ライフサイエンスコーパス: protein binding

1 tubular dysfunction in CKD, irrespective of protein binding.

2 n, and reveals changes in the stem-loop upon protein binding.

3 re prompted us to explore the possibility of protein binding.

4 in modeling the sequence specificity of DNA-protein binding.

5 e interaction is independent of nucleocapsid protein binding.

6 f sulfates, is important for heparan sulfate protein binding.

7 bserved and show differential sensitivity to protein binding.

8 , after correcting for differences in plasma protein binding.

9 l-tRNA synthetases and play roles in tRNA or protein binding.

10 conditionally disordered regions in unfolded protein binding.

11 form a complex that is stabilized by client protein binding.

12 the contribution of the solvation factor in protein binding.

13 other organelles, have limited capacity for protein binding.

14 NA binding surface, which is the site of BET protein binding.

15 etic molecules to impose steric effects upon protein binding.

16 ADP-ribose) strand and competes with DNA for protein binding.

17 e been useful in discovering new ligands for protein binding.

18 metalloproteinase and DNA deformations upon protein binding.

19 ively charged aptamers from the surface upon protein binding.

20 are generally unreactive unless activated by protein binding.

21 e kinetic measurement of fluorescent-labeled protein binding.

22 actory liver microsomes stability and plasma protein binding.

23 )Tc-PSMA-I&S was observed due to high plasma protein binding (94%) of the tracer.

24 This peptide showed relative high plasma protein binding abilities and a human plasma half-life o

25 s with a Galphai2 mutation that disables RGS protein binding accumulated in the perivascular channels

26 , the SP concentrations exceeded >2-fold the protein binding-adjusted EC90 for wild-type HIV-1; for D

27 7% of the SP showed concentrations above the protein binding-adjusted EC90.

28 hen cabotegravir exposure was well below the protein-binding-adjusted 90% inhibitory concentration.

29 ty, GECX enables the capture of low-affinity protein binding (affibody with Z protein), elusive enzym

30 mutation for two specific problems: protein-protein binding affinities and protein thermal stability

31 Although 1129 and 5C4 had similar pre-F protein binding affinities, the 5C4 neutralizing activit

32 aving no detectable influence on the protein-protein binding affinities.

33 proach to calculate the magnitude of protein-protein binding affinities.

34 antibody 1129) matched for isotype and pre-F protein binding affinities.

35 We developed a method to measure protein binding affinity dependence on the topology (top

36 Sequence variants that alter protein binding affinity may cause significant perturbat

37 Since experimental determination of protein-protein binding affinity remains difficult when performe

38 ein's structure due to a mutation influences protein binding affinity to metabolites and/or drug mole

39 also, protein-bound solutes, exhibiting high protein-binding affinity and dependence on tubular secre

40 Accordingly, the protein-binding affinity was found to be slightly higher

41 high dependence on tubular secretion but low protein-binding affinity.

42 , solubility, in vitro clearance, and plasma protein binding also hold in transformation space, but t

43 onucleotides (MTOs) provide increased plasma protein binding and biodistribution to liver, and increa

44 It is a fundamental motif for protein binding and chromatin dynamics, but the cellular

45 in the biointerfacial sciences, specifically protein binding and conformational changes, lipid membra

46 ween the GPR motif and the RGS domain upon G protein binding and examined whether RGS14 can functiona

47 udinal lattice compaction associated with EB protein binding and GTP hydrolysis.

48 ify the structure of an intermediate for RNA-protein binding and illustrate a general strategy to ach

49 discover that lysine acetylation impairs Rho protein binding and increases guanine nucleotide exchang

50 ral core of the protein that are absent from protein binding and interactions.

51 However, a quantitative description of protein binding and nuclease activation at off-target DN

52 An increasing number of studies are mapping protein binding and nucleotide modifications sites throu

53 DNA transactions, as well as interfere with protein binding and recognition.

54 that increased motif accessibility improved protein binding and regulatory activity.

55 ral diversity, which is believed to underpin protein binding and regulatory properties.

56 Protein binding and reporter-based assays further demons

57 rt exquisite spatiotemporal control over its protein binding and signaling activities in T cells.

58 aphic observations are reinforced by protein-protein binding and single cell-based flagellar motor sw

59 tion causes cytoplasmic localization, 14-3-3 protein binding and the phorphorylation of a terminal ph

60 tations affect U8 expression, processing and protein binding and thus implicate U8 as essential in ce

61 e series, the block copolymer maximized both protein binding and translocation efficiencies, closely

62 Chemical modifications can affect protein binding and understanding ASO-protein interactio

63 estigate the role of sequence segregation on protein binding and uptake into Jurkat T cells and HEK29

64 and spatially regulated ribosomal protein (r-protein) binding and ribosomal RNA remodelling events in

65 Our findings reveal that G-protein-binding and activation mechanisms are fundamenta

66 r and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity.

67 osed PP-InsP signal transduction mechanisms: protein binding, and a covalent modification of proteins

68 ccharide is functionally active, can restore protein binding, and allows activation of cell signaling

69 tosis and degradation, triggered by Hedgehog protein binding, and causing reduced levels of Ihog/Boi

70 kidney extraction and excretion, low plasma protein binding, and high metabolic stability as prefera

71 ed to represent footprints of MAC1-dependent protein binding, and Mac1 expressed in bacteria binds RN

72 adverse events was associated with ionicity, protein binding, and macrocyclic structure.

73 broad range of molecular weights, moieties, protein binding, and polarities were selected.

74 ion suppressor assay we demonstrate that p65 protein-binding apical stem-loop of U12 snRNA can be rep

75 Changes in DNA photochemical reactivity upon protein binding are interpreted as being mainly induced

76 says designed to identify ligands that block protein binding are much more challenging to develop; at

77 sed that the DNA shape variations induced by protein binding are required in the early stage of the b

78 roanalytical approaches capable of detecting protein binding are welcome.

79 ene expression compensated for inefficient B protein binding, as did suppressing mutations within gen

80 By ELISA-based DNA-protein binding assay and conventional gel shift assay,

81 Furthermore, using a virus overlay protein-binding assay (VOPBA) in combination with far-We

82 Using an ELISA-based protein-binding assay, the interaction of recombinant ca

83 Here, we use protein binding assays and functional studies in Xenopus

84 uraged in recent years to embrace high speed protein binding assays.

85 n-translation methodologies and quantitative protein-binding assays, we explored the folding state of

86 ethods underscores a need to further discuss protein binding assessments as they relate to medicinal

87 reduced histone H3K79 methylation and N-Myc protein binding at the ODC1 and E2F2 gene promoters and

88 with the same chelate classification without protein binding, at 5.2 (95% CI: 4.5, 6.0) per 10 000 ad

89 This enhances DNA accessibility to protein binding by 3-fold.

90 ssor regulatory activity and allele-specific protein binding by transcription factors of the TCF/LEF

91 face-to-volume ratios and subsequently large protein binding capacities are of interest for advanced

92 ous, has a CADD score of 29.6, and increases protein binding capacity in silico.

93 and adsorbed to a porous membrane with high protein binding capacity.

94 A protein binding cascade is studied in real time and in t

95 wing the construction of Cas9 complexes with protein-binding cassettes, artificial aptamers, pools of

96 their likelihood of fitting into VQIVYK tau protein binding channel model.

97 he coat protein constitute the core of the B protein binding cleft.

98 This process depends on a G protein-binding cluster (GPBC) in the M3-M4 loop of the

99 32/13 and mouse MIN6), and increased nuclear protein binding compared with the rs11708067-G allele.

100 monstrate that deconvolution of membrane and protein binding contributions allows for improved struct

101 The large number of these functional protein binding correlations point to a dynamic and hete

102 cellular ASO-binding proteins and found that protein binding could affect ASO potency.

103 Competitive gel-shift assays suggested that protein binding depends not only on the triple-helical s

104 d involves an RNA domain highly similar to a protein-binding domain in the RNAs of RNase P/MRP.

105 fragment thereof was conjugated to a target protein-binding domain that was capable of binding to a

106 ) modestly inhibited interaction between the protein binding domains of HIF-1alpha and p300.

107 A screen for inhibitors of the protein binding domains of p300 (CH1) and HIF-1alpha (C-

108 HLJ1 protein directly bound to catalytic and protein-binding domains of Src through its amino acid Y1

109 odules, two of which correspond to predicted protein-binding domains.

110 ed for coding variants altering postsynaptic protein-binding domains.

111 showed that both steric effects and protein-protein binding each regulate the mobility of receptors

112 alistic solvation-based model for predicting protein binding energy to estimate quantitatively the co

113 rence spectrum, ascribed to specific aptamer-protein binding events occurring within the nanoscale po

114 tory status with well-positioned phasing for protein binding events.

115 compounds that can disrupt critical protein-protein binding events.

116 We propose that agonist and G protein binding facilitate the formation of these electr

117 By overexpressing the N protein binding fragment of Nsp9 in infected Marc-145 ce

118 identifying new binding modes, and studying protein binding from a mixture of equilibrating isomers.

119 assessment of membrane affinity to uncouple protein binding from membrane interactions.

120 nd, fusion kinase inhibition shifted adaptor protein binding from the fusion oncoprotein to EGFR.

121 GBCAs known to be associated with protein binding had a higher rate of reactions, at 17 (9

122 ell as a Src homology 3 (SH3) domain and a G protein-binding homology region 1 (HR1) domain.

123 ith the cochaperone 78-kDa glucose-regulated protein (binding immunoglobulin protein) involve the C t

124 Reconstitution of membrane-protein binding in a liposome assay shows that the mecha

125 rints to determine any k-mer's potential for protein binding in a specific cell type and how this may

126 differences in transcriptional activity and protein binding in hematopoietic cells.

127 We found higher translocator protein-binding in slow decliners than fast decliners, w

128 nown about the detail behavior of loops upon protein binding including allostery.

129 ound 2'-modifications significantly affected protein binding, including La, P54nrb and NPM.

130 amples for all studied compounds with a high protein binding index.

131 m of IRE1 activation that relies on unfolded protein binding-induced oligomerization.

132 with an affinity comparable with other tRNA-protein binding interactions and with a molecular ratio

133 The results support that the BH3-only protein binding interface of Bcl-xL is much more dynamic

134 tial intrinsic heterogeneity at its BH3-only protein binding interface.

135 onformational changes and formation of the G-protein-binding interface.

136 ents leading to a cytoplasmic crevasse for G-protein binding is less well defined.

137 se (IS), which encompass membrane mechanics, protein binding kinetics and motion, and fluid flow in t

138 r purposes, including other enzyme assays or protein-binding ligands.

139 ve models of TF binding specificity based on protein binding microarray (PBM) data for 68 mammalian T

140 When training on protein binding microarray (PBM) data, we use robust reg

141 To address this problem, we performed protein binding microarray experiments on representative

142 on published data generated using universal protein-binding microarray (PBM) technology, which provi

143 a modified bacterial one-hybrid system with protein-binding microarray and chromatin immunoprecipita

144 h-throughput experimental methods, including protein binding microarrays (PBM) and high-throughput SE

145 o benchmark datasets, derived from universal protein binding microarrays (uPBMs), genomic context PBM

146 ictions based on motifs from methods such as protein-binding microarrays (PBMs) and systematic evolut

147 sequences per protein using custom-designed protein-binding microarrays (PBMs).

148 t on DNA binding activity and used universal protein-binding microarrays to assay sequence-specific D

149 n immunoprecipitation sequencing (ChIP-seq), protein-binding microarrays, and transcriptomic approach

150 ARR DNA-binding motifs, determined by use of protein-binding microarrays, were enriched at ARR10 bind

151 te (WTX101) is an oral first-in-class copper-protein-binding molecule that targets hepatic intracellu

152 gineering strategy that incorporates a serum protein binding motif onto a covalent side-chain staple

153 This variant lies within the consensus SH3 protein-binding motif by which SHANK2 may interact with

154 ial interactions is crucial to understanding protein binding motifs and cellular function, that is, a

155 Secondary structure elements that surround protein-binding motifs are evolutionarily conserved.

156 volved in specific biological functions like protein binding, nucleoside binding, neuron projection,

157 Plasma protein binding of (18)F-FDS was low (<0.1%), and metabo

158 or PS/(S)-cEt ASOs, and imply that altering protein binding of ASOs using different chemical modific

159 r drug development have been the high plasma protein binding of lead structures, interspecies discrep

160 , ERK1/2-mediated phosphorylation and 14-3-3 protein binding of the cytoplasmic amino-terminus of iRh

161 ng a new approach that visualizes unlabelled protein binding on DNA with changes in DNA conformation

162 of proteins is ubiquitous but the effects of protein binding on IAPP aggregation are largely unknown.

163 -molecule method to simultaneously visualize protein binding on single DNA molecules and changes in D

164 ther protected from chemical modification by protein binding or characterized by a loss of structure.

165 -seq is a powerful technology to measure the protein binding or histone modification strength in the

166 detect genomic regions showing differential protein binding or histone modification.

167 ructure adopted in the complex is induced by protein binding, or is instead intrinsic to the DNA sequ

168 It is a curated database; each glycan-protein binding pair is associated with at least one pub

169 Venous blood was drawn to compare protein binding, parent fraction, and radiometabolite co

170 In this method, one protein binding partner is labeled with a fluorophore, t

171 e hit compounds do not resemble the natural (protein) binding partner of Mcl-1, nor do they resemble

172 ty by Ca(2+) , nucleotides, phosphorylation, protein binding partners and other cellular factors is t

173 g partner is labeled with a fluorophore, the protein binding partners are mixed, and then, the comple

174 DNA-tagged human kinases to identify ligand:protein binding partners out of 32096 possible combinati

175 time-resolved information and probe multiple protein binding partners simultaneously, using small amo

176 dies on the interaction of PAR with its many protein binding partners.

177 iated by interaction with different lipid or protein binding partners.

178 In this study, we report protein-binding partners of PABPN1, which could provide

179 sses through their interactions with various protein-binding partners.

180 one gene may drive reciprocal changes in its proteins' binding partners.

181 his analysis reveals distinct structural and protein binding patterns across both transcriptomes, all

182 at intrinsic sequence patterns between intra-protein binding peptide fragments exist, they can be ext

183 The intra-protein binding peptide fragments have specific and intr

184 meable derivative of a high-affinity HIV Rev protein-binding peptide.

185 to N-methylation for the purpose of morphing protein-binding peptides into more serum-stable and cell

186 lumen were enriched for cell components and protein binding, poly (A) RNA binding and RNA binding we

187 for a comprehensive characterization of the protein binding preferences and the subsequent design of

188 Ligand-protein binding processes are essential in biological sy

189 tional characteristics, such as a distinct G-protein binding profile and cell responses after agonist

190 a manually curated compendium of genome-wide protein binding profiles in our online resource PAD.

191 ASIT with great potential due to its unique protein-binding properties.

192 lpha), cyclic AMP-responsive element binding protein binding protein (CBP), steroid receptor coactiva

193 hosphorylates and activates poly(A)- binding protein binding protein 1 (Pbp1), which then inhibits TO

194 n protein (GSKIP) is a cytosolic scaffolding protein binding protein kinase A (PKA) and glycogen synt

195 CBP (CREB (cAMP responsive element binding protein) binding protein (CREBBP)) and P300 (adenovirus

196 ting and mutagenesis analysis indicates that protein binding proximal to regulatory features such as

197 ic time scale for fluid flow relative to the protein binding rate.

198 conventional hemodialysis; a high degree of protein binding reduces the free fraction of toxins and

199 st to the nanomolar affinity of the N-WASP G protein-binding region for Cdc42.

200 and an increase in the surface area of the G-protein-binding region.

201 generates precise assignments of disordered protein binding regions and that it compares well with o

202 ing regions on protein, 2) the prediction of protein binding regions on RNA, and 3) the prediction of

203 mely RPI-Bind, for the identification of RNA-protein binding regions using the sequences and structur

204 to annotate, visualize and compare predicted protein-binding regions derived from ChIP-seq/ChIP-exo-s

205 tial ternary complex between Cdc42 and the G protein-binding regions of TOCA1 and a member of the Wis

206 mutational cost to chromatin and regulatory protein binding, resulting in mutation hotspots at regul

207 t are highly represented: actin/cytoskeletal protein binding, RNA binding, RNA splicing/processing, c

208 s study demonstrates that judiciously chosen protein-binding scaffolds can be adapted to obtain metal

209 inding SCN ligands, we devised a biophysical protein binding screen to identify SCN ligands through d

210 ive is to describe applications of different protein binding site comparison approaches to outline th

211 duce the fundamental principles of different protein binding site comparison methods.

212 associated with these efforts is determining protein binding site information for potential therapeut

213 hydrophilic and hydrophobic features of the protein binding site.

214 essing fast ps-ns timescale motions at the G protein binding site.

215 s so far; this site spatially overlaps the G-protein-binding site in homologous receptors.

216 teraction profiles suggest the presence of a protein-binding site in HsDHN3 that coincides with the K

217 e introduced a mutation (IM-AA) into the CaS protein-binding site in the C-terminal domain of CaV2.1

218 ystallographic fragment screening to map the protein-binding site of the aspartic protease endothiape

219 face of the receptor to the intracellular G protein-binding site.

220 we call a DNA carrier, allows positioning of protein binding sites at nanometer accurate intervals al

221 We identified mutations in protein binding sites correlating with differential expr

222 s of protein complexes and clustered protein-protein binding sites into similarity groups based on th

223 The global organization of protein binding sites is analyzed by constructing a weig

224 model reveals that a subset of preferential protein binding sites is responsible for the observed ch

225 r with fully disordered regions also provide protein binding sites recognized by the respiratory sync

226 hod for rapid and accurate identification of protein binding sites utilizing benign, near-UV photoact

227 While some protein binding sites were selectively localized, others

228 rbohydrates typically have low affinities to protein binding sites, and the development of carbohydra

229 Starting merely from the locations of protein binding sites, our model accurately predicts the

230 nome-wide chromatin marks or DNA-interaction protein binding sites, there is not yet an integrated so

231 ssing the genome-wide spatial correlation of protein binding sites.

232 y with regard to the location of stabilizing protein binding sites.

233 g active genes and clusters of architectural protein binding sites.

234 s rely on peak calling algorithms that infer protein-binding sites by detecting genomic regions assoc

235 pping coding and non-coding transcripts, and protein-binding sites on the two complementary DNA stran

236 cooperation of G4 and the adjacent putative protein-binding sites within the 5' UTR was necessary an

237 ecessor with new modules to predict IDRs and protein-binding sites within them.

238 binding sites reduced the molar substrate-to-protein binding stoichiometry to ~1.

239 rlying variation in partner-specific protein-protein binding strength and recognition specificity.

240 r relationship between mating efficiency and protein binding strength for interactions with Kds rangi

241 fs resemble HEAT repeats, ubiquitous helical protein-binding structures, but their sequences are inco

242 Furthermore, in vitro DNA-protein binding studies and downstream analysis in yeast

243 RUNX1 binding to the PCTP promoter using DNA-protein binding studies and human erythroleukemia cells

244 Molecular dynamics and protein binding studies establish that PTHR and SNX27 in

245 DNA-protein binding studies showed RUNX1 binding to consensu

246 ounds can also serve as reporter ligands for protein binding studies, as exemplified by studying inte

247 ncludes residues that are also involved in J-protein binding, suggesting a functional interplay among

248 is distal from previously described DNA- and protein-binding surfaces of the core domain.

249 dosis controls displayed higher translocator protein-binding than controls, especially in the frontal

250 ding of its involvement in RNA, channel, and protein binding that modulate calcium signaling, activit

251 This m(6)A-dependent regulation of protein binding through a change in RNA structure, terme

252 Predicted IDRs are annotated as protein binding through a novel SVM based classifier, wh

253 l mechanism by which nucleosomes control DNA-protein binding through increasing protein dissociation

254 II light chain, S100A10), a multifunctional protein binding to 5-HT receptors, in layer II/III neuro

255 studies, supported by in silico modeling of protein binding to calcium and phosphate, showed that mo

256 ed that HEPC74 primarily blocks HCV envelope protein binding to CD81, while HEPC98 primarily blocks b

257 Protein binding to DNA molecules sparsely labelled with

258 putation in similar, large systems including protein binding to DNA, viruses, and membranes.

259 r preference for membrane order, we measured protein binding to giant unilamellar vesicles (GUVs) con

260 ed peanut and soy extracts were used to test protein binding to human monocyte-derived dendritic cell

261 n previously used to investigate peptide and protein binding to lipid membranes, as it allows for ver

262 Quantification of protein binding to membrane proteins is challenging and

263 of glycation, conformational alterations and protein binding to RAGE receptors were assessed by Congo

264 complex architecture alters the kinetics of protein binding to SecB and confers strong antifolding a

265 in immunoprecipitation demonstrated MADS-RIN protein binding to specific CArG motifs present in the p

266 s harbor mutations in LTBP4, which encodes a protein binding to TGF-beta.

267 We propose that Ets-2 expression and protein binding to the ARRE-2 of the IL-2 promoter are p

268 vealed elongation factor 1 alpha (EF1a) as a protein binding to the G-quadruplex sequence.

269 The subsequent changes in protein binding to the membrane or activation of K(+), C

270 assay that allows for direct measurement of protein binding to the plasma membrane inside living cel

271 Protein binding to the RNA scaffold can induce structura

272 immobilized protein assays showed that hrp48 protein binding to the silencer RNA can recruit hrp36 an

273 unknown if this facilitation involves direct protein binding to the tightly bent DNA loop or an indir

274 scription inhibitors, by inhibiting aberrant protein binding to the toxic RNA, and by acting as RNase

275 oding RNA genes, carry mutations that affect protein binding to their promoters and alter expression

276 ratios may depend on competitive BER and NER protein binding to these lesions.

277 Mechanistically, SRPK2 promotes SR protein binding to U1-70K to induce splicing of lipogeni

278 ion of a Gaussian chain (such as an unfolded protein) binding to a sequence of receptors with matchin

279 alysis was used to study the fraction of EMD proteins binding to collagen.

280 stem cells to HH signaling, we searched for proteins binding to GLI proteins, the transcriptional ef

281 Proteins binding to the cytoplasmic tail of L-selectin r

282 -ligand binding measurements and competitive protein binding, to simultaneously detect and quantify p

283 ved axial-element component Hop1 biases axis protein binding towards small chromosomes.

284 hese motifs strongly associate with KRAB-ZNF protein binding, TRIM28 recruitment, and specific histon

285 The mechanism for hPg/M protein binding uncovered here may facilitate targeting

286 nd could explain the overlap in translocator protein binding values between patients with Alzheimer's

287 ous kinetic solubility, and estimated plasma protein binding values in ranges predictive of good ADME

288 However, when protein binding was coupled to strand-displacement DNA s

289 d voxel-wise comparison, 18-kDa translocator protein-binding was higher in high affinity binders, mix

290 Translocator protein-binding was measured using a simple ratio method

291 Translocator protein-binding was positively correlated with Mini-Ment

292 sion, protein mislocalization, and reduced G protein binding were identified as likely mechanisms of

293 ell lines was reduced, solubility and plasma-protein binding were improved while retaining potent ant

294 ch as cellular exchange, pore formation, and protein binding, which are intimately related to cell fu

295 rgeting domain organization and phospholipid-protein binding, which has implications for the ongoing

296 that the quadruplex formation disrupts CTCF protein binding, which results in an increase in hTERT g

297 tering DNA templates on a flowcell, HiTS and protein binding with a GAIIx instrument, and finally dat

298 enables in vitro quantification of membrane protein binding with ligands.

299 rapped nucleosomes, and that PHF1 alters DNA-protein binding within the nucleosome by decreasing diss

300 olunteers, suggesting increased translocator protein binding (z > 4.72).