ライフサイエンスコーパス: dicoumarol

1 uld be partially reversed by NQO1 inhibitor, dicoumarol.

2 f protein activity by pretreating cells with dicoumarol.

3 wn through the use of the inhibitor of NQO1, dicoumarol.

4 ns of coumarin compounds, we discovered that dicoumarol (a coumarin anticoagulant; 3,3'-methylenebis[

5 Several quinone reductases are inhibited by dicoumarol, a coumarin derivative.

6 The treatment of wild-type cells with dicoumarol, a known inhibitor of NQO1, also abolished TN

7 The incorporation of dicoumarol, a potent inhibitor of DT-diaphorase, interfe

8 ignaling cascades in activation of NFkappaB, dicoumarol also blocked NFkappaB activation in primary m

9 Dicoumarol, an NAD(P)H-dependent quinone oxidoreductase

10 Inhibition of adduct formation by dicoumarol, an NQO1 inhibitor, supported this finding an

11 f NQO1 inhibition and off-target effects for dicoumarol and its derivatives suggests that the ability

12 the antiproliferative mechanism of action of dicoumarol and possibly related pharmacophores may be me

13 more, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro

14 of NTR and its complexes with the inhibitor dicoumarol and three dinitrobenzamide prodrugs.

15 essed for off-target effects associated with dicoumarol and were found to have differing effects on s

16 The inhibitor dicoumarol appears to bind primarily by pi-stacking inte

17 We found that dicoumarol binds to bovine brain tubulin with a K(d) of

18 Dicoumarol blocked both the apoptotic responses and leth

19 Dicoumarol, Cibacron blue, chrysin, 7,8-dihydroxyflavone

20 Dicoumarol, currently in clinical use as an oral anticoa

21 E4, human PC5/6 and human PC7), showing that dicoumarol derivatives might be developed as either gene

22 tion, that cellular superoxide production by dicoumarol does not seem linked to NQO1 inhibition but m

23 NQO1- cells (H596, IMR-90) or dicoumarol-exposed NQO1+ A549 cells were resistant (LD50

24 The binding orientations of dicoumarol, flavones, and phenindone in the active site

25 This activity was cofactor independent and dicoumarol insensitive.

26 r studies generated results that explain why dicoumarol is a potent inhibitor and binds differently f

27 sign target and superoxide generation as the dicoumarol-mediated mechanism of cytotoxicity.

28 Additionally, inhibitors such as dicoumarol, N-acetylserotonin, and indomethacin blocked

29 y beta-lap was blocked by the NQO1 inhibitor dicoumarol or the PARP-1 inhibitor DPQ.

30 while a combination of FAD and the inhibitor dicoumarol overcome these alterations.

31 Dicoumarol prevented SAPK activation in vivo by chemical

32 Dicoumarol reduces the rate and extent of shortening, it

33 The concentration of dicoumarol required for inhibition of NQO1 varies accord

34 ituted with the NQO1 gene displayed relative dicoumarol resistance.

35 e that exposure to combinations of Taxol and dicoumarol results in a synergistic inhibition of cell d

36 activation of the former involved largely a dicoumarol-sensitive activity, whereas that of the latte

37 BZQ was not a substrate for the dicoumarol-sensitive enzyme in HCT116 cells.

38 t cancer cell lines, and the NQO1 inhibitor, dicoumarol, significantly protected NQO1-expressing cell

39 ductase, NQO1, displayed hypersensitivity to dicoumarol stress inhibition, whereas SAPK in cells reco

40 In addition, dicoumarol strongly potentiated TNFalpha-induced apoptos

41 with a K(d) of 22 microM and that 0.1 microM dicoumarol strongly stabilizes the growing and shortenin

42 ow toxicity of dicoumarols suggests that the dicoumarol structure will be a good starting point for d

43 oavailability and relatively low toxicity of dicoumarols suggests that the dicoumarol structure will

44 The competitive inhibitor of NQO1 dicoumarol synergized with rifampin to promote intracell

45 Disadvantages of using dicoumarol to inhibit NQO1 include its lack of specifici

46 its derivatives suggests that the ability of dicoumarol to kill cancer cells is independent of NQO1 i

47 The ability of dicoumarol to simultaneously inhibit SAPK and NFkappaB a

48 Dicoumarols were identified as a class of compounds that

49 ith A549 NSCLC cells treated with or without dicoumarol, were used to elucidate the mechanism of acti