ecology and evolution of this economically im

154 Previous studies of VPC in poplars have relied on plants propagated in vitro

155 erning pathways does not alter the timing of VPC fate specification [4, 5].

156 regulator of VPC, to modulate the timing of VPC in Populus tremula x alba, Zea mays, and Arabidopsis

157 and environmental variation in the timing of VPC indicates the potential for population-level adaptiv

158 Furthermore, we found that the timing of VPC, and therefore the time when increased plasticity is

159 of a fractal D to describe the clustering of VPCs in time.

160 we find that both VPCs and the daughters of VPCs are competent to respond to LIN-3, and VPC daughter

161 We also demonstrate that the daughters of VPCs specified to be 2 degrees can respond to LIN-3, ind

162 0, play a major role in preventing fusion of VPCs with hyp7 in the second larval stage.

163 To establish the functional import of VPCs, a critical stenosis was created in immunosuppresse

164 nclusion, the human heart contains a pool of VPCs that can be implemented clinically to form function

165 o the multipotent, signal-sensitive state of VPCs.

166 Only group PRh behaved congruently on VPC and DNMS, exhibiting a deficit at the easiest condit

167 Group H was impaired on VPC at delays > or =60 sec but had difficulty on DNMS on

168 One VPC expresses the primary (1 degrees ) fate in response

169 lag-2 is specifically transcribed in one VPC, named P6.p, in response to activation of EGFR/Ras/M

170 s (VPCs) and thereby inducing and patterning VPCs.

171 scular niches composed of c-kit-KDR-positive VPCs were identified within the walls of coronary vessel

172 ected by loss of Wnt function than posterior VPCs, and expression from WntColon, two colonsGFP transc

173 ted if Naja sputatrix venom preconditioning (VPC) reduces surgical brain injury (SBI)-induced neuroin

174 naling plays a permissive role in preventing VPCs from fusing with hyp7 and reevaluate the roles of W

175 also plays a significant role in preventing VPCs from fusing with hyp7.

176 wth factor signaling, is required to promote VPC fate plasticity during dauer and for normal vulval p

177 ification; (3) lin-26 is required for proper VPC fate execution; and (4) pvl-6 acts during vulval mor

178 ogression was reduced for patients receiving VPC (n = 56) versus PC (n = 52; hazard ratio = 0.76, one

179 with the PC control arm, patients receiving VPC had longer PFS, meeting the prespecified study end p

180 icantly different between patients receiving VPC or PC.

181 er control of the genetic program regulating VPC.

182 Pretreatment with an antagonist of S1P1, VPC 44116, prevented receptor internalization and degrad

183 postdauer third stage larvae, with the same VPC spatial-patterning events as in continuously develop

184 the orientation of the neighboring secondary VPC P7.p by signaling through the sex myoblasts (SMs), a

185 omized patient group (i.e., those who showed VPC suppression during initial antiarrhythmic drug titra

186 By examining the response of single VPCs to controlled doses of inductive signal in wild-typ

187 nal LIN-1::GFP protein is similar in all six VPCs before and after vulval induction, suggesting that

188 IN-12::GFP is expressed initially in all six VPCs, but appears to be reduced specifically in P6.p as

189 erconnected subnetworks corresponding to six VPCs.

190 subdomain (VPN) and a C-terminal subdomain (VPC).

191 tested on the visual paired comparison task (VPC), a test of recognition memory.

192 ntrols VPC cell fate, disrupts the temporary VPC quiescence.

193 We demonstrate that VPC-13789 suppresses AR-mediated transcription, chromati

194 This study demonstrates that VPC stimulates core promoters that are either independen

195 Our results indicate that VPC fate determination by intercellular signals is rever

196 We observed that VPC reduced brain edema and improved neurological functi

197 These results led us to postulate that VPC and DNMS, as previously administered to monkeys, wer

198 ges in plasticity caused by VPC suggest that VPC may be adaptive.

199 Our findings suggest that VPC reduces neuroinflammation and improves outcomes afte

200 Our analysis indicates that VPCs have L2-like and unique dauer stage features rather

201 odel the biological network that governs the VPC primary-secondary-tertiary pattern formation process

202 In this study, we investigated how the VPC processes temporal information during a time interva

203 Downregulation of apical LIN-12 in the VPC in which LET-23 is active is not affected.

204 LIN-12::GFP accumulation in VPCs and in the VPC lineages is dynamic and does not always reflect lin-

205 ulatory module that drives expression in the VPC P6.p in a Ras-dependent manner.

206 3 hypomorphic mutation, the daughters of the VPC closest to the anchor cell (AC), P6.p, are induced b

207 l repeat occurred in approximately 2% of the VPC population per day and correlated closely with inact

208 ts with fornix lesions performed well on the VPC task but were impaired on a spatial task (spontaneou

209 s a reduction of LIN-12 protein in P6.p, the VPC believed to be the source of the lateral signal.

210 In group TH/TF, the VPC impairment emerged earlier (30 sec); yet, once the n

211 This contextual shift underscores the VPC's adaptive role in interval estimation and highlight

212 The VPCs are born in the first larval stage.

213 The VPCs divide in the third larval stage (L3) of the wild t

214 The VPCs were connected by gap junctions to ECs, SMCs, and f

215 nt ligands act over a distance to affect the VPCs.

216 also acts in cell fate specification by the VPCs, via regulation of the Hox gene lin-39.

217 theless, the overall logic is similar in the VPCs and the HCG: EGF and/or WNT induce a 1 degree linea

218 d chromatin remodeling activities act in the VPCs to antagonize Ras activation through effects on pro

219 he major hypodermal syncytium and not in the VPCs to inhibit vulval fates.

220 ve regulator of lin-12/Notch activity in the VPCs, and found that SEL-2 is the homolog of two closely

221 rs, lin-17, mom-5 and mig-1, function in the VPCs.

222 a negative regulator of Wnt signaling in the VPCs.

223 BF and FOG-1 in the germ line but not in the VPCs.

224 can activate EGFR-Ras-MAPK signaling in the VPCs.

225 main and occurs at the apical surface of the VPCs.

226 n accumulates in the plasma membranes of the VPCs.

227 are required for generation/survival of the VPCs; (2) bar-1, mom-3/mig-14, egl-18, and sem-4 play a

228 and identity of the Wnt ligand acting on the VPCs are unknown.

229 essed at the axis of symmetry and orient the VPCs toward the center.

230 nd to the inductive signal requires that the VPCs do not fuse to the major hypodermal syncytium, hyp7

231 ates by regulating a signal from hyp7 to the VPCs or the physiological state of hyp7.

232 GF ligand may be the germ-line signal to the VPCs: the fog; fbf Muv phenotype depends on LIN-3 activi

233 or cells (VPCs): in wild-type animals, three VPCs are induced to form a single vulva, but, in fog; fb

234 The remaining three VPCs each adopt the non-vulval tertiary (3 degrees ) fat

235 duced phenotype, in which greater than three VPCs adopt induced cell fates.

236 Variation in leaf traits due to VPC are likely to provide distinct benefits under specif

237 Similar to VPC fate specification, each HCG cell adopts one of thre

238 arbitrary bend interconnects, as traditional VPC-designs restricted to principal lattice axes (i.e.,

239 diabetes diagnosis (VPC, 89.1%), treatment (VPC, 85.9%), and control (VPC, 95.6%) were within states

240 log mab-5, is expressed in the posterior two VPCs.

241 The two VPCs flanking the 1 degrees cell each express secondary

242 ndomly assigned 2:1:1 to receive vandetanib, VPC, or PC.

243 In vitro, VPCs were self-renewing and clonogenic and differentiate

244 ne-sided P = .098); median PFS was 24 weeks (VPC) and 23 weeks (PC).

245 when VPCs complete G1 and also controls when VPCs acquire the competence to respond to the intercellu

246 udes lin-4, lin-14, and lin-28 controls when VPCs complete G1 and also controls when VPCs acquire the

247 nhibitor or Zileuton, a 5-LOX inhibitor with VPC reversed the protective effects of VPC against neuro

248 to detect a reduced risk of progression with VPC versus PC (hazard ratio = 0.70; one-sided P < .2) an

249 peri-resection brain tissue was reduced with VPC.