ライフサイエンスコーパス: W-7

1 W-7 and chlorpromazine also lowered levels of phosphatid

2 W-7 did not affect heart rate, increases in QT intervals

3 nhibitors (fluphenazine, calmidazolium and a W-7 analogue) of the Ca2+-binding regulatory protein cal

4 KN-93 and W-7, a calmodulin inhibitor, decreased the open probabil

5 Calmidazolium and W-7 also activated a persistent inward current under who

6 the calmodulin inhibitors calmidazolium and W-7 in on-cell and excised patches.

7 ile calmodulin inhibitors (calmidazolium and W-7; each n = 5) decreased baseline CBF by an average of

8 in antagonists trifluoperazine dimaleate and W-7.

9 chelerythrine, 2-aminopurine, genistein, and W-7 and only partially or not at all by KN-62, wortmanni

10 bitors W-7 and W-13 reduced cAMP levels, and W-7 reduced cyst growth, suggesting that AC3 is involved

11 ubation with trifluoperazine (30 microM) and W-7 (150 microM) shifted it in the opposite, depolarised

12 e calmodulin antagonists trifluoperazine and W-7 and the Ca2+/calmodulin-dependent protein kinase II

13 phosphorylation, whereas trifluoperazine and W-7, antagonists of calmodulin, caused opposite depolari

14 effects of okadaic acid, trifluoperazine and W-7, which are commonly used in studies of protein phosp

15 Compared with control animals, W-7 reduced TdP inducibility without shortening the QT i

16 We report that the calmodulin antagonist W-7 and the calcium/calmodulin-dependent (CaM) kinase in

17 ed Akt activation, and calmodulin antagonist W-7 does not inhibit phosphotyrosine-associated PI-3 kin

18 in the presence of the calmodulin antagonist W-7 followed by insemination does not block cortical gra

19 nase blockade with the calmodulin antagonist W-7 reduced TdP in a dose-dependent fashion (4 of 7 indu

20 Calmodulin antagonist W-7 was effective in inhibiting calcium-promoted phospho

21 in the presence of the calmodulin antagonist W-7, indicating the vital selective role of calmodulin f

22 nitroguanidine and the calmodulin antagonist W-7, while the eNOS inhibitor L-N(5)-(1-iminoethyl)ornit

23 which is inhibited by calmodulin antagonist W-7.

24 M, and by the specific calmodulin antagonist W-7.

25 was prevented by the calmodulin antagonist, W-7.

26 vented by the calcium-calmodulin antagonist, W-7.

27 h could be blocked by calmodulin antagonists W-7 and calmidazolium and CaM kinase inhibitor KN-93.

28 The calmodulin antagonists W-7 and trifluoperazine inhibited Abeta formation and en

29 ment as did the calmodulin (CaM) antagonists W-7 and calmidazolium.

30 ructurally disparate calmodulin antagonists (W-7, trifluoperazine, and calmidazolium) resulted in the

31 y two structurally distinct CaM antagonists, W-7 and calmidazolium, and by CaM-dependent protein kina

32 When added during oscillations, both W-7, a calmodulin antagonist, and KN-62, a specific CaMK

33 of L-type Ca(2+) current was not affected by W-7.

34 Selective suppression of TdP inducibility by W-7, without shortening the duration of cardiac repolari

35 exchanger, and the response is inhibited by W-7, it is suggested that this protein may be calmodulin

36 Because that transition was not inhibited by W-7, the in vivo CDPK activation probably is not the res

37 on by serum and insulin is also inhibited by W-7.

38 n control animals, and this was prevented by W-7.

39 anced by calyculin A, and greatly reduced by W-7.

40 uch as the napthalenesulfonamide derivatives W-7/W-13, trifluoperazine, and calmidazolium, are used w

41 larizations, but pretreatment with high-dose W-7 did not prevent TdP in response to the L-type Ca(2+)

42 s between the photoreceptor and a downstream W-7-sensitive effector.

43 If two chemically different inhibitors (e.g. W-7 and trifluoperazine) produce similar effects, invest

44 oro-1-naphtha-lenesulfonamide hydrochloride (W-7) prevents induction of the photoregulated gene by ph

45 loro-1-naphthalenesulfonamide hydrochloride (W-7) than were PC-3 cells.

46 dependent, because the calmodulin inhibitor W-7 blocked the expression of the differentiation-specif

47 The calmodulin inhibitor W-7 decreased the proliferation of small SMCs and preven

48 Morulae exposed to the calmodulin inhibitor W-7 exhibited a dose-dependent delay in blastocoel forma

49 We have shown that the calmodulin inhibitor W-7 suppresses torsade de pointes (TdP) without shorteni

50 This includes the calmodulin inhibitor W-7, the phospholipase-C inhibitor U73122, and anti-psyc

51 lcium/calmodulin phosphodiesterase inhibitor W-7 but not by the protein kinase A inhibitor H-89 nor t

52 Finally, the calmodulin inhibitors W-7 and W-13 reduced cAMP levels, and W-7 reduced cyst g

53 cells pretreated with calmodulin inhibitors (W-7 or calmidazolium) exhibited an attenuated ERK respon

54 L-N5-(1-iminoethyl)ornithine, 10 micromol/L W-7, or incubating cells in pertussis toxin or 10 microm

55 brane region of the EGFR on model membranes; W-7/W-13 causes translocation of this peptide from membr

56 by the calmodulin (CaM) inhibitor 10 microM W-7 and partially inhibited by the phosphatidylinositol

57 A 4 hour exposure to 10 microM W-7 did not significantly alter cavitation, but attenuat

58 microm prazocin, 10 microm L-NIO, 10 microm W-7, 10 microm LY294002, 2 microm H-89, 10 microm ryanod

59 microm prazocin, 10 microm L-NIO, 10 microm W-7, 10 microm ODQ, 2 microm H-89 or 10 microm LY294002,

60 of 25 microM trifluoperazine and 100 microM W-7, two calmodulin inhibitors.

61 calmodulin inhibitors, monodansylcadaverine, W-7, and trifluoperazine, followed by measurement of cAM

62 inohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) (which are stimulators of the "contraction pathway"

63 inohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and chlorpromazine significantly lowered all higher

64 inohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) but not by its inactive isoform N-(6-aminohexyl)-1-

65 However, neither W-7, a calmodulin blocker, nor KN-93, a CaMKII inhibitor

66 show that the acute systemic application of W-7 and H-8 is hemodynamically tolerated and indicate th

67 Application of W-7, an inhibitor of the Ca2+-binding protein calmodulin

68 perpolarising shifts even in the presence of W-7.

69 of GPIbalpha; GPIbalpha-CaM) immobilized on W-7-agarose with a K(d) of 3.3 microM.

70 ion (PSS) containing either calmidazolium or W-7, both known antagonists of CaM.

71 t cells was revealed by the observation that W-7 was as effective as Casodex, an antiandrogen, in blo

72 In isolated perfused tubules, W-7 reversibly blocked vasopressin-stimulated urea perme

73 g, and 0 of 6 at 10 micromol/kg), but unlike W-7, H-8 did so by shortening the QT interval.

74 ed by pretreatment of the cell extracts with W-7.

75 otting, calcium-dependent precipitation with W-7 agarose beads, and reconstitution of calcium-mediate

76 h vehicle control, whereas pretreatment with W-7 (50 micromol/kg), an inhibitor of the intracellular