ライフサイエンスコーパス: GCP

1 GCP II activity was assayed in astrocyte cultures (4.4 p

2 GCP II also hydrolyzes gamma-glutamyl bonds in folylpoly

3 GCP II inhibitory assay revealed that (S)-2 is 40-fold m

4 GCP II is an enzyme that metabolizes N-acetyl-aspartyl-g

5 GCP-2 is induced in MG-63, but not A549 cells by TNF-alp

6 GCPs 2-6 constitute a family of homologous proteins.

7 GCPs cultured at 38 degrees C without ABA dedifferentiat

8 GCPs cultured similarly but at 38 degrees C and with 0.1

9 GCPs dedifferentiating at 32 degrees C require both 1-na

10 GCPs of tree tobacco can be isolated in sufficient numbe

11 ) cleaves granulocyte chemotactic protein 2 (GCP-2) and growth-related oncogene alpha (GROalpha), two

12 P-2), and granulocyte chemotactic protein 2 (GCP-2) but did not cleave interleukin-8.

13 for human granulocyte chemotactic protein-2 (GCP-2) as well as previously described CXC chemokine gen

14 emoattractants including Groalpha/KC, MIP-2, GCP-2, and MIP-1alpha, was observed in allografts retrie

15 eralized chronic periodontitis (GCP); and 4) GCP + AMI.

16 pressed in Purkinje cells and functions as a GCP mitogen in vitro, it is possible that Shh influences

17 eceived at least one dose of study drug at a GCP-compliant site and were included in the modified int

18 eceived at least one dose of study drug at a GCP-compliant site and were included in the modified int

19 elated well with the inhibitory potency in a GCP II assay.

20 Northern blots probed with a GCP II cDNA detected mRNAs exclusively in activity-posit

21 clinical trials in compliance with accepted GCP standards, supplemental attributes of an exemplary r

22 PPA), a previously discovered, orally active GCP II inhibitor.

23 aryotes gammaTuSCs associate with additional GCPs (4, 5, and 6) to form the core of the so-called gam

24 tency of these thiol-based compounds against GCP II was found to be dependent on the number of methyl

25 Our results suggest that all GCPs are incorporated into the helix via lateral interac

26 n levels were significantly elevated in AMI, GCP, and GCP + AMI groups compared to the control group.

27 in concentration to BMI was observed in AMI, GCP, and GCP + AMI groups.

28 tative CXC chemokines, GRO-gamma, NAP-2, and GCP-2, to attract and activate neutrophils.

29 ts were harvested and assayed for ENA-78 and GCP-2 by enzyme-linked immunosorbent assay.

30 lls demonstrated up-regulation of ENA-78 and GCP-2 chemokine mRNA.

31 ady state levels of intracellular ENA-78 and GCP-2 pre-mRNA and mRNA by the reverse transcription-pol

32 a more than 300-fold increase in ENA-78 and GCP-2 protein production.

33 stimulated a 10-fold increase in ENA-78 and GCP-2 RNA synthesis and a more than 300-fold increase in

34 PLRA methods and shortest for the CIGTS and GCP methods.

35 were significantly elevated in AMI, GCP, and GCP + AMI groups compared to the control group.

36 tration to BMI was observed in AMI, GCP, and GCP + AMI groups.

37 d generalized chronic periodontitis (LCP and GCP).

38 AgP and significantly different from LCP and GCP, but not from LAgP.

39 mal expression levels of mGluR2, mGluR3, and GCP II were determined for 10 regions of the postmortem

40 ortant step in medulloblastoma formation, as GCPs, remaining longer in the EGL proliferative niche, m

41 icial sublayers; and (3) whereas the average GCP proliferation in the external granular layer is prog

42 NAA]) and a cytokinin (6-benzylaminopurine), GCP expand, regenerate cell walls, dedifferentiate, and

43 oorganisms, we have studied the bifunctional GCP gene expression under fasting conditions and in cert

44 entration was associated with increased BMI, GCP, and AMI and may serve as a risk marker for these co

45 15 bp of the promoter 5' to a 225 bp GCP II fragment were essential for luciferase expression

46 tion frequency, positioning, and geometry by GCP-WD allows plant cells to build alternative cortical

47 e show that heat inhibits NO accumulation by GCPs and that L-N(G)-monomethyl arginine, an inhibitor o

48 At 38 degrees C, GCP acquire thermotolerance within 24 h, but their expan

49 d) and cytokinin (6-benzylaminopurine) cause GCPs to expand 20- to 30-fold, regenerate cell walls, de

50 f cerebellar granule neuron precursor cells (GCPs), located in the external granular layer (EGL) of t

51 Medulloblastomas arising from cerebellar GCPs are frequently driven by Shh pathway-activating mut

52 identified two isolated CBLs as H. contortus GCP-7 (33 kDa) and AC-4 (37 kDa).

53 In contrast, GCP-2 synthesis is only inducible in IL-1alpha-stimulate

54 is still unclear how GCP4-GCP6 (the non-core GCPs) may be involved in acentrosomal MT nucleation in p

55 eukin-1beta (IL-1beta), the chemokine CXCL6 (GCP-2), and the protease inhibitor elafin (PI3).

56 O-alpha, CXCL2/GRO-beta, CXCL5/ENA-78, CXCL6/GCP-2, CXCL7/NAP-2, and CXCL8/IL-8) were determined in b

57 h the N- and C-terminal domains of different GCPs are swapped, we show that the N-terminal domains de

58 hesis without significantly enhancing either GCP-2 gene expression or protein secretion.

59 stimulating a significant increase in either GCP-2 RNA synthesis or protein production.

60 iving Shh induced proliferation of embryonic GCPs.

61 incorporate value-added attributes to exceed GCP compliance.

62 II cDNA into PC3 cells, which do not express GCP II endogenously.

63 In the absence of beta1 expression, GCPs lose contact with laminin in the meningeal basement

64 fidence interval 0.76 to 0.87, P <0.001) for GCP.

65 urther, we discovered an unexpected role for GCP-WD in determining the geometry of microtubule-depend

66 nd folates are good candidate substrates for GCP II in vivo.

67 Pathogen carriers suffered mostly from GCP and seldom from LCP.

68 bulin, which forms a complex with GCP2-GCP6 (GCP for gamma -Tubulin Complex Protein).

69 al peptide (CRP) with the sequence GCP*(GPP*)GCP*G (single letter amino acid code: P* = hydroxyprolin

70 gher temperatures (34 degrees C or greater), GCPs expand only 5- to 6-fold; they do not regenerate wa

71 ate the molecular properties of cloned human GCP II (hGCP II), we analyzed the NAAG-hydrolytic activi

72 of this receptor by mouse GCP-2/CXCL6, human GCP-2, and IL-8/CXCL8 by binding, stimulation of GTPgamm

73 ssignment of these putative ligands in human GCP II.

74 90 and 761 bp portions of 5' region of human GCP II gene were able to drive the luciferase reporter g

75 nscriptional mechanisms regulating the human GCP II gene, a 3460 bp DNA fragment comprised of the pro

76 SVG cells, the proximal 240 bp of the human GCP II promoter (232 bp of the 5' UTR and 8 bp of 5' unt

77 LIX is no more closely related to human GCP-2 than to human ENA-78 and is more distant from both

78 evaluation system is set up according to ICH/GCP, World Medical Association Declaration of Helsinki,

79 Glutamate carboxypeptidase II (GCP II) catalyzes the extracellular hydrolysis of the ne

80 The enzyme glutamate carboxypeptidase II (GCP II) has been cloned from rat brain and human prostat

81 d to quantify glutamate carboxypeptidase II (GCP II) in order to explore a role for the metabotropic

82 epresentative glutamate carboxypeptidase II (GCP II) inhibitors, 2-(hydroxypentafluorophenylmethyl-ph

83 expression of glutamate carboxypeptidase II (GCP II) is reduced in selective brain regions in schizop

84 alytic enzyme glutamate carboxypeptidase II (GCP II) rapidly hydrolyzes NAAG into NAA and glutamate.

85 ith exogenous glutamate carboxypeptidase II (GCP II) using high-performance liquid chromatography (HP

86 yzing enzyme, glutamate carboxypeptidase II (GCP II), activity was normal in the knockout mouse brain

87 es to inhibit glutamate carboxypeptidase II (GCP II).

88 inhibitors of glutamate carboxypeptidase II (GCP II, EC 3.4.17.21).

89 Finally, we showed that the defect in GCP proliferation was similar in the cerebellar vermis a

90 Finally, pattern differences in GCP II gene promoter expression in SVG and LNCaP cells s

91 were statistically significantly elevated in GCP + AMI and AMI groups.

92 resses induction of auxin-regulated genes in GCP.

93 le of each of the two zinc-binding groups in GCP II inhibition.

94 Findings revealed a significant increase in GCP II protein and a reduction in mGluR3 protein in the

95 Atoh1 expression during a critical phase in GCP differentiation in which malignant transformation ma

96 ous evidence demonstrating their presence in GCP II-expressing tissues, these data suggest that both

97 and substrate ligands have been proposed in GCP II based on the amino acid sequence alignment to the

98 at Shp2 is not cell autonomously required in GCP.

99 parable to those in LAgP, but higher than in GCP or LCP for several species.

100 directly induced by Shh pathway activity in GCPs, murine medulloblastomas, and human medulloblastoma

101 ns act at least in part cell autonomously in GCPs to regulate their proliferation.

102 Hedgehog promotes polyamine biosynthesis in GCPs by engaging a non-canonical axis leading to the tra

103 reduced foliation at birth and a decrease in GCPs.

104 model in which beta1 integrin expression in GCPs is required to recruit a laminin-Shh complex to the

105 is dependent on beta1 integrin expression in GCPs.

106 Increased GCP II expression and low mGluR3 expression in the dorso

107 expression of Sna1 was sufficient to induce GCPs and medulloblastoma cell proliferation in the absen

108 uture clinical trials to assess drug-induced GCP II inhibition in biological matrices.

109 have shown that sonic hedgehog (Shh)-induced GCP proliferation is potentiated by the integrin ligand

110 hotic treatment in rodents did not influence GCP II or mGluR3 levels.

111 In contrast, both enantiomers of 3 inhibited GCP II with nearly equal potency.

112 Retroviral transduction of N-myc into GCPs induces expression of cyclin D1, E2F1, and E2F2, an

113 nitiator for the "TATA and CAAT" box lacking GCP II gene in the SVG cells.

114 ion of mCXCR1 and its proposed major ligand, GCP-2, positively correlated with paw swelling in murine

115 gree of Fu/HC polymorphism, largely limiting GCP to sibling offspring.

116 factor known to play a role in Shh-mediated GCP proliferation and medulloblastoma formation.

117 is problem, a group combined P-value method (GCP) is proposed, where the P-values are divided into mu

118 ominant engagement of this receptor by mouse GCP-2/CXCL6, human GCP-2, and IL-8/CXCL8 by binding, sti

119 the proposal, by others, that LIX is murine GCP-2.

120 0 repeat protein related to the animal NEDD1/GCP-WD protein, which interacts with the gamma-tubulin c

121 y in mammalian oocytes, and identified NEDD1/GCP-WD as a key regulator.

122 plex (gamma-TuRC) recruitment protein, Nedd1/GCP-WD, at the previously uncharacterized S460 residue i

123 In the absence of p75(NTR), GCPs continue to proliferate beyond their normal period,

124 escues the defective migration of Tis21-null GCPs and, remarkably, reduces the area of hyperplastic l

125 Cxcl3 is downregulated in Tis21-null GCPs of EGL and lesions; addition of Cxcl3 to cerebellar

126 Addition of GCP II inhibitors beta-NAAG, quisqualic acid and 2-(phos

127 cell line, constructs with 511 and 411 bp of GCP II gene fragments yielded highest transcriptional ac

128 Cleavage of GCP-2 and GROalpha by SpyCEP abrogated their abilities t

129 orrelates with a decrease in the duration of GCP proliferation.

130 lex, which may explain the low efficiency of GCP transfer.

131 In the absence of BG, inward invagination of GCP persists but is uncoupled from the folding of the Pu

132 tine nucleus) contained pronounced levels of GCP II message.

133 later stages also expressed higher levels of GCP mRNA and protein when they were shifted from normal

134 the cell specificity and regional pattern of GCP II expression in the rat nervous system by using Nor

135 rebellar development, we linked the rates of GCP proliferation to the different levels and localizati

136 hat fused B. schlosseri have higher rates of GCP than unfused colonies additionally provides a ration

137 The predicted amino acid sequence of GCP II displays similarities to aminopeptidases from Str

138 The early cohort of GCPs, despite being deficient for SMAD4, is still genera

139 rees C +/- ABA prevents dedifferentiation of GCPs by blocking cell cycle reentry at G1/S.

140 Finally, FGF promotes differentiation of GCPs in vitro and in vivo and halts proliferation of tum

141 proliferation and trigger differentiation of GCPs; its expression decreases in human medulloblastomas

142 ment proceeds, there is a rapid expansion of GCPs shortly before clonally related GCs exit the cell c

143 al domains define the functional identity of GCPs, whereas the C-terminal domains are exchangeable.

144 ults suggest that Tis21 induces migration of GCPs through Cxcl3, which may represent a novel target f

145 Previous structural analysis and modeling of GCPs suggest that all family members can potentially int

146 required to generate a sufficient number of GCPs for proper lobe growth.

147 but does lead to prolonged proliferation of GCPs and an increase in the overall size of the cerebell

148 Second, we found that the proliferation of GCPs and their response to SHH were severely impaired in

149 eletion does not affect the proliferation of GCPs but inhibits their differentiation and, chiefly, th

150 Proliferation of GCPs is regulated by the secreted signaling molecule Son

151 nisms by which Shh controls proliferation of GCPs remain inadequately understood.

152 ruit a laminin-Shh complex to the surface of GCPs and to subsequently modulate the activity of signal

153 the process of neoplastic transformation of GCPs, we generated a new medulloblastoma model by crossi

154 Treatment of GCPs with Shh prevents differentiation and induces a pot

155 ASPA deficiency does not affect the NAAG or GCP II level in the knockout mouse brain, if documented

156 y of interindividual germ cell "parasitism" (GCP) to histocompatible kin.

157 ents with generalized chronic periodontitis (GCP) and compare these results with serum levels of pati

158 : 84 with generalized chronic periodontitis (GCP), 65 with localized chronic periodontitis (LCP), and

159 ) AMI; 3) generalized chronic periodontitis (GCP); and 4) GCP + AMI.

160 Glucose-1,2-cyclic-phosphate (GCP) was proposed to be formed from UDP-Glc breakdown an

161 Harmonisation (ICH) Good Clinical Practice (GCP) guidelines, the accepted international ethical and

162 Helsinki (1989) and Good Clinical Practice (GCP).

163 site compliant with Good Clinical Practice [GCP]).

164 entre compliant with Good Clinical Practice [GCP]).

165 ere conducted using Good Clinical Practices (GCP) and in accordance with the ethical principles that

166 ing expansion of the granule cell precursor (GCP) pool.

167 s in the brain, and granule cell precursors (GCPs) are a common target of transformation in the pedia

168 e transformation of granule cell precursors (GCPs) in the developing cerebellum, but little is known

169 he proliferation of granule cell precursors (GCPs) is controlled by the secreted signaling molecule S

170 at proliferation of granule cell precursors (GCPs) is severely affected in the developing cerebellum

171 how that cerebellar granule cell precursors (GCPs) migrate along a gradient of brain-derived neurotro

172 t to arise from the granule cell precursors (GCPs) of the cerebellum.

173 s, we show that (1) granule cell precursors (GCPs) undergo predominantly symmetric division during po

174 ation of cerebellar granule cell precursors (GCPs), and its aberrant activation is a leading cause of

175 nd FGF signaling in granule cell precursors (GCPs), which are the most abundant neural progenitors in

176 reased apoptosis in granule cell precursors (GCPs).

177 us proliferation of granule cell precursors (GCPs).

178 tes the division of granule cell precursors (GCPs).

179 the late cohort of granule cell precursors (GCPs).

180 plastic EGL lesions, formed by preneoplastic GCPs.

181 ia based on the Glaucoma Change Probability (GCP) analysis, and two criteria based on point-wise line

182 output from the Glaucoma Change Probability (GCP) program of the Humphrey Field Analyzer (San Leandro

183 mental pathways for granule cell progenitor (GCP) neurogenesis.

184 transformation of granule cell progenitors (GCP) in the developing cerebellum.

185 Cerebellar granule cell progenitors (GCP) proliferate extensively in the external granule lay

186 migration and how granule cell progenitors (GCP) regulate cerebellar foliation.

187 tion of cerebellar granule cell progenitors (GCPs) in response to Sonic hedgehog (SHH) is severely re

188 e proliferation of granule cell progenitors (GCPs) in the EGL was also reduced, leading to reduced gr

189 R)) is highly expressed in the proliferating GCPs, but is downregulated once the cells leave the cell

190 rebellum, but is restricted to proliferating GCPs and Bergmann glia.

191 The proposed GCP method is applied to data from the Genetic Analysis

192 amma-tubulin, gamma-tubulin complex protein (GCP)2 and GCP3, whereas animals contain the gamma-tubuli

193 ring complex, gamma-tubulin complex protein (GCP)6, as a keratin partner in yeast two-hybrid assays.

194 nits and the gamma-tubulin complex proteins (GCPs) that exhibit biased localization toward MT minus e

195 d associated gamma-tubulin complex proteins (GCPs).

196 -tubulin and gamma-tubulin complex proteins [GCPs] 2, 3, and 4) and led to the identification of two

197 Cultured guard cell protoplasts (GCP) of tree tobacco (Nicotiana glauca) comprise a novel

198 ultured tree tobacco guard cell protoplasts (GCPs) are useful for studying the effects of heat stress

199 When guard cell protoplasts (GCPs) of tree tobacco [Nicotiana glauca (Graham)] are cu

200 bon generates graphite-conjugated pyrazines (GCPs) that are active for oxygen reduction electrocataly

201 ng Shh function in vivo dramatically reduces GCP proliferation.

202 tional mediators, the Gli proteins, regulate GCP proliferation in vivo, and tested whether they influ

203 edgehog (Shh), but the factors that regulate GCP differentiation remain a mystery.

204 Although pre-neoplastic cells resemble GCPs and tumor cells in many respects, they have a disti

205 iple-helical peptide (CRP) with the sequence GCP*(GPP*)GCP*G (single letter amino acid code: P* = hyd

206 eotides 5' of the transcription start sites, GCP-2 and ENA-78 show cell-specific differences in regul

207 240 bp may be important for tissue-specific GCP II expression.

208 ation of TrkB, the BDNF receptor, stimulates GCPs to secrete BDNF, thereby amplifying the ambient gra

209 he product, and they also showed synchronous GCP accumulation.

210 llular matrix protein vitronectin might tell GCPs when to stop dividing and begin differentiation.

211 ISHH results show that GCP II is expressed by virtually all astrocytes, by Berg

212 and total nucleation frequency, showing that GCP-WD controls gamma-TuRC positioning and function in t

213 ssignment of these residues and suggest that GCP II has a three-dimensional structure similar to othe

214 The data of the present study suggest that GCP II is expressed in the adult rat nervous system excl

215 The results suggest that GCP-2 gene expression is more tightly regulated in disea

216 In this study, we show that GCPs cultured for 12 to 24 h at 38 degrees C accumulate

217 The GCP expression appeared to be regulated primarily at the

218 The GCP methods determined progression earliest; however, th

219 The GCP mRNA and protein levels were elevated in early larva

220 The GCP program based on pattern deviation probability maps

221 The GCP-2 gene encodes a propeptide of 114 amino acid residu

222 Although the expression of both the GCP gene and lin-14 peaks at about the same time during

223 ssociated with rheumatoid arthritis, but the GCP provides smaller P-value.

224 f an exemplary research site that exceed the GCP criteria are also described.

225 and PI, GI, PD, and AL were also seen in the GCP group.

226 In contrast, removing Ptpn11 in the GCP lineage by Atoh1-cre has no effect on cerebellar dev

227 the entire cerebellum or selectively in the GCP lineage.

228 The AGIS, CIGTS, and one of the GCP and PLRA methods were relatively resistant to high v

229 that there was no significant change of the GCP at both mRNA and protein levels in the heterochronic

230 re induced by fasting, the regulation of the GCP gene is independent of the heterochronic lin-14 cont

231 Inhibition of the GCP II enzyme with NAAG peptidase inhibitors reduces the

232 Both coding and noncoding portions of the GCP-2 gene have very high nucleotide similarity to ENA-7

233 a long interspersed DNA-1 sequence 5' of the GCP-2 gene.

234 Isolation of the GCP-7 band by each peptide was preferentially inhibited

235 Among all the methods, only the GCP and ARTP can give the significance to identify a gen

236 Simulation shows that the GCP can effectively control the type I error rates and h

237 of active Shh signaling and showed that the GCP possessed a primary cilium with CEP290 at its base.

238 with glaucoma was 23.2% and 35.7% using the GCP program based on pattern deviation and total deviati

239 by applying the same criteria but using the GCP program based on total deviation probability maps.

240 residue mature peptide is identical with the GCP-2 protein previously isolated from MG-63 osteosarcom

241 Sequence analysis revealed that the GCPs share five regions of sequence similarity and defin

242 ar signal-regulated kinase 1; thermotolerant GCPs retain this polypeptide.

243 ylaminopurine to survive, but thermotolerant GCPs cultured at 38 degrees C +/- ABA do not require eit

244 rucei is composed of gamma-tubulin and three GCP proteins, GCP2-GCP4, and is primarily localized in t

245 ased with greater variability with the three GCP methods and decreased with all other methods.

246 GIS, 36% for CIGTS, 47% to 62% for the three GCP methods, and 72% and 84% for the two PLRA methods.

247 y and cell division, whereas the other three GCPs are not.

248 ansformants weakly expressed GFP, similar to GCP cultured at 32 degrees C in media lacking NAA.

249 esponsive transgene promoter in tree tobacco GCPs, suggesting that inhibition of cell expansion and c

250 possess potent inhibitory activities toward GCP II.

251 served peripheral protein of the gamma-TuRC, GCP-WD/NEDD1, associated with motile gamma-TuRCs and loc

252 However, the UMP . GCP complex was 4.8 degrees less closed than the glucose

253 resolution structure of the complex with UMP/GCP and a 2.8-A resolution structure of the complex with

254 ative clinical trial (ISRCTN 72102977) under GCP standards in Cameroon, laboratory confirmed BU patie

255 e center noncomparative clinical trial under GCP standards in Cameroon, laboratory confirmed BU patie

256 Twenty-one patients with untreated GCP (mean age: 46.0 +/- 8.8 years) and 16 patients with

257 LAgP, 37 with GAgP, 37 with LCP, and 27 with GCP.

258 , EPA, and AA were observed in patients with GCP when compared with patients with gingivitis (P = 0.0