ライフサイエンスコーパス: calmidazolium

1 did the calmodulin (CaM) antagonists W-7 and calmidazolium.

2 n is attenuated by the calmodulin antagonist calmidazolium.

3 calmodulin antagonists, trifluoperazine and calmidazolium.

4 ibitor, trifluoperazine, but not by another, calmidazolium.

5 h necessary and sufficient for inhibition by calmidazolium.

6 Calmidazolium (10 microM), a potent calmodulin inhibitor

7 Calmidazolium (100 nM), a calmodulin inhibitor, inhibite

8 tion of the Egr-1 induction by H89 (48%) and calmidazolium (35%), but not by mitogen-activated protei

9 or the calmodulin inhibitors mastoparan and calmidazolium (5 microM), did not alter the action of Ca

10 Preincubation with calmidazolium, a calmodulin antagonist, produced modest

11 ct was blocked by pretreating the cells with calmidazolium, a calmodulin inhibitor.

12 In the presence of calmidazolium, a CaM inhibitor, S235D showed high P(f) a

13 brane patches, Trp4 is activated strongly by calmidazolium, an antagonist of CaM, and a high (50 micr

14 that prevents CaM from binding to Trp3, and calmidazolium, an inactivator of Ca(2+)/CaM.

15 ucturally distinct inhibitors (fluphenazine, calmidazolium and a W-7 analogue) of the Ca2+-binding re

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

17 Calmidazolium and W-7 also activated a persistent inward

18 ongly activated by the calmodulin inhibitors calmidazolium and W-7 in on-cell and excised patches.

19 While calmodulin inhibitors (calmidazolium and W-7; each n = 5) decreased baseline CB

20 ructurally distinct CaM antagonists, W-7 and calmidazolium, and by CaM-dependent protein kinase II in

21 The calmodulin inhibitor, calmidazolium, and the tyrosine kinase inhibitor, genist

22 e derivatives W-7/W-13, trifluoperazine, and calmidazolium, are used widely to investigate the role o

23 s of calmodulin activity, compound 48/80 and calmidazolium, blocked both curvature and gravity-induce

24 this was inhibited by genistein, TMB-8, and calmidazolium but not by pertussis toxin or GF109203X.

25 Moreover, infusion of calmidazolium (calmodulin inhibitor) with GR-73632 preve

26 force production, we studied the effects of calmidazolium (CDZ) on steady-state force and the rate o

27 Exposure of myofilaments to calmidazolium (CDZ), which binds to cTnC and increases i

28 One of these compounds, calmidazolium chloride (CLC), rapidly and efficiently co

29 by use of the protofibril-stabilizing agent calmidazolium chloride.

30 th KN-62, or inclusion of the CaM inhibitor, calmidazolium, did not prevent agonist-induced inhibitio

31 retreated with calmodulin inhibitors (W-7 or calmidazolium) exhibited an attenuated ERK response to i

32 Moreover, channel activation was blocked by calmidazolium (IC(50) = 5 microm), suggesting a role for

33 The ACV-ACII fusion protein was inhibited by calmidazolium (IC(50), approximately 20 microM) as well

34 odulin antagonists, trifluoperazine, W7, and calmidazolium, impaired this cleavage, indicating comple

35 Calmidazolium inhibited the activities of both full-leng

36 is insensitive to adenosine analogs and that calmidazolium inhibits AC activity by a novel, noncompet

37 Blockade of calmodulin by calmidazolium or blockade of CaM kinase II with either K

38 ogical salt solution (PSS) containing either calmidazolium or W-7, both known antagonists of CaM.

39 Both nifedipine and calmidazolium partially blocked nocturnal increases in m

40 of the (Ca(2+)+Mg(2+))-ATPase, 10(-5) mol/L calmidazolium (R24571) was added to the isolated plasma

41 This calmidazolium-reduced activity could then be stimulated

42 dulin antagonists (W-7, trifluoperazine, and calmidazolium) resulted in the robust release of arachid

43 aM), pretreatment of islets with CaM blocker calmidazolium showed effects very similar to those of Sy

44 y alphaBgTx and by the calmodulin antagonist calmidazolium, suggesting that Ca2+ entry through alpha7

45 The application of the calmodulin inhibitor calmidazolium via the intracellular pipette solution did

46 Inhibition of ACIX by calmidazolium was mediated by direct interaction with th

47 almodulin-dependent kinase II, melittin, and calmidazolium were effective inhibitors of CLNMT and eac

48 pH (pH(o)), and by the calmodulin inhibitor, calmidazolium, whereas it is acutely activated by NH(4)(

49 modulin antagonists, trifluoperazine and the calmidazolium, with IC50 values of 0.25-1.5 microM.