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1 ciation from the receptor, or elimination of receptor reserve.
2 d for TPalpha-Galpha13 and in the context of receptor reserve.
3 tor apparently depends on the degree of P2Y1 receptor reserve.
4 g the SH interval indicated a small (10-20%) receptor reserve.
7 least two effectors with distinct levels of receptor reserve and that differentially reflect recepto
9 HC variant weak agonists require significant receptor reserve, because decreasing the level of T cell
11 ed in IP assays performed after reduction of receptor reserve by the alkylating agent, phenoxybenzami
12 knockdown of MORs revealed that depletion of receptor reserve does not account for presynaptic resist
13 ffects on CCL3L1 affinity, although possible receptor reserve effects obscure complete interpretation
14 c and postsynaptic responses suggests that a receptor reserve exists for presynaptic inhibition, but
17 n in female rats such that there is a larger receptor reserve for morphine-mediated antinociception.
18 gonist and Furchgott analysis revealed a low receptor reserve for the activation of GIRK channels but
19 e to the existence of a greater A1 adenosine receptor reserve for the inhibition of beta-ICa,L than f
20 r the activation of GIRK channels but a >90% receptor reserve for the inhibition of Ca(2+) events.
21 t, these data suggest a substantial level of receptor reserve for the PI response in mouse hippocampu
25 assess whether differences in the degree of receptor reserve might explain this discrepancy of resul
27 that the IP response exhibited a much larger receptor reserve than the AA response, and reduction of
30 tivity to low-potency agonists by decreasing receptor reserve without significantly altering receptor
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