ライフサイエンスコーパス: aminotriazole

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1 fers resistance to the histidine analogue, 3-aminotriazole.

2 2)O(2) and azide but not by hydroxylamine or aminotriazole.

3 like hydrogen peroxide or a prooxidant like aminotriazole.

4 e antagonized using the catalase inhibitor 3-aminotriazole.

5 and enhancers (deuterium oxide [D(2)O] and 3-aminotriazole [3-AT]) of oxidative damage, were also scr

6 tructure occur when genes are activated by 3-aminotriazole (3AT), an inducer of the transcriptional a

7 es in control cells and cells treated with 3-aminotriazole (3AT), an inducer of the transcriptional a

8 esponse to histidine starvation imposed by 3-aminotriazole (3AT).

9 ed by histidine starvation, using the drug 3-aminotriazole (3AT).

10 t of H(2)O(2) on ENaC P(o) was enhanced by 3-aminotriazole, a catalase inhibitor, and abolished by ov

11 Hypothyroidism was induced by aminotriazole administration.

12 e or pretreatment with a catalase inhibitor, aminotriazole, also affected BHA- and tBHQ-stimulated ER

13 catalatic activity of catalase, including 3-aminotriazole and azide, and inhibited by cyanide.

14 xide, whereas Yap2 activity is stimulated by aminotriazole and cadmium.

15 Leaky expression was eliminated using 3-aminotriazole and gene conversion was eliminated by usin

16 ZmMRP1 was induced by aminotriazole and to a lesser extent by menadione, where

17 H2O2 degradation, inhibition by boiling or 3-aminotriazole, and the approximate correspondence betwee

18 harmacological activity of a new series of 4-aminotriazoles as potent sigma1 receptor (sigma1R) ligan

19 minor phenotypes, including sensitivity to 3-aminotriazole, benomyl, and thiabendazole.

20 th this hypothesis, the catalase inhibitor 3-aminotriazole caused a significant increase in free radi

21 or mice treated with the catalase inhibitor aminotriazole, conditions in which intracellular steady

22 romoted the highest level of resistance to 3-aminotriazole (>100 mM) in constructs in which HIS3 was

23 vivo, using a rat model of goiter induced by aminotriazole, in which increased release of thyrotropin

24 ethylene or force and the catalase inhibitor aminotriazole induced ectopic cell death.

25 Aminotriazole, L-buthionine sulfoximine, and sodium azid

26 umoylation resulted in defective growth on 3-aminotriazole media and reduced basal and activated tran

27 In the absence of ETCBs, aminotriazole-mediated inactivation of catalase in PC-3

28 with the amino acid biosynthetic inhibitor 3-aminotriazole, or upon exposure to high concentrations o

29 or caf1 deletion suppressed the increased 3-aminotriazole resistance phenotype conferred by not muta

30 and mice treated with the catalase inhibitor aminotriazole, situations in which intracellular concent

31 In normal fibroblasts treated with aminotriazole to inhibit catalase, we found that peroxis

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