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1 treatment with the specific ADA inhibitor 2'-deoxycoformycin.
2 ndent on pharmacologic ablation of AAH by 2'-deoxycoformycin.
3 mycin is ribose, while it is deoxyribose for deoxycoformycin.
4 e, guanosine, and the picomolar inhibitor 2'-deoxycoformycin.
5 to malarial ADA complexes with adenosine or deoxycoformycin, 5'-methylthioribosyl groups are rotated
8 a 6-aminopurine source in the presence of 2'-deoxycoformycin, an inhibitor of adenine aminohydrolase
9 requirement for adenine or adenosine and 2'-deoxycoformycin, an inhibitor of parasite adenine aminoh
10 that exhibits an absolute requirement for 2'-deoxycoformycin, an inhibitor of the leishmanial adenine
11 ere performed to examine the binding of (8R)-deoxycoformycin and (8R)-coformycin to adenosine deamina
12 ns of mice treated with the ADA inhibitor 2'-deoxycoformycin (dCF) were elevated over 30-fold, sugges
14 much greater potentiating effect than did 2'-deoxycoformycin (DCF), although DCF is a more potent ADA
17 s treated with the specific ADA inhibitor 2'-deoxycoformycin exhibited features of the human disease,
18 axprt triple knock-out no longer required 2'-deoxycoformycin for growth and was avirulent in mice wit
19 n cannot proliferate indefinitely without 2'-deoxycoformycin or with hypoxanthine, guanine, xanthine,
20 es approximately 10(-13) M) (8R)-hydroxyl-2'-deoxycoformycin (pentostatin), a transition state analog
21 to determine the potential usefulness of 2'-deoxycoformycin (pentostatin), an inhibitor of adenosine
22 nosine and the adenosine deaminase inhibitor deoxycoformycin potentiated NT-induced Isc increase.
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