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1 significantly inhibits CaSR activity via non-competitive antagonism.
2 rine in quantitative agreement with complete competitive antagonism.
3 sible to modifying reagents and resistant to competitive antagonism.
4 ntial for allosterism but preferred only for competitive antagonism.
5 enhancement might be distinct from those for competitive antagonism.
6 ns of suramin are not consistent with simple competitive antagonism.
7 nse curve, consistent with the properties of competitive antagonism.
8 ther by reduction of available hormone or by competitive antagonism.
9  two different mechanisms; that is, a direct competitive antagonism and an apparently insurmountable
10 HR localization studies were consistent with competitive antagonism and blockade of nuclear transloca
11 toxin inactivates the 5-HT3 receptor through competitive antagonism and is a highly selective inhibit
12                        Little is known about competitive antagonism at physiological temperatures.
13                 Schild analysis demonstrated competitive antagonism between thioperamide and both clo
14                                              Competitive antagonism by bismuth subnitrate moderately
15 iperazinium, cytisine, and suberyldicholine; competitive antagonism by dihydro-beta-erythroidine, dec
16 a a mechanism independent of MSH and MC3/4-R competitive antagonism, consistent with either inverse a
17 ners; 2) gated importation by the thymus; 3) competitive antagonism for intrathymic niches; 4) tempor
18 ascorbic acid inhibited HPA activity via non-competitive antagonism from two allosteric sites, by cha
19 utions to common developmental pathways, and competitive antagonism governing downstream gene express
20  binding to apoferritin may be suggestive of competitive antagonism; however, this was not supported
21  functional relationship between agonism and competitive antagonism in the Cys-loop receptors, provid
22 uti in vivo represent a bipartite mechanism: competitive antagonism of agonist binding by the carboxy
23 of T cell activation: negative signaling and competitive antagonism of CD28:B7-mediated costimulation
24 at lack all neuronal MSH, thereby precluding competitive antagonism of MC-R by AgRP.
25  and all forms of Agrp tested, act solely by competitive antagonism of melanocortin action.
26           This result is consistent with the competitive antagonism of midazolam binding.
27                                Despite their competitive antagonism of NOS, M144V, like SCaM-1, exhib
28 ermeation and channel closure results from a competitive antagonism of protons at an intracellular Ca
29 ti's antilipolytic effect is exerted through competitive antagonism of the ACTH receptor (MCR-2).
30       The 12 most potent compounds displayed competitive antagonism of the human EP2 receptor with K(
31              These results describe specific competitive antagonism of the P2Y1 receptor by an adenin
32 e GIP binding site on the GIPr ECD, ensuring competitive antagonism of the receptor.
33                                              Competitive antagonism of TLR8 with non-targeting locked
34 s CBP and p300 have previously unrecognized, competitive antagonism to each other.
35 or mitochondria from the five strains due to competitive antagonism with molecular oxygen at complex