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1 cellular signal transduction and targeted as drug receptors.
2 inding can yield important information about drug-receptor and drug-drug interactions for a wide rang
3 ctural foundation for future optimization of drug-receptor binding and unbinding rates.
4 hich may be used for direct determination of drug-receptor binding interactions and for the rapid on-
5                                              Drug-receptor binding interactions of four agonists, ACh
6                       From DNA base pairs to drug-receptor binding, hydrogen (H-)bonding and aromatic
7 ane protein, was responsible for the altered drug-receptor binding.
8 on can be partially decoupled by varying the drug-receptor dissociation rate constant, k(off), and th
9 ould also aid drug discovery by establishing drug/receptor engagement.
10            These fundamental correlations on drug-receptor H-bond interactions may be generally usefu
11 r receptor exclusively activated by designer drug) receptor hM4Di in sensorimotor cortex and AAV-expr
12 r receptor exclusively activated by designer drugs) receptor hM4di abrogated spontaneous functional r
13 ropose that HERG inactivation stabilizes the drug-receptor interaction during membrane depolarization
14 nt for activity, but its precise role in the drug-receptor interaction has not been specifically inve
15 esses its receptor in the open pore, and the drug-receptor interaction is then stabilized by inactiva
16 e molecular mechanism of this double-faceted drug-receptor interaction may help in designing new ther
17 and in determining important elements of the drug-receptor interaction.
18 mbrane receptors provide valuable models for drug-receptor interactions across many important classes
19                                     Modeling drug-receptor interactions at the 3D level offers consid
20           This effect of a third molecule on drug-receptor interactions cannot be studied using tradi
21 ding sites, bound conformations and specific drug-receptor interactions for several allosteric modula
22  unnatural amino acid incorporation to probe drug-receptor interactions in functional G protein-coupl
23 d with studies using rabbit aorta to examine drug-receptor interactions in vascular smooth muscle.
24 d as an important factor in protein folding, drug-receptor interactions, and catalyst selectivities.
25 cokinetics, blood-brain barrier penetration, drug-receptor interactions, heavy metal toxicity, pharma
26 variation may be secondary to differences in drug-receptor interactions, patient's compliance and tol
27 he understanding of the structural bases for drug-receptor interactions.
28 alignments from SQ are consistent with known drug-receptor interactions.
29                                              Drug receptor kinetics is as a key component in drug dis
30  signaling in the translational control of a drug receptor KOR, which involves the mediator of netrin
31 ontributions of F1764 and Y1771 to a complex drug receptor site in the pore of Na+ channels.
32 residues that are analogous to the mammalian drug receptor site, and the lateral pore fenestrations.
33  receptors exclusively activated by designer drugs) receptors, we enhanced Gi/o- or Gs-protein-mediat

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