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 may be beneficial to reduce post-operative neuroinfl

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

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

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

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

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

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

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

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

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

12 5 in all VPCs reduces the sensitivity of all VPCs to inductive signal.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

70 The current VPC regime induced local skin inflammatory reaction limi

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

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

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

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

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

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

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

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

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

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

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

82 During VPC patterning, there is reciprocal modulation of endocy

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

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

85 Each VPC subnetwork contains 20 components.

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

87 veral consequences of dauer life history for VPC specification.

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

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

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

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

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

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

94 20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally red

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

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

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

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

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

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

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

102 actor, and lateral signaling between induced VPCs.

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

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

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

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

107 ave partially developed vulvae consisting of VPC progeny.

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

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

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

111 NA methylation in the genetic instability of VPC.

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

113 and contributes to the invariant pattern of VPC fates.

114 in generating the precise spatial pattern of VPC fates.

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

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

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

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

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

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

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

122 0, play a major role in preventing fusion of VPCs with hyp7 in the second larval stage.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 icantly different between patients receiving VPC or PC.

141 er control of the genetic program regulating VPC.

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

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

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

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

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

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

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

149 erconnected subnetworks corresponding to six VPCs.

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

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

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

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

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

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

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

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

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

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

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

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

162 3 hypomorphic mutation, the daughters of the VPC closest to the anchor cell (AC), P6.p, are induced b

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

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

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

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

167 The VPCs are born in the first larval stage.

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

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

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

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

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

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

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

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

176 a negative regulator of Wnt signaling in the VPCs.

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

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

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

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

181 n accumulates in the plasma membranes of the VPCs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 peri-resection brain tissue was reduced with VPC.