ライフサイエンスコーパス: ligand-binding affinity

1 CAM, but not the CCR2-CAM had a reduction in ligand binding affinity.

2 e inhibition without substantially affecting ligand binding affinity.

3 contains an on/off switch that regulates its ligand binding affinity.

4 f divalent cation binding sites that control ligand binding affinity.

5 taining the structural form with the highest ligand binding affinity.

6 +/- 0.1 hr); and occurred with no change in ligand binding affinity.

7 city, calcium dependent adaptation of T-site ligand binding affinity.

8 glutaminase kinetic activity and allosteric ligand binding affinity.

9 complexities with enhanced biostability and ligand binding affinity.

10 les for each target to validate the receptor-ligand binding affinity.

11 oach, named DeepDTAF, to predict the protein-ligand binding affinity.

12 otein core by tunicamycin also increases the ligand binding affinity.

13 ptor response without substantially altering ligand binding affinity.

14 tatus, thermostability, enzyme activity, and ligand binding affinity.

15 he receptor to agonists without changing the ligand binding affinity.

16 orrelation between coordination geometry and ligand binding affinity.

17 other motifs are responsible for maintaining ligand binding affinity.

18 coring functions made a useful prediction of ligand binding affinity.

19 or for these mutants fails to correlate with ligand binding affinity.

20 the amino terminus caused a reduction in the ligand binding affinity.

21 ory potency, it caused a dramatic decline in ligand binding affinity.

22 n with decreases in receptor mobility and in ligand-binding affinity.

23 ese constraints are released, thus enhancing ligand-binding affinity.

24 ing pocket without affecting the equilibrium ligand-binding affinity.

25 ity, substrate specificity, processivity and ligand-binding affinity.

26 hypoglycosylation and reduced extracellular ligand-binding affinity.

27 tified variants with enhanced expression and ligand-binding affinity.

28 at levels of cell growth correlate well with ligand-binding affinity.

29 ultimers, thereby reducing multimer size and ligand-binding affinity.

30 ligand levels, integrin levels, and integrin-ligand binding affinities.

31 suggests variable impacts of fatty acids on ligand binding affinities.

32 e properties, RNA 3D structures, and protein-ligand binding affinities.

33 of their electronic structure and different ligand binding affinities.

34 ol the aptamers' pre-folded states and their ligand binding affinities.

35 s contain mutations that result in increased ligand binding affinities.

36 ns on transactivation stem from differential ligand-binding affinities.

37 rential calcium ion dependence of calmodulin ligand-binding affinities, a system at the focal point o

38 te that GCPNet's predictions (1) for protein-ligand binding affinity achieve a statistically signific

39 Increased integrin ligand binding affinity (activation) is triggered by int

40 lin binding to integrin beta tails increases ligand binding affinity (activation).

41 Rapid modulation of ligand binding affinity ("activation") is a central prop

42 The rapid modulation of ligand-binding affinity ("activation") is a central prop

43 Undocking reduced ligand binding affinity allosterically and weakened the

44 bit thermoresponsiveness and (2) the protein-ligand binding affinities and dissociation rate constant

45 nce of two principal isoforms that differ in ligand binding affinities and in the packing of the aden

46 can be used as biosensors to measure protein-ligand binding affinities and kinetics with sensitivitie

47 how these heme pocket residues regulate the ligand binding affinities and physiological functions of

48 (TopologyNet) for the predictions of protein-ligand binding affinities and protein stability changes

49 Determination of ligand binding affinities and specificities of the gene

50 rrelate very well with those provided by the ligand binding affinities and the dissociation constants

51 ents between experimentally measured protein-ligand binding affinities and those predicted by the DFI

52 atures are greatly needed to predict protein-ligand binding affinity and accelerate the drug discover

53 tors contain an on/off switch that regulates ligand binding affinity and cell adhesion.

54 fected cells a nonglycosylated receptor with ligand binding affinity and coupling characteristics alm

55 We analyzed these proteins for ligand binding affinity and decay acceleration activity

56 ts in two forms: trans Pro300 SthK with high ligand binding affinity and fast activation, and cis Pro

57 plays a critical role in regulating integrin ligand binding affinity and function.

58 clic nucleotide binding domain in modulating ligand binding affinity and intramolecular communication

59 e help of a PEG spacer without affecting the ligand binding affinity and maintaining the stability of

60 well supported by virtual screening based on ligand binding affinity and molecular dynamic simulation

61 ional changes that include the modulation of ligand binding affinity and molecular extension.

62 ACTH(1-24) caused a significant decrease in ligand binding affinity and potency.

63 t individual residues in TM2 and TM5 play in ligand binding affinity and selectivity.

64 and the S252L/A315S double mutation on FGFR2 ligand binding affinity and specificity using surface pl

65 ns in FGFR2b also enhance and violate FGFR2b ligand binding affinity and specificity, respectively.

66 To determine the mechanism regulating ligand binding affinity and specificity, soluble FGFR1 a

67 influence of such functional groups on CYP2B ligand binding affinity and specificity.

68 distribution of nascent adhesions depend on ligand binding affinity and strength of pairwise interac

69 y suppressed in M phase due to a decrease in ligand binding affinity and the inability of epidermal g

70 ected by AR poly(Q) variation, we found that ligand binding affinity and the ligand-induced NH(2)- to

71 we review functional rationale from observed ligand-binding affinities and mutagenesis effects.

72 ted to predict protein-ligand binding sites, ligand-binding affinity and binding pose (conformation)

73 membrane-proximal domains modulate receptor ligand-binding affinity and dimerization efficiency.

74 Here, recent measurements of the intrinsic ligand-binding affinity and free energy of each integrin

75 s to membrane cholesterol with regard to the ligand-binding affinity and functional properties, inclu

76 Here, we reveal important differences in ligand-binding affinity and GC activity between mouse GC

77 ions alter receptor conformation to increase ligand-binding affinity and provide signaling in respons

78 These differences are not due to ligand-binding affinity and receptor abundance.

79 determining the integrin activation status, ligand-binding affinity and the type of ECM signals that

80 adhesion is regulated by changes in integrin ligand-binding affinity and valency through inside-out s

81 ype I, II, and III InsP3 receptors differ in ligand-binding affinity and whether such differences inf

82 Regarding doubly-functionalized ligands, binding affinity and stabilizing ability of Amt

83 The spectroscopic properties, ligand binding affinities, and steady-state kinetics of

84 s in the receptor has a nontrivial effect on ligand binding affinity, and suggest that such regions m

85 ptor subtypes differ in tissue distribution, ligand-binding affinity, and coupling to intracellular s

86 cell integrin expression level, and integrin-ligand binding affinity-are all quantitatively predictab

87 l penalties can be major determinants of RNA-ligand binding affinity as well as a source of binding c

88 catalytic activity and altered substrate or ligand binding affinity, as well as enabling the design

89 nt displayed depressed (3-fold) 1,25-(OH)2D3 ligand binding affinity at 4 degrees C, in vitro, althou

90 contrast to EGFR (ErbB1), ErbB3 retains high ligand binding affinity at an endosome-comparable pH in

91 a negatively cooperative model in which the ligand-binding affinity at either binding site in an EGF

92 oach is presented that estimates the protein-ligand binding affinity based on the given 3D structure

93 ens dimerization of LC8 and thus its overall ligand-binding affinity, because only the dimer binds li

94 The accurate prediction of protein-ligand binding affinity belongs to one of the central go

95 y can be implemented through differentiating ligand binding affinities between resting and active sta

96 vestigated whether the 10-fold difference in ligand-binding affinity between the mAHR and hAHR would

97 tor activation without a major effect on the ligand-binding affinities, but the Y273F mutant receptor

98 resource consuming to determine the protein-ligand binding affinity by experiments.

99 the hybrid-I-like domain interface increases ligand-binding affinity by mutationally introducing an N

100 endogenous ligand, GPR174 mutants with lower ligand binding affinities can be specifically activated

101 ye to monitor protein thermal unfolding, the ligand-binding affinity can be assessed from the shift o

102 ins annotations on: ligand-binding residues, ligand-binding affinity, catalytic sites, Enzyme Commiss

103 red to the wild type allele by measuring its ligand binding affinity, CCL2 scavenging efficiency, and

104 S-DPN (2), and we have compared the in vitro ligand binding affinities, coactivator binding affinitie

105 ome ligands showed good correlations between ligand binding affinity, coactivator binding affinity, a

106 trapped high-energy state displayed improved ligand binding affinity, compared with the wild-type enz

107 redictions is the common assumption that the ligand binding affinity contributions of noncovalent int

108 the half-bent conformation, indicating that ligand-binding affinity does not depend on conformation,

109 domain (betaPS-b58; V409D) greatly increased ligand binding affinity, explaining the increased cell s

110 d mutagenesis and evaluation of the relative ligand binding affinities for the mutant AhRs.

111 human GnRH receptor allosterically increased ligand binding affinity for GnRH II but had little effec

112 activation similar to the reductions seen in ligand binding affinity for HU210.

113 e from full to partial to none decreases the ligand binding affinity for human IgG1 (hIgG1) but incre

114 dence that the wild-type TSHR TMD influences ligand binding affinity for the ECD, possibly by alterin

115 ompetitive (direct) antagonists; 2) decrease ligand binding affinity for VLA-4 approximately 2 orders

116 We demonstrated a clear correlation between ligand-binding affinity for MR1, the presence of a coval

117 A novel scoring function to estimate protein-ligand binding affinities has been developed and impleme

118 Whereas protein-ligand binding affinities have long-established prominen

119 Ligand binding affinity, hormone-induced stimulation of

120 tuations: (i) can be effective modulators of ligand-binding affinities, (ii) are important determinan

121 time in-cell (19)F NMR that allows measuring ligand binding affinities in human cells by competition

122 populations of NMDA receptors with different ligand binding affinities in obese mice.

123 s provided evidence for the complete loss of ligand binding affinity in the transition state, indicat

124 correlation between measured and calculated ligand binding affinities including the free energy chan

125 The chimeric protein exhibited a cellular ligand binding affinity indistinguishable from that of t

126 es predictive of varying degrees of receptor-ligand binding affinities influence clinical outcomes in

127 (outside-in signaling) and for activation of ligand binding affinity (inside-out signaling).

128 was achieved via rapid and accurate protein-ligand binding affinity interaction studies which were p

129 Our prediction of ligand binding affinities is also in agreement with the

130 Rapid and accurate estimation of protein-ligand binding affinities is crucial for early-stage dru

131 tated to alanine, a significant reduction in ligand binding affinity is observed in the presence of W

132 ses, allowing the determination of essential ligand binding affinities (K(D)).

133 etry (AS-MS) method for quantitative protein-ligand binding affinity (Kd) measurements in large compo

134 rat HNF-4alpha1 has a crucial impact on the ligand binding affinity, ligand specificity and secondar

135 ed markedly lower surface expression, normal ligand binding affinity, markedly lower G-protein coupli

136 sion/clustering (rather than through altered ligand binding affinity) may be highly relevant towards

137 mine experimentally the relation between the ligand binding affinities measured in solution and the d

138 hod provides chemical information to protein/ligand binding affinity measurements.

139 , locating small molecule binding, measuring ligand-binding affinity, monitoring protein folding and

140 latest methods in the prediction of protein-ligand binding affinities, mutation induced globular pro

141 imulating hormone (TSH)-induced reduction in ligand binding affinity (negative cooperativity) require

142 tion in Chinese hamster ovary cells enhanced ligand binding affinity, not valency, and did not alter

143 The differences in ligand binding affinities observed in this study are pos

144 Here, we present crystal structures and ligand binding affinities of periplasmic binding protein

145 e did not correlate with previously reported ligand binding affinities of the EDCs.

146 ophila alphaPS2betaPS integrins to probe the ligand binding affinities of these invertebrate receptor

147 647-labeled conjugate allowed measurement of ligand binding affinities of unlabeled hA(2A)AR antagoni

148 e plasmon resonance showed a NOTA-conjugated ligand binding affinity of 1 nM.

149 CHT1 mediated choline uptake by reducing the ligand binding affinity of CHT1 without significantly al

150 Cellular regulation of the ligand binding affinity of integrin adhesion receptors (

151 They explain the observed variability in the ligand-binding affinity of a GPCR when coupled to differ

152 Quantitative estimates of the ligand-binding affinity of human and rat AhR were obtain

153 f the region did not significantly alter the ligand-binding affinity of RXR at equilibrium.

154 signal transduction, IL-2Ralpha controls the ligand-binding affinity of the receptor complex.

155 hat covalent adaptation primarily alters the ligand-binding affinity of the receptor off-state (K(D1)

156 dels in which covalent adaptation alters the ligand-binding affinity of the receptor on-state, the ma

157 of water for protein carboxylate or thiolate ligands, binding affinities of 50-250 microM, and a slow

158 which cannot be explained based upon altered ligand binding affinity or receptor number.

159 zation, and downregulation, without changing ligand binding affinity or receptor-G protein coupling.

160 been shown to have no significant effect on ligand-binding affinity or cooperativity, or on spectros

161 chine learning scoring functions for protein-ligand binding affinity prediction have been found to co

162 Therefore, ligand binding affinity prediction needs to consider how

163 used as the local input feature for protein-ligand binding affinity prediction.

164 e responsible for the broad diversity of TLR ligand-binding affinity, providing a testable hypothesis

165 zation of scoring functions based on protein ligand-binding affinity rather than structural stability

166 -promoted down-regulation, without affecting ligand binding affinity, receptor-G protein coupling, or

167 Predicting absolute protein-ligand binding affinities remains a frontier challenge i

168 unction, even when the overall structure and ligand-binding affinity remains unaltered.

169 nduced integrin conformational unbending and ligand-binding affinity revealed conditions under which

170 and ModE, it is possible to speculate about ligand-binding affinities, selectivity and evolution.

171 ing remote residues that induce differential ligand binding affinity shifts for GnRH I and II.

172 Thermal shift assays used to measure ligand binding affinity show that the binding of LA is s

173 N terminus of the GFP did not alter receptor ligand binding affinity, signal transduction, or the pat

174 vs double-stranded DNA) and defined protein-ligand binding affinities spanning >10 orders of magnitu

175 nt improvements recently reported in protein ligand binding affinity, stability, expression and enzym

176 rrelation between charge/dipole polarity and ligand binding affinity, structure-function studies were

177 mined their surface expression of FPR, their ligand binding affinity, their G-protein coupling, and t

178 entified mutations which specifically affect ligand binding affinity thus aiding the definition of re

179 gical phosphorylation by MAP kinase, reduces ligand-binding affinity, thus negatively regulating the

180 n-line chromatographic determination of drug/ligand binding affinities to the immobilized opioid rece

181 nant of ligand physiochemical properties and ligand binding affinity to a biological transporter.

182 we developed an approach for quantifying the ligand binding affinity to the beta-end of the Hb centra

183 l framework for the determination of protein:ligand binding affinities together with the comprehensiv

184 teins are now known to modulate the in vitro ligand binding affinity, trafficking, and second messeng

185 ool in drug discovery for predicting protein-ligand binding affinities, transport properties, and poc

186 old higher than the parental cells, with the ligand binding affinity unchanged.

187 tant exhibited a modest decrease (4-fold) in ligand binding affinity using the fluorescent probe 1-an

188 Changes in ligand-binding affinities via molecular mechanics/genera

189 a quantitative, cell-free, assessment of MR1 ligand-binding affinity was lacking.

190 mational changes in the receptor that alters ligand binding affinities, we have obtained additional c

191 Phospholipase C signaling and ligand-binding affinity were reduced by carboxyl (C)-ter

192 iversity around these residues modulates TCR ligand-binding affinities, whereas V gene usage correlat

193 dy reveals that IFNAR1 flexibility modulates ligand-binding affinity, which, in turn, regulates biolo

194 assay permits straightforward measurement of ligand-binding affinities with receptor-either in vitro

195 erged enthalpy and entropy estimates produce ligand binding affinities within 1.5 kcal/mol of experim

196 Accurate predictions of ligand binding affinities would greatly accelerate the f

197 These mutants possess the highest monovalent ligand-binding affinity yet reported for an engineered p