ライフサイエンスコーパス: binding assay

1 with WT RGS2 in a flow cytometry competition binding assay).

2 etagamma in a FRET-based Gbetagamma-PLC-beta binding assay.

3 .6 +/- 0.1 nM in a rat cortex P2X7R membrane binding assay.

4 y HSA-bound LCFAs such as the albumin-cobalt binding assay.

5 tion constants were evaluated by competitive binding assay.

6 hat were below the limit of detection in the binding assay.

7 fluorescence polarization-based PAR-protein binding assay.

8 d values measured by an indirect competitive binding assay.

9 ized the results obtained in the radioligand binding assay.

10 proteins to alpha4beta7 in an in vitro cell binding assay.

11 tein receptor); this was confirmed by a RELN-binding assay.

12 a detection limit of 58ngmL(-1) as a direct binding assay.

13 zyme-linked immunosorbent assay (ELISA)-type binding assay.

14 mg (+/-0.64), was obtained with a saturation binding assay.

15 ated a fluorescence polarization competition binding assay.

16 wn in co-immunoprecipitation experiments and binding assays.

17 f Xvelo recruit both RNA and mitochondria in binding assays.

18 as inferred by competition and GTPgamma(35)S binding assays.

19 teractions that are not detected in solution binding assays.

20 using in silico predictions and MHC class II binding assays.

21 e mapping short peptide antigens in antibody binding assays.

22 when tested in the in vitro and in live-cell binding assays.

23 l with the values determined in radio ligand binding assays.

24 and LysRS for ES7 were confirmed by in vitro binding assays.

25 n recent years to embrace high speed protein binding assays.

26 eceptors and examined these events in direct binding assays.

27 trongly with the RFXAP component in in vitro binding assays.

28 nd mouse PEDF promoter regions, confirmed by binding assays.

29 ibrils, which cannot be mimicked by in vitro binding assays.

30 phoretic mobility shift and ethidium bromide binding assays.

31 using a yeast two-hybrid screen and in vitro binding assays.

32 immunohistochemical studies, and competition binding assays.

33 as frequent-hitting fragments in biophysical binding assays.

34 They are also employed in fluorescent binding assays.

35 using surface plasmon resonance and in vitro binding assays.

36 ene promoter regions and by the promoter DNA-binding assays.

37 ctivity with the other 3 GSTs using antibody binding assays.

38 molecular docking analysis and experimental binding assays.

39 HBP1-S107C in either cell-based or cell-free binding assays.

40 ocytosis assays and heterologous competitive binding assays.

41 dictate the caliber and robustness of ligand binding assays.

42 RP with one candidate, RhoC, by in vitro RNA binding assays.

43 espectively as calculated using fluorescence binding assays.

44 in inflamed tissue by mass spectrometry and binding assays.

45 applicable to pulldown and kinetic activity/binding assays.

46 GPCRs to be used for instance in FRET-based binding assays.

47 Rs were evaluated using flow cytometry-based binding assays.

48 validated through steady-state fluorescence binding assays.

49 rent dust contaminants in a radio-ligand TTR binding assay; 2,2',4,4'-tetrahydroxybenzophenone, perfl

50 were evaluated in a radioligand displacement binding assay, a [(35)S]GTPgammaS binding assay, and in

51 iven luciferase induction in vivo, PPARgamma binding assays (affinity comparable to pioglitazone and

52 was confirmed by a comprehensive cell-based binding assay against a library of CTLA-4 mutants and by

53 an automated fluorescence-based competition binding assay, allowing the pKi values of several well-k

54 NMR titration experiments and in vitro DNA binding assays also show that, within the heterodimeric

55 n CPSF30, we identify using quantitative RNA-binding assays an N-terminal lysine/arginine-rich motif

56 to RAGE receptors were assessed by Congo red binding assay and a brown staining method.

57 the Wnt9A promoter, shown by oligonucleotide-binding assay and by chromatin immunoprecipitation assay

58 By ELISA-based DNA-protein binding assay and conventional gel shift assay, we succe

59 -11 were tested in vitro using a competitive binding assay and ex vivo using a rat aortic ring bioass

60 e evidence via motif predictions, an in vivo binding assay and genetic experiments that the Rpd3/Sin3

61 We developed a modified C1q-binding assay and hypothesized that C1q-binding dnDSA co

62 induced activation of mGluR2 in the membrane-binding assay and in primate cortex, hippocampus, and st

63 for amyloid-beta was evaluated by saturation binding assay and in vitro autoradiography using post-mo

64 ed for nineteen M1 PAMs in the [(3)H]PT-1284 binding assay and the EC50 values of these ligands in a

65 . (2016) describe a novel cell-based peptide-binding assay and use it to analyze the binding specific

66 hich meet the requirements for use in ligand-binding assays and absorption, distribution, metabolism,

67 hIP-qPCR (quantitative PCR), oligonucleotide-binding assays and analytical ultracentrifugation.

68 tally validate our simulations, using ligand binding assays and antibodies to monitor the conformatio

69 Ia receptors was investigated in competition binding assays and autoradiography using a fresh cardiac

70 ical shift perturbation analysis, orthogonal binding assays and cell fluorescence microscopy studies

71 Using in vitro binding assays and electron microscopy on recombinant fr

72 ergy transfer measurements, combined with PG-binding assays and fitting of the crystal structures of

73 d components were tested in mouse eosinophil-binding assays and flow cytometry-based cell death assay

74 Here, we use protein binding assays and functional studies in Xenopus egg ext

75 sequences were evaluated using quantitative binding assays and HLA-DRB1 tetramers.

76 and 56 TFs extracted from in vitro HT-SELEX binding assays and in vivo ChIP-seq data, respectively.

77 hesized and evaluated in CB1 receptor (CB1R) binding assays and iNOS activity assays.

78 ly, quantitative fluorescence anisotropy RNA binding assays and isothermal titration calorimetry expe

79 e interactions are not predicted by in vitro binding assays and prevailing cell wall models.

80 Through in vitro binding assays and saturation transfer difference (STD)

81 electron microscopy and radioligand receptor binding assays and shown to require beta-arrestin2, a mu

82 Here, we use direct monobody-binding assays and single-channel recordings of a Fluc c

83 ing, which was extensively validated through binding assays and site-directed mutagenesis of function

84 Equilibrium and stopped-flow binding assays and size exclusion chromatography were co

85 Pulldown and immunofluorescence binding assays and surface plasmon resonance were used t

86 ings are supported by results of competitive binding assays and the similarity of the x-ray structure

87 oth muscle cells (SMC) was measured by a DNA-binding assay, and ii) lipopolysaccharide (LPS)-induced

88 splacement binding assay, a [(35)S]GTPgammaS binding assay, and in a competition association assay th

89 Genetic sequencing, glycan-array receptor-binding assays, and ferret studies reveal the H7N9 virus

90 Using crosslinking analogs, click chemistry, binding assays, and functional assays, we identified G-p

91 circular dichroism, fluorescence-based lipid-binding assays, and in silico structural prediction.

92 ted low-affinity binding to LRP6 in in vitro binding assays, and inhibition of LRP6 or critical signa

93 phomimetic (T73D/S189D) constructs, in vitro binding assays, and phosphatase activity assays, we demo

94 and performed autoradiography, [H-3]-AV-1451 binding assays, and quantitative tau measurements in pos

95 nding and increased CTCF binding in promoter-binding assays, and risk allele carriage diminished tran

96 el compounds were assessed using radioligand binding assays, and the compounds with the highest affin

97 s (5 and 27) were tested in [(35)S]GTPgammaS binding assays, and their RTs appeared correlated to the

98 3 ECD proteins in Wnt signaling and receptor binding assays, and we engineer novel high-potency RSPOs

99 Binding assays are not yet available for GPR55 screening

100 NMR binding assays are routinely applied in hit finding and

101 Ligand-binding assays are the linchpin of drug discovery and me

102 Implementation of a DNA binding assay as a prescreen and models in DNA allowed r

103 calorimetric, fluorescence, and hydrodynamic binding assays, as well as bulk solution and single fila

104 Competitive binding assays based on the lectin Concanavalin A (ConA)

105 bsequent computational modeling and liposome binding assay both suggest that the conformational flexi

106 gnizes sialylated sulfated glycans in glycan-binding assays, but the identities of endogenous sialosi

107 + and 15 who were AMR-, were assayed in C1q-binding assays (C1q Screen; One Lambda, Inc. Canoga Park

108 r reporter strains, in vivo and in vitro DNA-binding assays combined with 5'RACE, that BrlR binds to

109 Direct binding assays, combined with site-directed mutagenesis,

110 Subsequently, using binding assays, computational docking and cellular studi

111 Gel-shift binding assays confirm that N1 methylation interferes wi

112 Cell-based receptor binding assays confirm that Q8 is a CysLT1 antagonist an

113 Activity and lipid-binding assays confirm that these peptides act via a rec

114 Lipid binding assays confirm the role of the two basic patches

115 The Blitz competition binding assay confirmed target binding of NUCC-555 to th

116 An in vitro binding assay confirmed that RTA selectively recognizes

117 Immunoprecipitation and ELISA-style binding assays confirmed a direct interaction between EM

118 Fluorescent lipid-binding assays confirmed that the protein is highly sele

119 Enzymatic and lectin binding assays confirmed that WT and R345W F3 are both p

120 Immunohistochemistry and in vitro binding assays confirmed the involvement of macrophageli

121 A RELN-binding assay confirms that CTR truncation significantly

122 In a competition binding assay, DAB4 bound EL4 murine thymic lymphoma cel

123 Biochemical and in vitro binding assay data demonstrated that xylan chains are at

124 NovaScreen binding assay data for ER (human, bovine, and mouse) and

125 Co-immunoprecipitation binding assays demonstrate phosphorylated Mad and Dullar

126 /deuterium exchange experiments and in vitro binding assays demonstrate that Lsm11, in addition to in

127 Whole cell binding assays demonstrated BBA33-dependent binding to h

128 In contrast, solid-phase activity and binding assays demonstrated reduced specific activity an

129 Flow cytometry and PIP2 reporter-binding assays demonstrated that ABCA1 led to PIP2 redis

130 ed with transcriptome analysis and Runx1 DNA-binding assays demonstrated that granulocytic/monocytic

131 Binding assays demonstrated that PEDF-R bound the 44-mer

132 complementation assays and affinity capture-binding assays demonstrated that soluble G37R-hSOD1 effi

133 vitro screening with radioligand competition binding assays demonstrated variable affinity for mu (MO

134 y, combining electrophysiological and direct binding assays, demonstrates that hEAG1 channels are sub

135 Split ubiquitin-binding assays detected interactions between Hsp90 and C

136 preparations makes conventional competition binding assays difficult to interpret.

137 In radioligand binding assays, EGF and TGFalpha exhibited increased aff

138 eptor using a high-concentration radioligand binding assay enabled the identification of moderate aff

139 Microarray-based binding assays facilitate the discovery of protein ligan

140 hromatin immunoprecipitation assay, in vitro binding assay, flow cytometry, and confocal microscopy.

141 binding and presented a new method to ligand binding assay for D1R.

142 s inactive in a [(3)H]astemizole competitive binding assay for hERG liability screening.

143 development of a fluorescence-based, direct binding assay for the detection of type II and III DFG-o

144 odular way consisting of orthogonal in vitro binding assays for ligand screening and verification of

145 se chain reaction, Western blotting, and DNA binding assays (for transcription factors).

146 ompounds includes, among others, cannabinoid binding assays, functional studies, and surface plasmon

147 latory motif prediction, in vivo protein-DNA binding assays, genetic analyses and monitoring of epige

148 ffinities were measured (pH, temperature and binding assay) had significant effects on prediction acc

149 Our label-free binding assays have further provided the interaction str

150 ious endothelial cells (ECs) and in in vitro binding assays (ii) MYPT1 targets and stimulates PP1c to

151 peptide was determined using GLP-1 receptor binding assays, immunocytochemistry for the receptor and

152 and the scintillation proximity radioligand binding assay improved our understanding of substrate bi

153 ined with a homogenous conformation-reporter binding assay in a microfluidic device, that a substanti

154 s of purified PllA with a glycan array and a binding assay in solution.

155 -Barre syndrome, which was confirmed by cell binding assays in all four patients.

156 tibody binding to beta1-integrin subunit and binding assays in different cell lines, primary neurons,

157 t]) was determined using in vitro homogenate binding assays in human, monkey, and rat cerebellum.

158 Abeta and SORLA was further corroborated by binding assays in rat kidney extracts.

159 Binding assays in the absence and presence of actin reve

160 ulting ASO conjugates were evaluated in ASGR binding assays, in primary hepatocytes, and in mice.

161 synthetic mimics of trehalose dimycolate in binding assays, in structural studies by x-ray crystallo

162 a patens as well as in vivo and in vitro RNA binding assays indicate that HCF145 has been recruited i

163 Conversely, steady-state binding assays indicate that more rigid lipid compositio

164 Importin binding assays indicate that nuclear access occurs via a

165 Surface plasmon resonance and cell-binding assays indicated that both antibodies likely int

166 of vaccine-induced F-specific antibodies by binding assays indicated that packaging conferred substa

167 Human serum albumin binding assays indicated that the retained carboxyl grou

168 Substrate binding assays indicated that UDP and fructose, respecti

169 e approach, coupled with subsequent in vitro binding assays, indicated that BBA33 binds to collagen t

170 Capture also correlated with results of Env binding assays, indicating that greater immunogenicity r

171 ked immunosorbent assay (ELISA)-based ligand-binding assays, it is difficult to evaluate the residual

172 workflow is presented by hybridizing ligand binding assay (LBA) with liquid chromatography-high-reso

173 Screening of a compound library in a DRAK2 binding assay led to the identification of an isothiazol

174 urement of EDA levels combined with receptor-binding assays might be of relevance to aid in the diagn

175 The results from fluorescent binding assays, molecular docking and dynamics demonstra

176 nd Cry1Ca protein in the food chain; and (2) binding assays of Cry1Ac, Cry2Aa and Cry1Ca to midgut br

177 Spectroscopic and SDS-PAGE binding assays of Sin a 2 and Ara h 1 with different pho

178 In vitro(99m)Tc-HYNIC-TCP-1 binding assays on HCT 116 cells indicated a mean Kd of 3

179 Unlike ligand-binding assay, our method is not prone to interferences

180 erence did not reach significance with a C1q-binding assay (P=0.06).

181 ate concentrations measured by using protein-binding assays (PBAs) also showed this pattern but to a

182 Binding assays performed in microtiter plates, by two-di

183 The binding assay, performed on isolated islets, showed a li

184 These models, combined with peptide binding assays, provide evidence for multiple interactio

185 Mutagenesis analysis and in vitro binding assays provided additional evidence to show that

186 The topology-dependent binding assay provides a robust and easily implemented m

187 A novel URAT1 binding assay provides support for direct interaction wi

188 In solid phase ELISA-based ligand binding assays, purified pentameric H2O2-treated CRP bou

189 lower IC50 than aflibercept in VEGF receptor binding assays (RBAs) and retaining activity upon releas

190 or VEGF binding, inhibition of VEGF receptor binding assays (RBAs), and VEGF-driven in vitro models o

191 protein (gCDeltamuc) in cell culture and GAG-binding assays, respectively.

192 otential target of resveratrol, and in vitro binding assay results using resveratrol-conjugated Sepha

193 Equilibrium binding assays reveal that the POT1-TPP1 complex binds G

194 Facilitated allergen-binding assays revealed a highly significant (P < .001)

195 Our binding assays revealed an association of LANA with NAP1

196 Binding assays revealed direct interaction between Kar1

197 Cell-free carbohydrate binding assays revealed that AMPK autophosphorylation ab

198 cally, in silico docking, gene reporter, and binding assays revealed that His323 of the PPARgamma lig

199 iguingly, coimmunoprecipitation and in vitro binding assays revealed that mortalin facilitates PP1alp

200 Protein-DNA binding assays revealed that MtRecD binds efficiently to

201 Competition binding assays revealed that the anti-SEE antibodies rec

202 gical evaluation in calcium mobilization and binding assays revealed the importance of alkyl substitu

203 integrase were identified using AlphaScreen binding assays, revealing that the integrase interacts w

204 ding due to technological advances in glycan binding assays, reverse genetic systems for influenza an

205 irst measured with the use of a radioprotein-binding assay (RPBA) (1988-2006) and, afterwards, with t

206 Furthermore, the dimeric rsFcgammaR binding assay sensitively detected greater Fc receptor a

207 Using solid-phase binding assays, serum and recombinant L-ficolins were sh

208 lycine in the binding pocket, whereas ligand-binding assays show that glycine binds with nanomolar af

209 A binding assay showed a specific interaction between GPVI

210 Binding assays showed high affinity and selectivity of s

211 Binding assays showed strong interaction of purified Fli

212 y, immunohistochemical staining and in vitro binding assays showed that apoE co-localized and bound m

213 In vitro binding assays showed that Eaf3/5/7 specifically stimula

214 Furthermore, in vitro binding assays showed that TH directly binds the substra

215 Binding assays showed that the decrease in killing was l

216 th cross-linking experiments and competition-binding assays showed that the fully disordered isolated

217 The structure, together with RNA binding assays, shows that the selection of 5'-splice si

218 nd competitive S-adenosyl-l-methionine (SAM) binding assay suggest that these compounds likely confer

219 In vitro ligand-binding assays suggest that CTDP-32476 is a potent and s

220 In vitro DNA binding assays suggest that Zta has high affinity for al

221 Transcriptional profiling and DNA-binding assays suggested that Cmr directly represses dos

222 he establishment of a homogeneous BRET-based binding assay suitable for both detailed kinetic studies

223 ntial measurements, and charged nanoparticle binding assays support a negative surface charge state f

224 Binding assays supported this hypothesis, highlighting a

225 this reporter assay and our previous ligand binding assay tested on the same dust extracts.

226 onstrate using a fluorescence anisotropy DNA-binding assay that the previously reported XPA DBD binds

227 ocetin cofactor activity assay, and collagen-binding assays that provide insight into a different fun

228 This was supported by the use of nucleotide-binding assays that revealed an increase in the affinity

229 ncoded binding pathways, so we utilized cell binding assays that specifically detect binding mediated

230 f novel chimeric HA proteins and competitive binding assays, that sequential infection of ferrets wit

231 nd an enzyme-linked immunosorbent assay-type binding assay, the equilibrium dissociation constant (Kd

232 Using an ELISA-based protein-binding assay, the interaction of recombinant calmodulin

233 In a fluorescence competitive binding assay, the selective ligand binding was observed

234 factor (VWF) activity include a new platelet-binding assay, the VWF:GPIbM, which is subject to less v

235 In glycan-binding assays, the H10 viruses preferentially bound "av

236 In addition, a competitive binding assay to detect cardiac Troponin I (cTnI) was us

237 s study was to assess the ability of the C1q-binding assay to identify clinically significant de novo

238 y available fluorescence polarization ligand binding assay to investigate the binding potency of flam

239 Applying this binding assay to two yeast TFs, we demonstrate that sequ

240 We used the data from three in vitro ToxCast binding assays to assess OASIS, a quantitative structure

241 n design, phage display, and high-throughput binding assays to create an improved light inducible dim

242 In this study, we use Ab-binding assays to demonstrate that Streptococcus pneumon

243 NMR, X-ray crystallography, mutagenesis and binding assays to determine the structure and function o

244 direct telomerase activity and nucleic acid binding assays to explain how naturally occurring mutati

245 recipitation (RIP) combined with competitive binding assays to identify novel primary targets of miR-

246 we have employed single molecule telomerase binding assays to investigate the function of the TEN do

247 autoradiography, and [H-3]-AV-1451 in vitro binding assays to the study of postmortem samples from p

248 ncers, together with high-throughput in vivo binding assays, to systematically dissect the contributi

249 ys, far-UV CD spectroscopy, the thioflavin T binding assay, transmission EM, and molecular dynamics s

250 DNA binding assays uncovered the DNA-binding site of ThrR an

251 and unbound motifs, we performed an in vitro binding assay using 12,000 mouse RNA sequences with the

252 )Lu-PSMA I&T was determined in a competitive binding assay using LNCaP cells.

253 combination of an in vitro lysophospholipid binding assay using purified protein and transport assay

254 A URAT1 binding assay using radiolabeled verinurad revealed that

255 analysis of a panel of conventional affinity binding assays using a suite of aptamers for the small m

256 Binding assays using fluorescent 2'/3'-O-(N-methylanthra

257 inding affinity was measured via competition binding assays using hB1R-expressing Chinese hamster ova

258 = 97, total) were synthesized and tested in binding assays using purified A*0101 and B*0801 molecule

259 In vitro binding assays using purified proteins showed strong aff

260 Binding assays using purified recombinant proteins demon

261 bromelain IgE inhibition and concanavalin A binding assays using sera of cypress pollen-sensitized p

262 Furthermore, using a virus overlay protein-binding assay (VOPBA) in combination with far-Western bl

263 The prognostic value of a C3d-binding assay was further confirmed in an independent co

264 An in vitro binding assay was performed on COLO205 cells treated wit

265 A novel AdoMet binding assay was used to accurately determine the equil

266 Using a novel fluorescence binding assay, we find that an aromatic residue at this

267 d affinity matrices and a radiolabeled lipid binding assay, we reveal that S1P directly interacts wit

268 Here, using in vitro binding assays, we examined the relationship between the

269 ation methodologies and quantitative protein-binding assays, we explored the folding state of heterol

270 Using in vitro binding assays, we find that RNF11 can directly compete

271 performing a promoter activity assay and DNA binding assays, we firmly demonstrated the key role of t

272 In binding assays, we found that phosphorylation of Thr(6)

273 ed in our head-to-head comparison of aptamer binding assays, we further developed and evaluated a set

274 ysis, LPCAT3 promoter assays, and direct DNA binding assays, we have mapped the functional PPAR-respo

275 opy, molecular dynamics (MD) simulations and binding assays, we offer evidence that a structural alte

276 Through mutation analysis and binding assays, we show that Gle1 inhibits Ded1 by reduc

277 Here, using quantitative in vitro binding assays, we show that the IQ domain of IQGAP1 is

278 By molecular docking and receptor binding assays, we showed that c-CA itself is neither an

279 ll as monoamine oxidase (MAO) and functional binding assays were conducted to investigate possible ne

280 Steady-state kinetic analyses and binding assays were consistent with Sirt1 S-nitrosation

281 First, radioligand binding assays were performed to determine affinity and

282 In vitro binding assays were performed with (18)F-FPyKYNE-losarta

283 In vitro kinase and binding assays were used to identify the most potent com

284 Ligand-binding assays were used to quantitate ligand affinity.

285 Recent in vitro binding assays, which exclude the effects of the cellula

286 ditionally been characterized by radioligand-binding assays, which have low temporal and spatial reso

287 A BRET-based competition binding assay with 4 was also established and used to de

288 Using ligand binding assays with cysteine-rich domains-fused p75 neur

289 species, are designed as surface-competitive binding assays with fluorescence readouts.

290 ll receptor of type I NKT cells in real time binding assays with high affinity, only a few activate t

291 fluorescence, autoradiography and homogenate binding assays with homologous and heterologous blockade

292 ated part of the sensor chip, and subsequent binding assays with label-free lectins.

293 Using [(3)H]dofetilide-binding assays with membranes of human Kv11.1-expressing

294 Modeling of ligand binding to CB1R and binding assays with native and mutant (Ile105Met) hCB1Rs

295 Binding assays with phage expressing NP41 confirmed bind

296 Binding assays with purified recombinant proteins showed

297 mbined expression studies and in situ ligand-binding assays with the analysis of genetically altered

298 Selected probes were tested in competition binding assays with unlabeled competitors in order to de

299 tial effects on the radioligand used for the binding assay, with (R,R)-68 potentiating the radioligan

300 ns, this work is the first to utilize direct binding assays, X-ray crystallography, and modeling, to