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1 yldopamine, N-acetyloctopamine (naOA), and N-acetylserotonin.
2 inistration of the BH4 synthesis inhibitor N-acetylserotonin (15 mg/kg IV) before the 30-minute occlu
4 melanocyte samples acetylated serotonin to N-acetylserotonin and tryptamine to N-acetyltryptamine.
5 ditionally, inhibitors such as dicoumarol, N-acetylserotonin, and indomethacin blocked sepiapterin re
6 ry to produce and metabolize serotonin and N-acetylserotonin, and its activity is determined by topog
7 cholesterolemic rabbits, pretreatment with N-acetylserotonin completely abolished the ischemic PC-ind
9 nt, and four analytes; N-acetyloctopamine, N-acetylserotonin, N-acetyltyramine, and N-acetyldopamine
12 etyl-N2-formyl-5-methoxykynuramine (AFMK), N-acetylserotonin (NAS), and 5-methoxytryptamine (5-MT).
13 er skin to 3H-metabolites corresponding to N-acetylserotonin (NAS), melatonin, and 5-methoxytryptamin
15 alkylamine N-acetyltransferase (AANAT) and N-acetylserotonin O-methyl transferase (ASMT), two enzymes
16 e terminal enzyme for melatonin synthesis, N-acetylserotonin-O-methyltransferase (ASMT), was cloned f
17 acetyl octopamine, N-acetyldopamine, naTA, N-acetylserotonin, OA, dopamine, tyramine, and serotonin a
18 in (or tryptamine) with acetyl-CoA to form N-acetylserotonin (or N-acetyltryptamine) and is responsib
21 MT, EC 2.1.1.4) catalyzes the methylation of acetylserotonin to complete the synthesis of melatonin i
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