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 otein core by tunicamycin also increases the ligand binding affinity.

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

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

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

7 +/- 0.1 hr); and occurred with no change in ligand binding affinity.

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

9 glutaminase kinetic activity and allosteric ligand binding affinity.

10 orrelation between coordination geometry and ligand binding affinity.

11 other motifs are responsible for maintaining ligand binding affinity.

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

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

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

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

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

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

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

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

20 hypoglycosylation and reduced extracellular ligand-binding affinity.

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

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

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

24 of their electronic structure and different ligand binding affinities.

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

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

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

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

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

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

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

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

33 Undocking reduced ligand binding affinity allosterically and weakened the

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

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

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

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

38 Determination of ligand binding affinities and specificities of the gene

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 Ligand binding affinity, hormone-induced stimulation of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 Therefore, ligand binding affinity prediction needs to consider how

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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