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1 d be blocked by cotreatment with SQ22536 (an adenylate cyclase inhibitor).
2 ated by dideoxyadenosine (5 nmol; n = 4), an adenylate cyclase inhibitor.
3 nosine monophosphate (cAMP); addition of the adenylate cyclase inhibitor 2',5'-dideoxyadenosine to th
4 ry when the preparation was pre-treated with adenylate cyclase inhibitors 2',3'-dideoxyadenosine (DDA
5 8-bromo-cAMP, and was blocked by H89 or the adenylate cyclase inhibitor 9-(tetrahydro-2-furanyl)-9H-
6 s or amiloride; treatment with either of two adenylate cyclase inhibitors; and application of AMP-PNP
7 en pre-treatment was with a guanylate and an adenylate cyclase inhibitor combined, NO donors had no e
8 as with a guanylate cyclase inhibitor and an adenylate cyclase inhibitor combined; in that situation,
10 h the MAPK specific inhibitor (U0126) or the adenylate cyclase inhibitor dideoxyadenosine (ddA) aboli
13 zed by pretreatment with protein kinase A or adenylate cyclase inhibitors, H89 and di-deoxyadenosine,
14 ase inhibitor methylene blue (M-BLU) and the adenylate cyclase inhibitor MDL combined; or (iv) the ni
17 lin-1-one (ODQ) or cystamine (CYS); (ii) the adenylate cyclase inhibitors nicotinic acid (NIC-A), 2',
18 ibitory only when pre-treatment was with the adenylate cyclase inhibitors nicotinic acid (NIC-A), 2',
19 -kappaB activation, and dideoxyadenosine, an adenylate cyclase inhibitor, prevented the hCG effect on
20 -chelators, Fe++-chelator, CYP450 inhibitor, adenylate cyclase inhibitor, protease inhibitors, and ni
21 urthermore, pretreatment of ganglia with the adenylate cyclase inhibitor SQ 22, 536, or the phosphodi
22 imic or occlude clonidine's actions with the adenylate cyclase inhibitor SQ 22536 nor with the non-sp
25 uppression of mitogenesis is reversed by the adenylate cyclase inhibitor SQ22536, and implicates cAMP
31 se effects are reduced in the presence of an adenylate cyclase inhibitor, yet persist in the presence
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