ライフサイエンスコーパス: PPADS

1 PPADS (100 microM) and suramin (300 microM) reduced the

2 PPADS [pyridoxal phosphate-6-azo(benzene-2,4-disulfonic

3 PPADS abolished this post-contraction increase in discha

4 PPADS and 2',3'-O-(2,4,6-trinitrophenyl)-ATP blocked alp

5 PPADS and suramin also reduced contractions to exogenous

6 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) (0.1-100 microM) and suramin (1-300 microM) inhib

7 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) at 10 microm.

8 hosphate-6-azo (benzene-2,4-disulfonic acid (PPADS) but not by the 5-HT3 antagonist tropisetron or th

9 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) was given.

10 l phosphate-6-azophenyl-2,4-disulfonic acid (PPADS), a P2X antagonist, attenuated the responses of gr

11 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), and more potently activated by 3'-O-(4-benzoyl)b

12 phosphate-6-azophenyl-2',5'-disulfonic acid (PPADS), pyridoxal-5'-phosphate-6(2'-naphthylazo-6-nitro-

13 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS).

14 phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, 10 micromol/L) reduced the control fEPSP amplitud

15 hosphate-6-azophenyl-2', 4'-disulfonic acid (PPADS; 20 microm).

16 phosphate-6-azophenyl-2',4' disulfonic acid (PPADS; a P(2X)-purinoceptor antagonist; 3 x 10(-5) mol/L

17 osphate-6-azophenyl-,2',4'-disulphonic acid (PPADS) and Mg2+ produced concentration-dependent inhibit

18 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS), blocking Ca(2)(+)-dependent exocytosis from neur

19 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS).

20 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM) or alpha,beta-methylene ATP (50-100 mi

21 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microm), reduced constrictions in MA but not i

22 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 10 microM).

23 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS, 100 microM).

24 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 10 microM) or an NK(3) tachykinin receptor antago

25 hosphate-6-azophenyl-2',4'-disulphonic acid (PPADS; 100 microM), but not the adenosine receptor antag

26 ent apyrase, the purinergic receptor agonist PPADS, the calcium chelator BAPTA-AM, and calpain inhibi

27 is-1,3,5-na phthalene-trisulphonic acid) and PPADS (pyridoxal phosphate-6-azophenyl-2',4'-disulphonic

28 cotinic cholinergic receptor antagonist) and PPADS (P2X receptor antagonist).

29 We found that both OxATP and PPADS significantly improved functional recovery and dim

30 ion molecule-1 (ICAM-1), whereas suramin and PPADS decreased both ATPgammaS-induced and basal ICAM-1

31 Suramin and PPADS often reduced ongoing activity, and blocked the ex

32 by ivermectin but insensitive to suramin and PPADS, and it permeated the large cation N-methyl-d-gluc

33 Suramin and PPADS, general P2Y receptor blockers, and MRS2578, an in

34 ivity to the antagonists NF449, suramin, and PPADS was conferred by the nature of the extracellular l

35 uramin (14 micromol (kg body wt)-1 i.v.) and PPADS (17 micromol (kg body wt)-1 i.v.) antagonized the

36 The nonselective P2 antagonist PPADS or the P2Y1-selective antagonist MRS2179 failed to

37 d 2MeS-ATP mimics, while the P2XR antagonist PPADS blocks, the observed enhancement of the frequency

38 administration of the purinergic antagonist PPADS (1 or 3 mug kg(-1)).

39 this response by the P2 receptor antagonist PPADS suggests that bradykinin-induced micturition facil

40 pyrase or the purinergic receptor antagonist PPADS.

41 d in the presence of P2 receptor antagonists PPADS (10 microm) and suramin (5 microm).

42 eceptors with the broad-spectrum antagonists PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate

43 ed by non-specific P2X receptor antagonists, PPADS or suramin.

44 ere partially attenuated by 1 mm suramin but PPADS (80 microm) had no effect.

45 The effects were attenuated by PPADS, an antagonist to P2X receptors.

46 (ED50 22 +/- 5 nmol) and this was blocked by PPADS (17 micromol (kg body wt)-1 i.v.); unidentified va

47 sEPSC facilitation was blocked by PPADS (30 microm) and the selective P2X(3) receptor anta

48 ied in Ca2+/Mg2+-free medium, and blocked by PPADS or oxidized ATP.

49 The effect was blocked by PPADS, a protein kinase C inhibitor (bisindolylmaleimide

50 n-dependently (1-30 micromol/L) inhibited by PPADS (50%-inhibitory concentration, 3 micromol/L).

51 neurons from P2X2-/- mice were unaffected by PPADS but were blocked by mecamylamine.

52 /- 9 nmol), an action that was unaffected by PPADS or suramin.

53 he 6-azophenyl-2',4'-disulfonate derivative (PPADS), in which the phosphate group was cyclized by est

54 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS), 2'-deoxy-N6-methyladenosine 3',5'-bisphosphate (

55 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS), and to a lesser degree the nonspecific ectonucle

56 xal-phosphate-6-azophenyl-2',4'-disulfonate (PPADS, a P2 receptor blocker) decreased the ventilatory

57 H)) ZD7288, or by the purinoceptor inhibitor PPADS.

58 the P2 receptor antagonists suramin and iso-PPADS.

59 wer than PPADS (IC50 98.5 +/- 5.5 nM) or iso-PPADS (IC50 42.5 +/- 17.5 nM), although unlike PPADS its

60 Likewise, PPADS abolished the group IV afferent responses to stati

61 c receptor antagonists suramin (100 microm), PPADS (20-50 microm), and apyrase (80 U/ml), in contrast

62 now tested the hypothesis that injection of PPADS (10 mg kg(-1)) attenuated the responses of group I

63 Previously we have shown that injection of PPADS, a P2 receptor antagonist, into the arterial suppl

64 Suramin (200 microM) or PPADS (200 microM) applied by intra-arterial perfusion e

65 CI), we delivered P2X7R antagonists OxATP or PPADS to rats after acute impact injury.

66 nyl-2',4'-disulphonic acid tetrasodium salt (PPADS; 10 pmol) depressed the reflex bradycardia (by app

67 or (IC50 10.2 +/- 2.6 microM) was lower than PPADS (IC50 98.5 +/- 5.5 nM) or iso-PPADS (IC50 42.5 +/-

68 In the present study, we found that PPADS attenuated the group III afferent responses to sta

69 ADS (IC50 42.5 +/- 17.5 nM), although unlike PPADS its effect was reversible with washout and surmoun

70 bited the peak amplitude of the IJP, whereas PPADS had no effect.

71 lunted by blocking purinergic receptors with PPADS (0.1-1 mM; intravesically).