ライフサイエンスコーパス: FK-506

1 -loading capacity are additive with those of FK 506.

2 vitamin E, MnTBAP, L-N-acetyl-cysteine, and FK-506.

3 rapamycin reversed the inhibitory actions of FK-506.

4 w cells followed by antilymphocyte serum and FK-506.

5 s with aortic banding, LVH was unaffected by FK 506 (0.3 mg.kg-1.d-1) or even higher doses of CsA (10

6 tojanin I, is inhibited by cyclosporin A and FK-506 (0.5 microM), two drugs that specifically block t

7 Mice received tacrolimus (FK-506, 0.1 mg/kg per day)/mycophenolate mofetil (MMF, 6

8 FK-506 (2 microM), a specific blocker of PP2B, reduced t

9 ne during hyperglycemia declined less in the FK-506 (28%) and CsA groups (29%) compared with controls

10 Yet the calcineurin inhibitor FK-506 (500 nM) did not prolong the openings of human ch

11 smmPBj14 were treated with one of two drugs: FK-506, a potent immunosuppressive agent, or PMPA, a pot

12 ere treated with cyclosporine and seven with FK-506 along with prednisone and azathioprine post-PTX.

13 FK-506 also accelerated the rest decay of SR Ca2+ conten

14 FK-506 also inhibited potentiation of cAMP levels when c

15 FK-506 also inhibits Na(+)-Ca2+ exchange, although this

16 , and 9 were immunosuppressed with 0.5 mg/kg FK 506, although the remaining groups with 1 mg/kg FK 50

17 alcineurin antagonists cyclosporin A and the FK-506 analogue, ascomycin, diminished costimulatory mol

18 statistically lower in patients treated with FK-506 and CsA (5.05+/-0.47 and 5.05+/-0.42 mg/kg/min) a

19 e after arginine stimulation observed in the FK-506 and CsA groups as compared with controls (754%+/-

20 differences on low maintenance doses between FK-506 and CsA.

21 e effects of low dose maintenance therapy of FK-506 and Cyclosporin A (CsA) in 14 patients 1 year aft

22 FK-506 and cyclosporin inhibited augmentation of cAMP le

23 apy (anti-alphabeta-TCR monoclonal antibody, FK-506, and anti-lymphocyte serum).

24 mediated by IL-2R, but not by cyclosporin A, FK-506, and prednisone, which suppress signals mediated

25 PCB 95 and FK 506 are used to examine the relationship between ryan

26 DA-approved drugs, we identified tacrolimus (FK-506) as the most potent activator of ALK1 signaling i

27 d glucocorticoid-inducible kinase (SGK1) and FK 506 binding protein 5, genes known to be important in

28 FKBP6 has a putative N-terminal FK-506 binding and peptidylproyl isomerase (rotamase) do

29 FKBP6 shows homology to the FK-506 binding protein (FKBP) class of immunophilins.

30 FK-506 binding protein (FKBP) has been reported to be cl

31 The immunophilin, FKBP20-2, belongs to the FK-506 binding protein (FKBP) subfamily that functions a

32 With HF, expression of RyR2 and FK-506 binding protein 12.6 (FKBP12.6) were reduced, whe

33 can microarray techniques, the intracellular FK-506 binding protein 4 (FKBP4) was identified to bind

34 rivative induced rapid dimerization of FKBP (FK-506 binding protein) and FRB (FKBP-rapamycin binding

35 t of potent nonimmunosuppressive ligands for FK-506 binding proteins (FKBPs).

36 onventional PPIases, cyclophilins and FKBPs (FK-506 binding proteins).

37 s a previously uncharacterized member of the FK-506-binding protein (FKBP) gene family down-regulated

38 ppressive ligand of the immunophilin FKBP12 (FK-506-binding protein 12 kDa), has previously been show

39 ng protein-like 1 (AIPL1) is a member of the FK-506-binding protein family expressed specifically in

40 s, the calcium-binding protein S100P and the FK-506-binding protein FKBP51, was decreased following a

41 The rough endoplasmic reticulum-resident FK-506-binding protein FKBP65 can be isolated from chick

42 y-6-nitro-7-sulfonyl-benzo[f]quinoxaline) or FK-506 blocked the hypoxic seizure-induced increase in C

43 llular cAMP levels; the inhibitory effect of FK-506 but not of cyclosporin A was attenuated by rapamy

44 tion of apoptosis was markedly suppressed by FK-506 calcineurin inhibitor.

45 FK-506 can inhibit the activity of FKBP, thereby reversi

46 at the commonly used immunosuppressive agent FK-506 can inhibit TRPC6 activity in vivo.

47 In most cells, FK-506 caused an increase in SR Ca2+ content during stea

48 immunosuppression or in the presence of MMF/FK-506 combination.

49 Preincubation of cells with 0.1 microM FK-506 completely prevented carbachol-induced augmentati

50 FK-506 did not affect SR Ca2+ uptake but modestly decrea

51 ics, and in an earlier report we showed that FK-506 enhanced the fibrogenic process in in vivo and in

52 Rapamycin, an agent that competes with FK-506 for the immunophilin, FK binding protein 12, does

53 , although the remaining groups with 1 mg/kg FK 506, from day 0 to 4 after transplant.

54 owever, at day 15 rats receiving 1 mg/day of FK 506 had a significantly lower number of apoptotic cel

55 We conclude that FK-506 increases the fraction of SR Ca2+ released during

56 Ca2+ current were unaltered, suggesting that FK-506 increases the fraction of SR Ca2+ released during

57 eas these two indicators represent increased FK-506-independent DNA turnover activities in thymocytes

58 FK-506-induced synaptic potentiation was expressed in ad

59 The immunosuppressants cyclosporin A and FK-506 inhibited the increase in APP mRNA and holoprotei

60 Intracellular addition of EGTA or FK-506 into CN-15-transfected cells induced an up to 5-f

61 yte profiles, renal function parameters, and FK 506 levels in the postoperative period up until eithe

62 magnesium losses, which correlated with high FK 506 levels.

63 electrolyte abnormalities continue, to which FK 506-mediated renal toxicity might contribute.

64 yclosporine, azathioprine, 6-mercaptopurine, FK-506, methotrexate) were identified and compared with

65 Short course tacrolimus (FK-506) monotherapy was withdrawn at postoperative day 2

66 mmunosuppressive agents (e.g., cyclosporine, FK-506, mycophenolate mofetil, azathioprine, OKT-3, anti

67 provide further evidence that the actions of FK-506 on cholera toxin-treated gastric chief cells are

68 on between immunophilin FKBP12 and Ry1R with FK 506 or rapamycin completely eliminates PCB 95-enhance

69 e inhibition of postsynaptic CaN activity by FK-506 or an autoinhibitory peptide induced synaptic pot

70 lls were dialyzed with either cyclosporin A, FK-506, or calcineurin autoinhibitory peptide (structura

71 PBMC proliferation was blocked in vitro with FK-506, pig-tailed macaques treated preinoculation with

72 cineurin inhibitors, cyclosporin A (CsA) and FK 506, prevent pressure-overload LVH using 2 standard r

73 Since the discovery that FK-506 promotes neurite outgrowth, considerable attentio

74 ssants mycophenolic acid, cyclosporin A, and FK-506 provide a potential explanation for a reduced inc

75 neurin inhibitors, such as cyclosporin A and FK-506, rely upon binding sites on both subunits for com

76 FK 506 selectively eliminates PCB 95-induced Ca2+ releas

77 FK-506 significantly increased steady state twitch Ca2+

78 in vivo administration of the CaN inhibitor FK-506 significantly suppressed hypoxic seizures, and po

79 he immunosuppressive drugs cyclosporin A and FK-506 suggest that it is involved in both positive and

80 and graft survival rates have improved with FK-506 (Tacrolimus) immunosuppression.

81 udy subjects received either cyclosporine or FK-506/tacrolimus as part of their immunosuppressive reg

82 the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calci

83 (P = 0.003) in the presence of anti-CD3/MMF/FK-506 treatment for liver-Tx and BM-Tx, respectively.

84 Synaptic potentiation induced by FK-506 was significantly attenuated by co-injecting BAPT

85 inhibitor and immunosuppressant tacrolimus (FK-506) was prevented by Npas4 overexpression.

86 -tailed macaques treated preinoculation with FK-506 were not protected from acutely lethal disease.

87 essed by the calcineurin-dependent inhibitor FK-506, which has no effect on these activities in thymo

88 the peptide inhibition is not reversed with FK-506, which indicates a distinct mechanism.