ライフサイエンスコーパス: competition assay

1 acterial quorum sensing, is detected using a competition assay.

2 MRT, and STAMP) using our recently developed competition assay.

3 VS in human macrophage-like THP-1 cells in a competition assay.

4 hya site bases shown to be important in the competition assay.

5 The top hits were assayed in an in vitro competition assay.

6 devised a high-throughput fluorescence-based competition assay.

7 s, we have developed a functional antagonist competition assay.

8 binding enriched BMV replicase in a template competition assay.

9 o inhibited AA activation of PLC delta1 in a competition assay.

10 the values obtained by a fluorescence-based competition assay.

11 r in structure were used as competitors in a competition assay.

12 (RBAs) using an enzyme-linked immunosorbent competition assay.

13 g mutants failed to compete for binding in a competition assay.

14 tides of the same sequence were present in a competition assay.

15 alian or avian viruses using a plasmid-based competition assay.

16 neutralizing antibody were tested in direct competition assays.

17 and lysozyme than the wild type in in vitro competition assays.

18 ic acids were able to displace the tracer in competition assays.

19 ith Als2cr4 recombinant proteins and peptide competition assays.

20 ges at 37 degrees C measured by fluorescence competition assays.

21 n blotting, solid-phase epitope mapping, and competition assays.

22 nzyme-linked immunosorbent assay (ELISA) and competition assays.

23 based on coimmunoprecipitation and in vitro competition assays.

24 sing escape mutants, structure analyses, and competition assays.

25 ntially diminished viral fitness in in vitro competition assays.

26 ) coexpressing HER2 and EGFR was assessed in competition assays.

27 ent to direct IAB5 to an ectopic promoter in competition assays.

28 has been difficult to define by conventional competition assays.

29 by using methylation protection and binding/competition assays.

30 ogies are generally applicable to any growth competition assays.

31 pitopes were identified by ELISA and binding competition assays.

32 periments with deletion mutants, and peptide competition assays.

33 nd fitness during infection were measured by competition assays.

34 rom RAW264.7 cells by performing a series of competition assays.

35 F resistance mutations was studied in growth competition assays.

36 ion inhibitor as measured by exchange factor competition assays.

37 ability to grow in the lung, as measured by competition assays.

38 ces B and C bound DnaK with high affinity in competition assays.

39 human natural killer cells was evaluated by competition assays.

40 avidity for PU.1, as determined by gel shift competition assays.

41 ntiparallel native FRT sites in dilution and competition assays.

42 direct comparison of protein activity and by competition assays.

43 tested against wild-type pfcrt in co-culture competition assays.

44 ng, we used mutagenesis coupled with acetate competition assays.

45 was true for infectious virus, including in competition assays.

46 ld decreased GAS recovery in isogenic strain competition assays.

47 M(-1)s(-1) at pH 7.4 through two independent competition assays.

48 Center-of-Tree (COT) protein through fitness competition assays.

49 s were identified using ex vivo head-to-head competition assays.

50 d and changes in fitness were assessed using competition assays against genetically marked, surrogate

51 When the prsW mutant was tested in competition assays against its isogenic parent in the ha

52 irmed each of these phenotypes in one-on-one competition assays against otherwise-wild-type lacZ muta

53 In peptide competition assays, all HR-B mutants at residue 462 reve

54 lasmon resonance based vitronectin-PAI-1-SMB competition assay allowed us to conclude that 1) only th

55 yses,trans-protection analyses, and in vitro competition assays, allowed us to identify novel effecto

56 Intestinal persistence competition assays also demonstrated that the rpoN mutan

57 embranes, as determined using a cytochrome c competition assay, although Sj-FABPc interacted to a gre

58 Competition assays among FBABIRT and BIRT derivatives de

59 mutagenesis, as shown by both a fluorescent competition assay and a polarity sensitive dye, badan.

60 Completion of the competition assay and complementation rescue system take

61 n binding assay, gel electrophoresis binding competition assay and confocal microscopy.

62 is dysfunctional in an Escherichia coli CRP competition assay and has been proposed as a potential s

63 n by the determination of IC(50) values in a competition assay and surface dissociation constants (K(

64 ceptor were measured using a (3)H-Mibolerone competition assay and varied from 18% of nilutamide bind

65 esponsive mRNA target candidates in both RIP competition assays and expression profiling experiments

66 Competition assays and molecular docking simulations sug

67 Guanosine triphosphate analog competition assays and mutagenesis analysis, performed t

68 Cross-competition assays and mutational analyses showed eviden

69 Using peptide competition assays and NMR spectroscopy, we conclude tha

70 Competition assays and structural mapping revealed two n

71 ads to reduced plaquing, fitness defect in a competition assay, and reduced tissue cyst formation in

72 PP-stabilized microtubules was assessed by a competition assay, and their influence on microtubule po

73 inity of amychelin was determined using EDTA competition assays, and a biosynthetic cluster was ident

74 m kinetic analyses, microtubule (MT) binding competition assays, and hydrogen/deuterium-exchange stud

75 In vitro gel shift assays, competition assays, and immunoprecipitations (IPs) revea

76 plex, the relative loop stability known from competition assays, and the relative loop size known fro

77 g, fitness was evaluated by growth curve and competition assays, and vanA presence was determined by

78 etection limits for unmodified toxins in the competition assay are comparable to values reported prev

79 ding affinity with lectins by a fluorescence competition assay are determined.

80 as characterized by kinetic, saturation, and competition assays at membrane preparations of Chinese h

81 ngth of the polyphenols was also tested in a competition assay based on the fluorescence quenching of

82 A competition assay, based on a validated chemical kinetic

83 Here we show, by using a direct competition assay between doxycycline-resistant and doxy

84 A competition assay between GDP and GDP analogues in the G

85 Additionally, data from a competition assay between SLA and single-stranded RNA (s

86 A competition assay between the DeltatoxRS and wild-type V

87 Results from an in vitro binding competition assay between the wild-type FlhD(4)C(2)-prot

88 We now show, using competition assays between ATP and GTP, that GTP is the

89 Analysis of competition assays between PA1 and TIF2 with an exogenou

90 We demonstrated that in in vivo competition assays between the rpoE mutant and the WT ma

91 In in vivo competition assays between the rpoN mutant and a wild-ty

92 Nodule competition assays between the wild type and the nwsB mu

93 Site-directed mutagenesis, competition assays between wild-type and mutant NDK prot

94 r dominance has repeatedly been supported in competition assays between Xenopus laevis and X. boreali

95 In a competition assay, both soluble CD163 and Fn14/TweakR we

96 within its central hydrophobic patch, and in competition assays, both CSP-1 and CSP-2 interacted with

97 Finally, we show how a competition assay can be set up to perform focused libra

98 We show that this general ELISA-based competition assay can be used to quantify small molecule

99 directed mutagenesis and sucrose octasulfate competition assays collectively indicate that the negati

100 An in vivo competition assay compared the colonization levels of th

101 ase in the competitive index in colonization-competition assays comparing the mutant strain with both

102 Peptide competition assays confirm that a candidate clathrin box

103 Competition assays confirmed that RSV MA binds inositol

104 Neutralization competition assays confirmed that the peptide NWFDITNWLW

105 Competition assays, cross-linking experiments, limited p

106 IC(50) (10.9 nM) derived from a biochemical competition assay (DELFIA) that measures the level of in

107 Efflux and substrate competition assays demonstrate that NAD is a preferred s

108 In vivo competition assays demonstrate that noninducing flavonoi

109 A tissue culture-based competition assay demonstrated that the HBD effectively

110 An HIF-1 binding and competition assay demonstrated that the HRE sequence fro

111 However, peptide competition assays demonstrated a 6-fold difference in t

112 Competition assays demonstrated a marked advantage to be

113 Competition assays demonstrated that accumulation and lo

114 Competition assays demonstrated that Ad/GFP-ABP-PEG-HCBP

115 Competition assays demonstrated that both immunophilins

116 the direct assay is superior to that of the competition assay, detection limits for unmodified toxin

117 7)-10(8) M(-1)s(-1) range as determined by a competition assay developed here.

118 Data from molecular docking and substrate competition assays established that the primary molecula

119 Using a reporter-based high-throughput competition assay, followed by deep sequencing, we measu

120 mycin derivatives, which matched well with a competition assay for Hsp90alpha.

121 ng to target sites on immobilized DNA, and a competition assay for inhibition of the HMGA2-DNA comple

122 describe a novel, patient serum-independent competition assay for pathogenicity screening of FH19-20

123 We describe a supramolecular surface competition assay for quantifying glutamine uptake from

124 In addition, we developed a competition assay for the oligonucleotides between the s

125 As a demonstration of the potential of the competition assay for unlabeled toxin detection, we conc

126 tant analysis, a high-throughput subtractive competition assay, for genotypically defined M. tubercul

127 A fluorescence polarization competition assay has been developed to screen for inhib

128 Growth competition assays have been developed to quantify the r

129 Pooled mutant competition assays have shown that the Mycobacterium tub

130 Using an FA competition assay, host ACSLs were found to activate Ct

131 er analysis using lectin staining and lectin competition assays identified that AAV1 and AAV6 use eit

132 screening pluripotency-associated factors by competition assay; (ii) setting up an inducible compleme

133 Finally, we demonstrate an Affimer-based competition assay, illustrating the potential of Affimer

134 in virulence relative to the wild type by a competition assay in BALB/c mice.

135 In an in vitro growth competition assay in mouse intestinal mucus, the rpoN mu

136 An SSA competition assay in which either diverged or identical

137 were similar to those obtained with a growth competition assay in which the relative proportion of ea

138 Oat1, mOat3, and mOat6, a fluorescence-based competition assay in Xenopus oocytes as well as wild-typ

139 their DeltasfaA and DeltasbnD mutants using competition assays in a murine abscess model and invasio

140 Competition assays in BALB/c mice revealed that mutants

141 By using antibody and oligonucleotide competition assays in electrophoretic mobility shift ana

142 By using antibody and oligonucleotide competition assays in electrophoretic mobility shift ass

143 s determined by yeast two-hybrid and in vivo competition assays in H. pylori cell-culture infection s

144 Consequently, competition assays in laboratory conditions may not refl

145 han wild type as measured by intraperitoneal competition assays in mice.

146 tro binding of biotinylated Cry proteins and competition assays in midgut protein vesicles showed wea

147 Finally, we show using competition assays in suckling mice that inhibition of m

148 -kappaB "isogenic" viral strains in pairwise competition assays in T-cell lines, primary cells, and t

149 ributes to pellicle formation and fitness in competition assays in the Gram-negative Pseudomonas aeru

150 During competition assays in vitro, an irs4-null (Deltairs4) mu

151 Using competition assays in vivo, we show that each of the hil

152 Competition assays indicate that although both substrate

153 Substrate competition assays indicate that template misalignment,

154 Heparin competition assays indicated that this may be a result o

155 t most perform better than parental lines in competition assays, indicating that there is a trade-off

156 Previous bulk competition assays indirectly measured the loop lifetime

157 age its incorporation, together with the RIP competition assay, into existing target prediction and v

158 The calorimetric competition assay introduced here overcomes this limitat

159 Pollen competition assays involving various combinations of AGL

160 The model-based competition assay is also unique in being able to order,

161 Using fluorescence anisotropy competition assays it is shown that PEA-15 competes for

162 With dialysis and competition assays, it was unambiguously demonstrated th

163 affinity was too weak to measure in the dye competition assays (Kd > 55 microM).

164 Using a new competition assay, NELF-A and NELF-B are each shown to a

165 In direct competition assays, no specificity for pregenomic RNA wa

166 ation required prior to analysis because the competition assay obviates the need to fluorescently lab

167 Competition assays of these nine acid tolerance response

168 This flow cytometry-based growth competition assay offers advantages over current assays

169 We developed an ELISA-based competition assay on these air plasma-treated plates and

170 Head-to-head competition assays on agar plates indicate that two-dime

171 automated, and allows one to perform F-actin competition assays on similar sized proteins.

172 ptors using this method without performing a competition assay or increasing the protein concentratio

173 the paternal signal was not visible in sperm competition assays or as allelic imbalance in sperm.

174 d transurethrally either at an ~1 : 1 ratio (competition assay) or individually (monoinfection).

175 A significant advantage of the competition assay over reported profiling assays is the

176 Competition assays provide a means to assessing possible

177 Competition assays provide evidence that DNA strand sepa

178 Therefore, an equilibrium competition assay provides a quick and facile method to

179 e mixture of the two competing ligands, this competition assay provides accurate and precise values f

180 inant human MMP20 were compared by substrate competition assay, pull-down assay, and surface plasmon

181 ce resonance energy transfer and an in vitro competition assay revealed that activated GRs competed f

182 Moreover, an on-microarray competition assay revealed that the capture of the PPI b

183 Competition assays revealed excellent binding and select

184 In vitro competition assays revealed that both Ca(2+)/calmodulin

185 Peptide competition assays revealed that the DEF2 peptide could

186 Competition assays revealed that the dominant HGM commen

187 Competition assays revealed that the two binding pockets

188 , employing a fluorescence polarization (FP) competition assay, revealed that among several alpha/bet

189 Studies on sugar uptake, including competition assays, revealed that MRT was a sucrose and

190 By using a competition assay, several peptides derived from the BH3

191 Substrate competition assays show that in solution zebularine is r

192 Coimmunoprecipitation and competition assays show that the trans-sialidase/parasit

193 In silico modeling and FRET-based competition assay showed that EGCG physically interacts

194 Direct in vivo competition assays showed a 5-fold competitive advantage

195 ELISA-based competition assays showed altered capacities of the aged

196 lysis of mutations in the hya site using DNA competition assays showed that apo-IscR most likely reco

197 Competition assays showed that both cleaved products are

198 Competition assays showed that PEDF can bind heparin and

199 lative IC(50) values from gel mobility shift competition assays showed that the -759-bp GRE has a 2-f

200 Competition assays showed that the decrease in activity

201 Competition assays showed that the rate of binding (t((1

202 Competition assays showed that TIA-1 apparently binds wi

203 Competition assays showed that VP35 interacted specifica

204 CMP-Kdo synthetase inhibition and competition assays showing that Kdo and D-Ara, a precurs

205 es CLEC18A-1 binding to GLPS-F3, and a sugar competition assay shows that CLEC18 preferentially binds

206 ore allowed a highly robust and miniaturized competition assay sufficient for high-throughput screeni

207 Competition assays suggest that FH and C4BP have distinc

208 ut all phases of the cell cycle, and subunit competition assays suggested that hTERT-hTR interaction

209 Competition assays suggests that COBRA binds individual

210 We developed a mechanical single-molecule competition assay that allows online observation of bind

211 ed directly by the antibody array and (ii) a competition assay that employed unlabeled toxins as repo

212 comparably stable, as confirmed by a direct competition assay that established an equilibrium 55:45

213 a homogeneous fluorescence polarization (FP) competition assay that requires neither labeled primers/

214 We have developed a novel competition assay that uses a gold nanoparticle (Au NP)-

215 ence by flow cytometry allowed us to perform competition assays that demonstrated the high probabilit

216 Using a competition assay, the affinity of UDP-Glc was determine

217 Using a template competition assay, the core promoter of ca. 20 nucleotid

218 In a competition assay, the presence of purified rHagB decrea

219 rough the use of single-hit and multiple-hit competition assays, the catalytic core of pol eta was fo

220 oretic mobility gel shift assay (EMSA)-based competition assays, the kl-TSS was found to occupy a dif

221 egion 17-31 of PTH-(1-31) and assessing, via competition assays, their effects on binding to the wild

222 In dansylamide-competition assays, these designs showed 46-64-fold impr

223 (Con A) was determined using a fluorescence competition assay to be 0.289 +/- 0.003 muM, which repre

224 e (WT) virus were competed in a head-to-head competition assay to determine how different clones grew

225 We used a biosensor competition assay to determine whether there were corres

226 We have developed a novel, biosensor-based competition assay to directly address this important que

227 Here, we employ a competition assay to evaluate the role of this region in

228 essential genes and a high-throughput growth competition assay to measure fitness with unprecedented

229 We have developed a multiple-cycle growth competition assay to measure HIV-1 replication efficienc

230 Using a competition assay to measure relative affinities of puri

231 We used peptide competition assays to demonstrate that Cdh1p interacts d

232 c-specific fluorophore, Zinpyr-1, is used in competition assays to determine the kinetic and thermody

233 ase activity of I-AniI in vitro and utilized competition assays to probe the relationship between the

234 ite and complement these data with gel-based competition assays to provide a detailed structural unde

235 fluorescence complementation and two-hybrid competition assays to show that PTS represses KNOX1 prot

236 de-affinity profiling and nucleotide-binding competition assays, to characterize comprehensively (S)G

237 Third, using ciprofloxacin competition assay, TOP2-mediated DNA cleavage induced by

238 rescent probe binding has been assessed in a competition assay using the natural LFA-1 ligand ICAM-1

239 HB synthesis exist in agreement with in vivo competition assays using Acanthamoeba castellannii or hu

240 tant (Ki) of 0.02 nM measured in radioligand competition assays using cloned human receptors.

241 We then performed competition assays using clones of both morphs from diff

242 Moreover, in vitro competition assays using Cr-DFO and FO clearly demonstra

243 Competition assays using nitrocefin efflux and covalent

244 In direct competition assays using pooled human urine inoculated w

245 Competition assays using purified molecules demonstrated

246 Competition assays using recombinant human NK(2) recepto

247 Moreover, an alternative competition assay utilizing Trp --> DNQX quenching for d

248 A competition assay was designed using TREX1 dominant muta

249 A fluorescence anisotropy-based coactivator competition assay was developed to measure the specific

250 efine the receptor binding domain of LsbB, a competition assay was performed in which a systematic co

251 An in vivo mouse challenge-competition assay was used to determine if the mutants w

252 Using DNA binding competition assays we found that Dna2 has substrate stru

253 tomic force microscopy, confocal images, and competition assays) we characterized this reagent and de

254 nalytical ultracentrifugation, and CD4-based competition assay, we demonstrate that the stoichiometry

255 Using a competition assay, we demonstrated that a pyelonephritis

256 Using a plasmid competition assay, we have measured the stability of ori

257 NA affinity chromatography and cross-linking competition assays, we also demonstrate that the heterog

258 Using in vitro liposome binding and competition assays, we demonstrate that mVps24p selectiv

259 Using competition assays, we demonstrate that overexpression o

260 Using in vitro pulldown and competition assays, we demonstrate that this motif binds

261 Using in vitro transcription template competition assays, we observed that p300 forms a stable

262 Furthermore, a series of ligand competition assays were carried out on a single lectin s

263 ted by subtype C HIV-1 were constructed, and competition assays were carried out to compare the fitne

264 Flow cytometry-based receptor competition assays were developed to monitor concentrati

265 In this report, in vivo and in vitro competition assays were used to test whether females hav

266 The technique consists of a competition assay where the toxins in solution compete w

267 We also performed competition assays, which suggested that CaM and S100A1

268 monoclonal antibodies were used to develop a competition assay with a six-channel portable SPR biosen

269 face plasmon resonance-enhanced fluorescence competition assay with a surface-bound antibody is descr

270 involved in binding to cells, we performed a competition assay with C3 and RGD peptide or with a mono

271 8R RNase A to be 0.57 +/- 0.05 nM by using a competition assay with fluorescein-labeled G88R RNase A.

272 tty acid to the antibody, and to implement a competition assay with free fatty acid (undecanoic acid)

273 e-binding site in tubulin, as confirmed by a competition assay with N,N'-ethylenebis(iodoacetamide) a

274 In a direct competition assay with palmitate, all the polyunsaturate

275 We also undertook a novel transfection competition assay with ZnT cDNAs to confirm that the dri

276 Using ligand competition assays with (125)I-labeled GH-RH antagonist

277 e found on MX-1 tumor membranes using ligand competition assays with (125)I-labeled GHRH antagonist J

278 Using competition assays with a selective MMP-12 inhibitor as

279 Binding competition assays with anti-CXCR4 antibodies show that

280 Competition assays with ApoE4, ApoE3, and Tau revealed t

281 Competition assays with CD4 and mAbs F105 and b12 sugges

282 ce of domain II also provides selectivity in competition assays with genomes from related phages.

283 Competition assays with hTSP-1 and Vn revealed the R1ab-

284 Competition assays with human kinesin-5 (Eg5) only parti

285 ll as in hypernucleation and paclitaxel site competition assays with isolated tubulin than the other

286 emolysis of chicken red blood cells (cRBCs), competition assays with monoclonal antibody (MAb) C179,

287 Competition assays with nucleotide analogs showed a rema

288 Competition assays with peptide-epoxide scanning librari

289 hat it confers a fitness advantage in growth competition assays with Pseudomonas putida.

290 PtdE-binding activities was confirmed using competition assays with PtdE-containing liposomes.

291 Through competition assays with sarcoplasmic reticulum vesicles

292 To investigate FVIII endocytosis, competition assays with soluble receptor ligands, bindin

293 Electrophoretic mobility shift assay and competition assays with the CRE2 element indicates that

294 Competition assays with the heterologous E. coli system

295 sRICs to bind HER2 or HER3 was determined in competition assays with unlabeled Fab or HRG on cells ex

296 he presence of deoxycholate and bile, and in competition assays with wild-type cells both in vitro an

297 However, in competition assays, with 6 of the 7 pairs, clade B strai

298 ntage for the wild type over the mutant in a competition assay within the lungs of A/J mice.

299 The utility of this competition assay would be greatly increased if the posi

300 Extending from the direct assay, the competition assay yields information on the presence, id