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 a recently established NanoBRET-based ligand binding assay.

3 formed by laser Doppler flowmetry and lectin-binding assay.

4 ity was measured by IgE-facilitated allergen binding assay.

5 and poorly bound to Abeta in an ELISA-based binding assay.

6 ta-1 interaction using an ELISA-style ligand binding assay.

7 y established "epitope-stealing" HLA/peptide-binding assay.

8 ed using the competitive proxy ligand-ESI-MS binding assay.

9 y Western blot analysis and by a radioligand binding assay.

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

11 ized the results obtained in the radioligand binding assay.

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

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

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

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

16 ated a fluorescence polarization competition binding assay.

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

18 .6 +/- 0.1 nM in a rat cortex P2X7R membrane binding assay.

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

20 Ca(2+) imaging assay and a [(3)H]ketanserin binding assay.

21 fication strategy and the associated aptamer binding assay.

22 binding assay and an HPLC-based competition binding assay.

23 tify IL-36 antagonists using a novel TR-FRET binding assay.

24 ned using [(3)H]CP55940 and [(35)S]GTPgammaS binding assays.

25 ives were synthesized and tested by in vitro binding assays.

26 idated these predictions through competitive binding assays.

27 d their interaction through multiple protein-binding assays.

28 helial sites, using SPR and microtiter-based binding assays.

29 eting the threshold required for radioligand binding assays.

30 the crystal structure, was validated in RNA-binding assays.

31 stic patterns in high-resolution protein-DNA binding assays.

32 espectively as calculated using fluorescence binding assays.

33 eceptors and examined these events in direct binding assays.

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

35 in inflamed tissue by mass spectrometry and binding assays.

36 applicable to pulldown and kinetic activity/binding assays.

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

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

39 validated through steady-state fluorescence binding assays.

40 wn in co-immunoprecipitation experiments and binding assays.

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

42 sized compounds, were studied in competition binding assays.

43 adenosine receptors, performing radioligand binding assays.

44 s well as FRET-based kinetic and equilibrium binding assays.

45 al new motifs that are validated by in vitro binding assays.

46 mass spectrometry (MS), and split-ubiquitin binding assays.

47 an interactions, and limitations in existing binding assays.

48 , single turnover kinetics, and RNA affinity-binding assays.

49 s (sigma1Rs) were determined via competitive binding assays.

50 set using surface plasmon resonance and cell binding assays.

51 ilar to Ins(1,4,5)P(3) and 15-fold weaker in binding assays.

52 sing single molecule atomic force microscope binding assays.

53 l to promote more accurate and robust ligand binding assays.

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

55 Compared with ligand binding assays, a major advantage of mass spectrometry-b

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

57 dates that were validated through a panel of binding assays against the purified antigen.

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

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

60 Using a fluorescence polarization 30S-binding assay and a new crystal structure of the methylt

61 :03, we used an UV-mediated peptide exchange binding assay and an HPLC-based competition binding assa

62 After in vitro testing via competition binding assay and autoradiography, [(18)F]PF-NB1 emerged

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

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

65 group, and both a surface plasmon resonance binding assay and in vivo xenograft mouse model results

66 d physiological membranes in both a liposome-binding assay and MIN6 cells.

67 ses.IMPORTANCE Evidence from both phenotypic binding assay and structural study support the observed

68 . (2016) describe a novel cell-based peptide-binding assay and use it to analyze the binding specific

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

70 l activity in a battery of assays, including binding assays and an assay that mimics molecular recogn

71 Human Fc receptor binding assays and analysis of antibody-cell interaction

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

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

74 ex via mutational analysis combined with RNA-binding assays and cell-based frameshifting reporter ass

75 Using drug-binding assays and computational docking, we show that t

76 In vitro DNA binding assays and crystallographic studies reveal the Z

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

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

79 ensitivity ELISA and ELISpot assays, peptide-binding assays and HLA-II tetramer staining, we focused

80 formation capture (Hi-C) analysis, chromatin binding assays and immunofluorescence, we show that, by

81 d from in vitro high-throughput EpiSELEX-seq binding assays and in vivo methylated TFBSs from the MeD

82 nding sequence, both in in vitro biochemical binding assays and in vivo studies of differentially met

83 ere investigated in fluorescence-based lipid binding assays and in-silico docking simulations.

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

85 Competitive cell binding assays and internalization assays were performed

86 of peanut-allergic patients, competitive IgE-binding assays and mediator release assays were performe

87 Using competitive binding assays and molecular modeling, we established th

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

89 We further demonstrate by in vitro binding assays and super-resolution microscopy in vivo t

90 Using solid-phase binding assays and surface plasmon resonance experiments

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

92 thod to high-throughput transcription factor binding assays and use it to explore a fitness landscape

93 d the binding affinity is 2.7 nM (rat cortex binding assay) and 15.9 nM (human P2X7 receptor).

94 (SPMChs) and PBMC B2AR numbers (radioligand binding assay) and signaling (cyclic AMP ELISA) were ass

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

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

97 studies of the ETA protein, through a direct binding assay, and pharmacological and genetic approache

98 onance, fluorescence microscopy, competitive binding assays, and animal studies.

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

100 reacted between H7 and H3 haemagglutinins in binding assays, and had accumulated significantly more s

101 ased mutations, in vitro deamination and DNA binding assays, and HIV-1 restriction assays identify R2

102 alyse the results with respect to mutational binding assays, and hypothesize a mechanism for HEXIM bi

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

104 ap association assays, pulldown and integrin-binding assays, and live-cell imaging, we demonstrate th

105 itation, LOX enzymatic activity, solid-phase binding assays, and proteomics analyses, we report that

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

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

108 ion, native affinity purifications, in vitro binding assays, and SILAC-based quantitative proteomics,

109 r docking, nuclear magnetic resonance, lipid-binding assays, and surface plasmon resonance, this work

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

111 iological examination, serotyping, congo-red binding assay, antibiogram-testing, and PCR-monitoring o

112 ustrated that some pharmacologically related binding assays are highly correlative and may be substit

113 NMR binding assays are routinely applied in hit finding and

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

115 vity analysis using biochemical activity and binding assays are useful but can be costly and are ofte

116 upported by isothermal titration calorimetry binding assays as well as modeling studies.

117 ized by saturation, kinetic, and competition binding assays at the human, guinea pig, and mouse H(2)

118 ons between sperm and neutrophils as well as binding assays between sperm and recombinant Siglec-Fc c

119 heir phospholipid preferences using liposome binding assays, biolayer interferometry and isothermal t

120 alysis of the results of HLA-A*02:01 class I binding assays carried out in the presence and absence o

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

122 We then designed a robust binding assay compatible with high-throughput screening

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

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

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

126 the loss of nuclease activity, fluorescence binding assays confirm the CTD retains its DNA binding c

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

128 An in vitro binding assay confirmed that RTA selectively recognizes

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

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

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

132 s, carried out using the proxy ligand ESI-MS binding assay, confirmed that GD1b binding to CTB(5) is

133 A RELN-binding assay confirms that CTR truncation significantly

134 emonstrate that high-throughput in vitro DNA binding assays coupled with unbiased computational analy

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

136 ational and transcriptional analysis and DNA-binding assays, DdlR was found to be a direct activator

137 Co-immunoprecipitation binding assays demonstrate phosphorylated Mad and Dullar

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

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

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

141 x-loop-helix (bHLH) domain of Ascl1, and DNA-binding assays demonstrated that this interaction interf

142 obsolete, core concepts behind conventional binding assay design.

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

144 In vitro and in vivo RNA-binding assays disclosed that these glycoprotein mRNAs a

145 Single-molecule binding assays enable the study of how molecular machine

146 ble and has advantages over microtiter-based binding assays, especially under flow conditions.

147 rofiles evaluated using in vitro competition binding assays, ex vivo rat aortic ring bioassays and BR

148 anced thermal and pH stability and (b and c) binding assays exploiting antibodies or functional nucle

149 Radioligand binding assays first showed that they bind to the intrac

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

151 We describe here an affinity binding assay for HBeAg, which takes advantage of G-quad

152 rter, we have developed an improved sandwich binding assay for HBeAg.

153 An in vitro binding assay for MIF-1/MIF-2 to the CD74 ectodomain (sC

154 ance energy transfer (NanoBRET)-based ligand binding assay for SMO providing a sensitive and high thr

155 We established a NanoBRET-based binding assay for SMO with superior sensitivity compared

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

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

158 Analytical technologies based on binding assays have evolved substantially since their in

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

160 as determined in LNCaP cells via competitive binding assays (IC(50)) and dual-tracer radioligand and

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

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

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

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

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

166 etic polymorphism using in vitro competition binding assays in human brain and heart; assess whether

167 Although ligand binding assays in microwells provide a promising approac

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

169 Binding assays in the absence and presence of actin reve

170 ssay is superior to commonly used SMO ligand binding assays in the separation of specific from non-sp

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

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

173 we used molecular dynamics simulations, DNA binding assays, in vitro ubiquitination reactions, and D

174 that is present in all the current receptor binding assays, including those employing viruses or pre

175 oplasmic proximal tagging with a biophysical binding assay increases the precision with which transme

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

177 ried out comprehensive in vitro activity and binding assays, indicating that the oxidative protein fo

178 More importantly, the solution phase binding assay is directly applicable to identifying glyc

179 tivity, and throughput of traditional ligand-binding assay (LBA) and liquid chromatography-tandem mas

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

181 Using antibody-binding assays, measurements of virus infectivity, and a

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

183 ent-fixing DSAs identified by a positive C3d binding assay (n=73, 54%) had a higher risk of transplan

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

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

186 hesized compounds were tested in radioligand binding assay on rat cortex against [(3)H]-cytisine and

187 ctivity, cardiomyocyte nuclear extract-based binding assays, overlap with human cardiac tissue DNaseI

188 Using a combination of TNKS-binding assays, PARP activity assays, and analytical ult

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

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

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

192 Enzymatic and binding assays reveal that MORC4 has ATPase activity, wh

193 Gain and loss of function as well as genomic binding assays revealed a direct transcriptional control

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

195 High-resolution genomic binding assays revealed that Gsx2 binds both monomer and

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

197 In vitro binding assays revealed that Rap bound directly to purif

198 Protein-lipid binding assays revealed that RavD selectively binds phos

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

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

201 Ligand binding assays routinely employ fluorescently-labeled pr

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

203 In vitro binding assays show that helix 1, but not helix 2, is es

204 Our fluorescence polarization binding assays show that ZF4 has higher affinity for hFi

205 In vitro DNA-binding assay showed that TRIM28 knockdown increased the

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

207 In vitro binding assays showed that both gmAhr proteins bind to 2

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

209 In the NanoBRET-based binding assay, SMO is N terminally tagged with nanolucif

210 on this specific binding, a soluble oligomer-binding assay (SOBA) was developed as an indirect probe

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

212 gnition of RALF23 by LLG1, LLG2 or LLG3, and binding assays suggest that other RALF peptides that sha

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

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

215 complex, which was revealed by 7-methyl-cap-binding assays, suggesting inhibition of cap-dependent t

216 sequence coupled with in vitro brush border binding assays suggests that it functions as an oligomer

217 Binding assays supported this hypothesis, highlighting a

218 eptide-protein docking analysis and in vitro binding assay that identify epitopes with high affinity

219 ly, we identify key principles for designing binding assays that are optimally suited for a given det

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

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

222 We first demonstrate, via a [(35)S]GTPgammaS-binding assay, that drug activity is retained after conj

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

224 In in vitro HLA-binding assays, the 2 CD4+ T-cell specificities (amino a

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

226 n, washout experiments, and [(35)S]GTPgammaS binding assays, then validated 17b as the covalent antag

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

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

229 mbine proximity labeling and single molecule binding assays to discover transmembrane protein interac

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

231 ion followed by mass spectrometry and direct binding assays to identify proteins that associated with

232 We demonstrated that performing bacterial binding assays to mucins using SPR is feasible and has a

233 Here we used RNA chemical footprinting and binding assays to test this model and further probe the

234 ssay that we term SaMBA (saturation mismatch-binding assay) to investigate the role of DNA conformati

235 mutations, followed by in vitro and in vivo binding assays, to determine conserved surface residues

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

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

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

239 A correlation of binding assays used in this analysis illustrated that so

240 This label-free molecular binding assay uses in-line holographic video microscopy

241 contacts was further confirmed in a NanoBRET binding assay using a Nano luciferase tagged PC4 acting

242 an EC(50) of 942 nM in the [(35)S]GTPgammaS binding assay using mouse striatal membranes but was ina

243 A URAT1 binding assay using radiolabeled verinurad revealed that

244 ganic chemistry and evaluated in radioligand binding assays using FAP-expressing HT-1080 cells.

245 immunoreactivity was determined by cellular binding assays using MKN-45 gastric carcinoma cells.

246 = 97, total) were synthesized and tested in binding assays using purified A*0101 and B*0801 molecule

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

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

249 esent study, the fluorescence-based cofactor-binding assay was adapted to detect binding of the beta-

250 A fluorescence polarization (FP)-based binding assay was combined with biolayer interferometry

251 A Luminex binding assay was developed and used to assess simultane

252 Methods: A competitive binding assay was performed using Chinese hamster lung (

253 Methods: A competitive binding assay was performed using Chinese hamster lung (

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

255 ghput Forster resonant energy transfer-based binding assay, we found that one of our synthetic analog

256 Guided by a surface plasmon resonance (SPR) binding assay, we selected six hybridomas that produced

257 Using DNA binding assays, we demonstrate that heme disrupts bindin

258 purified enzymes for prenylation and protein-binding assays, we demonstrate that SmgGDS-607 different

259 Using cell-based Notch signaling and ligand-binding assays, we evaluated differences in NOTCH1 and N

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

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

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

263 Using bio-layer interferometry-based binding assays, we found that this antibody interacts wi

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

265 tion and fractionation methods, and in vitro binding assays, we mapped the Coy1 regions responsible f

266 Using immunoprecipitation and DNA-binding assays, we now show that the formation of mAKAPb

267 ss-subtype peptide microarrays and multiplex binding assays, we probed the magnitude and breadth of c

268 In direct binding assays, we show here that MA binds to Env CTs.

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

270 Using cryo-electron microscopy and binding assays, we show that S309 recognizes an epitope

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

272 proteins and surface plasmon resonance-based binding assays, we show that the MHC-Ib family furnishes

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

274 Competition binding assays were conducted with (3)H-PK11195 and the

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

276 s, radiochemistry, stability and radioligand binding assays were performed for the novel tracer (64)C

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

278 Mutagenesis and quantitative binding assays were then used to validate the crystallog

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

280 Radioligand binding assays were used to obtain structure-activity re

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

282 A direct peptide array-whole cell binding assay, where the peptides are conjugated to a ce

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

284 have also evolved to rapid, high-throughput binding assays, which have replaced often cumbersome and

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

286 Methods: In vitro binding assays with (18)F-BMS-986192 were performed on h

287 fibrils and viscous gels validated using dye-binding assays with amyloid-specific probes, congo red a

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

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

290 Quantitative binding assays with known and novel CIFs suggest that th

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

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

293 Competition binding assays with monoclonal antibodies isolated from

294 Binding assays with phage expressing NP41 confirmed bind

295 Binding assays with purified recombinant proteins showed

296 hook residues for binding, and quantitative binding assays with synthetic peptides presenting the HC

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

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

299 nels, can be used to perform single molecule binding assays without the need to directly label the an

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