ライフサイエンスコーパス: H-7

1 H-7 also inhibited 0.5 microM PDB-induced facilitation o

2 H-7 can enhance OF in the presence of trabecular obstruc

3 H-7 increased outflow facility, causing a partial loss o

4 H-7 increases trabecular outflow facility in monkeys by

5 H-7 inhibited the electrically evoked contractions in a

6 H-7 partially restored baseline outflow facility measure

7 H-7 significantly increased outflow facility after singl

8 (ECA), a Rho kinase inhibitor (Y-27632), and H-7 (serine/threonine kinase inhibitor), were examined f

9 tin), but not by inhibiting cGK (KT-5823 and H-7).

10 hibitors including Rp-8-pCPT-cGMPS, H-8, and H-7 as well as by ATPgammaS.

11 ly reported retardatory effects of BIS-I and H-7 on behavioural recovery after UL.

12 lls were grown in culture, treated with BDM, H-7, and latrunculin B, and then fixed, stained for beta

13 modified by inhibition of protein kinase C (H-7), the addition of antioxidants (vitamin E or superox

14 Concurrent H-7 enhanced outflow facility by 73% +/- 18% (n = 12, P

15 In contrast, H-7, a nonspecific protein kinase C inhibitor, attenuate

16 lphonyl)-2-methylpiperazine dihydrochloride (H-7; 10 microM).

17 he serine-threonine protein kinase inhibitor H-7 (1 mM, five rats; 10 mM, five rats).

18 the broad-spectrum protein kinase inhibitor H-7 (10 microM) had no effect on the resting membrane po

19 application of the protein kinase inhibitor H-7 after LTP induction can reverse the increased RC3/ne

20 ocked by the broad spectrum kinase inhibitor H-7 and by the protein kinase A-specific inhibitor H-89.

21 he serine/threonine protein kinase inhibitor H-7 and the immunosuppressive drug rapamycin and require

22 The serene-threonine kinase inhibitor H-7 had no effect when microinjected at the time of de-a

23 ide (CHX), with the protein kinase inhibitor H-7, or with the immunosuppressive drug rapamycin.

24 th the non-specific protein kinase inhibitor H-7.

25 ncentrations of the protein kinase inhibitor H-7.

26 The PKC inhibitor H-7 (50-100 microM) inhibited the CS- or eserine-facilit

27 ein, but not the protein kinase C inhibitor, H-7.

28 bFGF, the protein kinase C (PKC) inhibitor, H-7; calphostin C, or the PKC activator, PMA; and protei

29 of muscles with protein kinase A inhibitors H-7 and KT5720 completely suppressed the activation of E

30 The protein kinase C inhibitors H-7 and staurosporine dose dependently reversed the inhi

31 the non-selective protein kinase inhibitors H-7 (100 microM), H-8 (50 microM) and HA-1004 (100 micro

32 or by PMA was blocked by the PKC inhibitors H-7 (30 microM) or GF109203X (1 microM).

33 ene expression was blocked by PKC inhibitors H-7 (30 microM).

34 either the protein kinase C (PKC) inhibitors H-7 (30 microM) and GF109203X (1 microM) or the PKC acti

35 The protein kinase C and A inhibitors, H-7 and H-8, or the cyclooxygenase inhibitor, indomethac

36 Three-hundred micromoles of intracameral H-7 doubled facility in iridectomized + CM- disinserted

37 Bis-I and Iso-H-7 significantly retarded the disappearance of spontane

38 stilled water, six rats), PKC inhibitor [Iso-H-7 (10 mM, four rats; 50 mM, five rats) or bisindolemal

39 The effects of Iso-H-7 were dose-dependent: more nystagmus quick phases (p<

40 ase C, including bisindolylmaleimide, K252a, H-7, and calphostin C, were unable to mimic this effect

41 (5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and N-[2-(p-bromocinnamyl-amino)ethyl]-5-isoquinoli

42 5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) and then recorded on videotape for 15 minutes.

43 5-Isoquinolinylsulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase C, the enzyme typic

44 5-isoquinolinesulphonyl)-2-methylpiperazine (H-7; 100 microM), by the PKC inhibitor calphostin C (10

45 In cultured HTM and SC cells, 100 microM H-7 caused a rapid loss of filamentous actin staining bu

46 eral infusion for 90 minutes with 100 microM H-7 increased trabecular and total outflow facility by 1

47 ad inhibition of protein kinases (100 microM H-7), inhibition of PKA (10 microM H-89), nor inhibition

48 Twenty millimolar BDM, 100 microM H-7, and 1 microM latrunculin B increased outflow facili

49 , but only at 6 and 24 h post-UL in the 1 mM H-7 group.

50 greater than controls (p<0.05) in the 10 mM H-7 group at 4, 5, 6 and 48 h post-UL, but only at 6 and

51 Four 5-microl drops of 400 mM H-7 applied topically followed 2 hours later by anterior

52 re, and either single or sequential doses of H-7 or RGD peptide were added.

53 Furthermore, inclusion of H-7 (100 microM), BAPTA (10 mM), AA (50 microM), antioxi

54 In contrast, presynaptic injection of H-7 significantly depressed LTP but not basal transmissi

55 In contrast, treatment with ECA, Y-27632, or H-7 triggered changes in cell shape and reduced actin st

56 ein, a tyrosine kinase inhibitor, and GFX or H-7, PKC inhibitors, abolished both VEGF-induced PKC act

57 protein kinase inhibitors (staurosporine or H-7) or specific protein kinase C inhibitors (GF109203x,

58 by pretreatment with either staurosporine or H-7, two selective, pharmacological PKC inhibitors.

59 -isoquinolinylsulfonyl)-2-methyl-piperazine (H-7), a proposed myosin light-chain kinase inhibitor; an

60 isoquinolinylsulphonyl)-2-methyl-piperazine (H-7).

61 pertussis toxin, an inhibitor of G-proteins, H-7 or staurosporine, inhibitors of protein kinase C, or

62 This suggests that H-7 may be useful in treating glaucoma, even in the pres

63 Outflow facility response to H-7 was measured by two-level constant pressure perfusio

64 cility, and the outflow facility response to H-7.

65 ry effects of IL-13 on TNF were sensitive to H-7, neomycin, and wortmannin, suggesting that the pathw

66 te inactivation were greatly attenuated with H-7, calphostin C, or PKCi, but not with H-89 or PKAi.

67 Pretreatment with H-7 blocked these effects.