ライフサイエンスコーパス: protein binding

1 mposition and oligonucleotide flexibility to protein binding.

2 been hindered by complexities unique to RNA-protein binding.

3 if bent DNA conformations are 'captured' by protein binding.

4 ecommendations exclude HD due to strong drug-protein binding.

5 gonized by C-rich motifs and correlated with protein binding.

6 decreased enhancer activity and differential protein binding.

7 tory factors, which interact through protein-protein binding.

8 ing to hCD80-positive tissue and high plasma protein binding.

9 rated in water/propanol mixing and in ligand/protein binding.

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

11 metalloproteinase and DNA deformations upon protein binding.

12 ively charged aptamers from the surface upon protein binding.

13 are generally unreactive unless activated by protein binding.

14 e kinetic measurement of fluorescent-labeled protein binding.

15 actory liver microsomes stability and plasma protein binding.

16 two conformations can significantly modulate protein binding.

17 regulated by a domain predicted to engage in protein binding.

18 reatment of drug toxicity due to strong drug-protein binding.

19 lf-life of 5.2 h, consistent with reversible protein binding.

20 cleosome disk participates only minimally in protein binding.

21 their effectiveness as low-MW competitors of protein binding.

22 ne methylation is a key regulator of protein-protein binding.

23 sensus predictors of disorder and disordered protein binding.

24 residues were necessary for efficient 14-3-3 protein binding.

25 ty, histone modification, transcription, and protein binding.

26 ing dsDNA while maintaining the integrity of protein binding.

27 ss of activity due to host cell, tissue, and protein binding.

28 Low protein binding (21%), large volume of distribution (190

29 icles was implemented to resist non-specific protein binding; 4) application of anti-PSA antibody mod

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

31 I&F was only slightly delayed by high plasma protein binding (94%-95%), and very low accumulation in

32 In allosteric proteins, binding a ligand can affect function at a dist

33 enhanced mechanical properties and preserved protein binding able to sustain, for over six weeks in v

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

35 The SSB-IDL fusions maintain DNA and protein binding activities in vitro, although cooperativ

36 causing zinc loss and inhibition of DNA and protein binding activities, leading to dyserythropoiesis

37 subset of LOTUS domains display both RNA and protein binding activities.

38 s mechanism of action; spectrum of activity; protein binding; activity in the presence of surfactant,

39 ively high log D(7.4) values and high plasma protein binding, adding to their stability.

40 ic lymph were 1.6- and 16.9-fold higher than protein binding-adjusted IC(90) (PA-IC(90)) of LPV for H

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

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

43 to complete a calculation framework for RNA-protein binding affinities, including a unified free ene

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

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

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

47 nd target related information (e.g. compound-protein binding affinity data).

48 mulations quantify protein diffusion and DNA-protein binding affinity, dependent on macromolecular de

49 TX attenuates ABI by converting inhibitory, protein-binding aggregates into nonbinding coaggregates,

50 tion and free-energy calculations of protein-protein binding, along with experimental validation, we

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

52 Using protein binding analyses and degradation assays with sub

53 ng non-canonical Wnt signaling via a novel G-protein binding and activating (GBA) motif.

54 1007 demonstrated significantly higher blood protein binding and bone uptake than the other tracers.

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

56 vivo performance may result from high plasma protein binding and extensive biliary excretion.

57 g the identification of chromatin-associated protein binding and genomic footprinting analysis from a

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

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

60 terol to PS ASOs and their effects on plasma protein binding and on enhancing ASO potency in the musc

61 irectly and indirectly (through irreversible protein binding and processing to the derived adducts) w

62 sphorylation of glutamate receptors mediates protein binding and receptor trafficking, ultimately con

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

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

65 -cellular localization, protein translation, protein binding and translation efficiency.

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

67 nd lung heparan sulfate potently block spike protein binding and/or infection by pseudotyped virus an

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

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

70 elle, with cytoplasmic and membrane-embedded proteins binding and diffusing according to distinct par

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

72 Ps crown pentons/hexons and mediate tegument protein binding, and CATCs bind and rotate all five peri

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

74 cular RNA-RNA kissing loop dimerization, RNA-protein binding, and intramolecular RNA tetraloop-tetral

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

76 as possible to increase solubility, decrease protein binding, and maintain the high antischistosomal

77 cts, in vivo antinociceptive effects, plasma protein binding, and metabolic stability.

78 is initiated by transient rather than stable protein binding, and the protein-RNA binding dynamics gr

79 Using this approach, protein-binding aptamers that otherwise have minimal eff

80 to characterize target-binding affinities of protein-binding aptamers.

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

82 ant and purified enzymes for prenylation and protein-binding assays, we demonstrate that SmgGDS-607 d

83 ments and their interaction through multiple protein-binding assays.

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

85 osing effects on ribosome binding, substrate-protein binding, ATPase activity and in vivo function, s

86 ion of nucleus ruptures, consistent with LEM-protein binding being a key function of BAF during membr

87 e against condensation and to visualise ParB protein binding by fluorescence.

88 e RI sensitivity was utilized to demonstrate protein binding by using bovine serum albumin and detect

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

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

91 cularly important: deformations arising from protein binding commonly fall within this range, but the

92 o shows significant improvements in imputing protein binding compared to the top models in the ENCODE

93 32/13 and mouse MIN6), and increased nuclear protein binding compared with the rs11708067-G allele.

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

95 these mutations have differential effects on protein binding depending on the domains in which they o

96 On cells, spike protein binding depends on both heparan sulfate and ACE2

97 The overall effect of methylation on protein-protein binding depends ultimately on the balance betwee

98 ng of the HS oligosaccharides that represent protein binding determinants.

99 he interplay between nascent RNA folding and protein binding determines the fate of transcripts remai

100 ake rate constant calculations (k(1)); (iii) protein binding (different calculations and measurement

101 spanning pore, and a lid strand comprising a protein-binding DNA aptamer to block the channel entranc

102 tion mechanism from nature, which uses decoy protein-binding DNA sites, named DNA sponge, to modulate

103 mutant lacking the Lap2, emerin, Man1 (LEM)-protein binding domain.

104 ng a defective mutation in Opn3's putative G protein-binding domain also exhibited a reduction in glu

105 tured C-terminal half of CHT7 with predicted protein binding domains, but not the canonical CXC DNA b

106 lecular recognition of glycosides, either by protein binding domains, enzymes, or synthetic receptors

107 intrinsically disordered proteins (IDPs) and protein binding domains.

108 ally, we demonstrate distinct roles for Zeb2 protein-binding domains, suggesting that Zeb2 partners c

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

110 inetics of expression, protein transport, or protein binding dramatically alter the distribution of t

111 utrophin) retains most of the structural and protein binding elements of dystrophin(5).

112 ain and STI1 motif (1-2) of Ubqln4 support J protein binding, essential for SV40 infection.

113 ion of variants at amyloid-beta A4 precursor protein-binding family B member 2 (APBB2; chromosome 4,

114 lization, dependence of KASH proteins on SUN protein binding for NE enrichment, and direct SUN-KASH b

115 yl groups, and experiments show that protein-protein binding free energies are sensitive to the exten

116 compute the effect of methylation on protein-protein binding free energies.

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

118 was complicated by our inability to uncouple protein binding from DNA condensation.

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

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

121 e frequencies but also their contribution to protein binding in a cellular context is applicable to o

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

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

124 expression of target genes via differential protein binding in cardiac cells, indicating that they a

125 NP, rs4730222, exhibits differential nuclear protein binding in electrophoretic mobility shift assays

126 Chimeric RNAs and clustered protein binding in fRIP and eCLIP experiments align with

127 ssociation constants for nonspecific protein-protein binding in the Kd ~ 10-mM regime.

128 s and decreased transcriptional activity and protein binding in vitro, providing a plausible molecula

129 en region is a fundamental task in analyzing protein binding intensity or chromatin accessibility.

130 eparan sulfate (HS) mediates a wide range of protein binding interactions key to normal and pathologi

131 h functions specified by atomic-level ligand-protein binding interactions.

132 al opening and creating the capsid auxiliary protein binding interface.

133 us mechanisms, including disruption of the G protein-binding interface, loss of protein stability, or

134 downstream responses through the canonical G-protein-binding interface.

135 s, or distorted variations) found at protein-protein binding interfaces.

136 changing a protein binding motif will alter protein binding, it has been shown that single nucleotid

137 Lastly, we discuss how ligand-protein binding kinetics are more appropriate than equil

138 further show that it is possible to quantify protein binding kinetics by counting the binding of indi

139 The modelling of protein-protein binding kinetics is important for the developmen

140 CI: 25%, 48%; 23 of 64 administrations) and protein-binding linear (31%; 95% CI: 1%, 94%; [one of se

141 Its high sensitivity to protein binding makes it particularly suitable for fragm

142 iched proteins binding strongly and depleted proteins binding marginally, while highlighting cooperat

143 We introduce the HT nextPBM (nuclear extract protein-binding microarray) approach to study DNA bindin

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

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

146 Here we use protein-binding microarrays (PBMs) to comprehensively an

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

148 effect of single nucleotide polymorphisms on protein binding might be under selection, with the non-r

149 ng extracellular matrix regulation, unfolded protein binding, mitochondrial function, and inflammator

150 tion surface, which greatly influences Spike protein binding mode.

151 Xist requires Repeat-A, a protein-binding module in its first two kilobases (2kb),

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

153 While it is clear that changing a protein binding motif will alter protein binding, it has

154 ition, revealing a new role for this protein-protein binding motif.

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

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

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

158 Lastly, we study real-time protein binding on ssDNA-SWCNTs, obtaining agreement bet

159 double bond appears to have no influence on protein binding or activity of ASO fatty acid conjugates

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

161 id-packing order during the initial stage of protein binding, or any further change during the insert

162 rgininamide, a ligand mimic of TAR's cognate protein binding partner Tat, is able to restore a native

163 in protein folding by describing a novel TPR-protein binding partner, Pgamma, and revealing that this

164 argininamide (ARG), a mimic of TAR's cognate protein binding partner, the transactivator Tat.

165 that LTs can modulate the activity of their protein-binding partner.

166 microRNA (miRNA) processing, the role of the protein binding partners in facilitating the requisite s

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

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

169 ls distinct cellular localizations, specific protein binding partners, and hundreds of microproteins

170 interaction between two basally colocalized protein binding partners.

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

172 o be inactive and to be poorly recognized by protein binding partners.

173 are essential to identify and validate novel protein binding partners.

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

175 bitors often function as molecular decoys of protein-binding partners or nucleic acid targets, while

176 We conclude that by complexing with their protein-binding partners TEP1 and Ro, respectively, thes

177 EZH2 can alter the affinity of EZH2 for its protein-binding partners to regulate cancer cell state t

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

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

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

181 0), "hydrolase activity" (NCSTN and XRCC6), "protein binding" (PICALM, STX4, GPNMB, VASP, extended-sy

182 relation to the static structure of a target protein binding pocket.

183 mphipathic alpha-helices predicted to form a protein-binding pocket and overlapping with minimal tran

184 bind, similar to small molecule occupancy of protein binding pockets, thus creating the potential to

185 y to form secondary structures and telomeric protein binding, pose a challenge to BIR and increase th

186 hemical properties and corresponding overall protein-binding potential of individual fragments.

187 information and can also be applied to other protein binding problems such as protein-DNA and protein

188 o show that at small separation, the protein-protein binding process contains two consecutive phases

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

190 Analysis of the plasma-protein binding profiles of the ASO-conjugates by size-e

191 es lighter coat color through changes in its protein binding properties.

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

193 By taking advantage of the inherent serum-protein-binding property of lipid motifs and their tende

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

195 ataxin-2, also known as Pbp1 (polyA binding protein-binding protein 1), is an intrinsically disorder

196 The Ras GTPase-activating protein-binding protein G3BP1 is a central regulator of

197 netic modifier cAMP-response element-binding protein-binding protein/p300 and thereby up-regulated TH

198 R signaling and the importance of lipid- and protein-binding proteins in regulating second messenger

199 nding (Q2 = 80 +/- 1%) and worst for protein-protein binding (Q2 = 69 +/- 0.8%).

200 ff-rate Modified Aptamer) nucleic acid-based protein-binding reagents allows for biomarker discovery.

201 betaarrs are known to act as adaptor proteins binding receptors and various effectors, but it

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

203 p90 are important for interaction with the J-protein binding region of DnaK.

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

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

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

207 howed distinct spatial clustering near known protein binding regions.

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

209 ro, with a genetic dissection of the protein-protein binding relationships that organize compartment

210 Our SCRIBER (SeleCtive pRoteIn-Binding rEsidue pRedictor) method takes advantag

211 proof-of-principle through the prediction of protein binding residues will be relevant for many other

212 incorporated FunFams into the prediction of protein binding residues.

213 Accurate predictions of protein-binding residues (PBRs) enhances understanding o

214 Knowledge of protein-binding residues (PBRs) improves our understandi

215 are over 30 sequence-based predictors of the protein-binding residues (PBRs).

216 tion elements and preventers of non-specific protein binding, respectively.

217 re the first layer generates a prediction of protein-binding, RNA-binding, DNA-binding and small liga

218 studies provide evidence for a non-catalytic protein-binding role for choline kinase alpha.

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

220 e modulated by several mechanisms, including protein binding, self-association, subcellular localizat

221 tic exploration of how a drug interacts at a protein binding site and allows for the rank-ordering of

222 site in the middle domain of Hsp90 and the J-protein binding site of Hsp70 in both E. coli and yeast.

223 y processes require the determination of the protein binding site structure, which can be achieved vi

224 est electrostatics-guiding DNA to a specific protein binding site-as the main driving force defining

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

226 between the ligand-binding pocket and the G-protein-binding site in the G-protein-coupled receptor s

227 s shifted by more than 20 angstrom and the G-protein-binding site is a shallow groove rather than a c

228 in the sorting of membrane lipids around the protein-binding site to prepare it for viral assembly.

229 gic receptor (beta(2)-AR), targeted at the G-protein-binding site, enhance Gs activation and cyclic A

230 compassing the ligand-binding site and the G protein-binding site.

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

232 cify the location, number, and strength of N-protein binding sites (valency).

233 e repeat sequences, self-chains, RNA binding protein binding sites and CpG islands within the flankin

234 bal structural features, such as RNA-binding-protein binding sites and reactivity differences at sing

235 s for understanding stacking interactions in protein binding sites and tuning their strength in the c

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

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

238 ing 63.5 muM ligands and 0.83 muM accessible protein binding sites, the signal enhancement provided b

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

240 genome-wide assays for nucleosome location, protein binding sites, three-dimensional interactions, a

241 to long ssDNA substrates containing multiple protein binding sites.

242 ChIP-seq) to obtain a genome wide profile of protein binding sites.

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

244 fied by peak calling correspond to annotated protein-binding sites and/or have stable predicted secon

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

246 The identification and characterization of protein-binding sites for ligands are crucial for the un

247 ternal flexibility to the polymer and forges protein-binding sites to ensure polymer function.

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

249 To develop mass spectrometry for mapping protein-binding sites, we implemented a new carboxyl gro

250 molecular recognition and the flexibility of protein-binding sites.

251 studies, support a mechanism for cooperative protein binding solely by DNA allostery.

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

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

254 SWCNTs, obtaining agreement between enriched proteins binding strongly and depleted proteins binding

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

256 DNA-protein binding studies showed RUNX1 binding to consensu

257 -OMe) modification at gap position 2 reduced protein-binding, substantially decreasing hepatotoxicity

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

259 Slow off-rate modified aptamer (SOMA) protein-binding technology was used to quantify 1310 kno

260 ork for further improvements in modeling RNA-protein binding that can be tested by prospective high-t

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

262 drophobic and van der Waals interactions for protein binding; they also use their main chain and side

263 methylation within the IRX2 gene body, CTCF protein binding, three-dimensional (3D) chromatin intera

264 ortions that are similar to those induced by protein binding-thus prepaying some of the energetic cos

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

266 ibited angiotensin-converting enzyme 2-spike protein binding to a greater degree than controls.

267 y (MRBLE-pep) that simultaneously quantifies protein binding to a library of peptides directly synthe

268 However, D614G does not alter S-protein binding to ACE2 or neutralization sensitivity of

269 SARS-CoV-2 spike protein binding to angiotensin-converting enzyme 2 (ACE2

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

271 onfirm that changes D510G and I529T reduce S protein binding to DPP4 but show that this reduction onl

272 that considers experimental data of protein-protein binding to generate a complex between GCase and

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

274 using experimental data for maltose binding protein binding to maltose, and for two carbonic anhydra

275 Quantification of protein binding to membrane proteins is challenging and

276 tion 1) (PIAS1) was identified as a cellular protein binding to N.

277 ELTA enables the biophysical measurements of protein binding to PAR of a defined length, detection of

278 Neither mutation modulated S protein binding to sialic acids, S protein activation by

279 Protein binding to small molecules is fundamental to man

280 ize the SARS-CoV-2 infection and block Spike protein binding to the ACE2 receptor, and biodistributio

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

282 CoV-2) infection begins with the viral spike protein binding to the human receptor protein angiotensi

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

284 ul for quantification of peripheral membrane protein binding to the PM in living cells.

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

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

287 such as TARP (transmembrane AMPAR regulatory protein) binding to alpha-actinin-stabilized PSD-95, and

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

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

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

291 relatively low aqueous solubilities and high protein binding values.

292 ers have utilized non-covalent chemistry for protein binding, very recently covalent engagement to no

293 ogy analysis of the adductome indicated that protein binding was a major function of adducted protein

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

295 er affinity for FAP in vitro, whereas plasma protein binding was higher for [(18)F]FGlc-FAPI.

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

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

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

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

300 ead led to enhanced AKAP (A-kinase anchoring protein) binding with preferential localization of the h