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1 -loading capacity are additive with those of FK 506.
2 blocked by co-infusion of the CaN inhibitor, FK-506.
3 w cells followed by antilymphocyte serum and FK-506.
4 vitamin E, MnTBAP, L-N-acetyl-cysteine, and FK-506.
5 rapamycin reversed the inhibitory actions of FK-506.
6 s with aortic banding, LVH was unaffected by FK 506 (0.3 mg.kg-1.d-1) or even higher doses of CsA (10
7 tojanin I, is inhibited by cyclosporin A and FK-506 (0.5 microM), two drugs that specifically block t
10 ne during hyperglycemia declined less in the FK-506 (28%) and CsA groups (29%) compared with controls
12 smmPBj14 were treated with one of two drugs: FK-506, a potent immunosuppressive agent, or PMPA, a pot
13 the combined effect of AMD3100 and low-dose FK-506 (AF) can reduce the adhesion score significantly
14 ere treated with cyclosporine and seven with FK-506 along with prednisone and azathioprine post-PTX.
18 , and 9 were immunosuppressed with 0.5 mg/kg FK 506, although the remaining groups with 1 mg/kg FK 50
19 alcineurin antagonists cyclosporin A and the FK-506 analogue, ascomycin, diminished costimulatory mol
20 statistically lower in patients treated with FK-506 and CsA (5.05+/-0.47 and 5.05+/-0.42 mg/kg/min) a
21 e after arginine stimulation observed in the FK-506 and CsA groups as compared with controls (754%+/-
23 e effects of low dose maintenance therapy of FK-506 and Cyclosporin A (CsA) in 14 patients 1 year aft
26 mediated by IL-2R, but not by cyclosporin A, FK-506, and prednisone, which suppress signals mediated
28 DA-approved drugs, we identified tacrolimus (FK-506) as the most potent activator of ALK1 signaling i
29 d glucocorticoid-inducible kinase (SGK1) and FK 506 binding protein 5, genes known to be important in
33 The immunophilin, FKBP20-2, belongs to the FK-506 binding protein (FKBP) subfamily that functions a
35 can microarray techniques, the intracellular FK-506 binding protein 4 (FKBP4) was identified to bind
36 rivative induced rapid dimerization of FKBP (FK-506 binding protein) and FRB (FKBP-rapamycin binding
39 D (SlyD) and Thermococcus gammatolerans SlyD FK-506-binding protein (FKBP) domains suitable for prese
40 s a previously uncharacterized member of the FK-506-binding protein (FKBP) gene family down-regulated
41 ppressive ligand of the immunophilin FKBP12 (FK-506-binding protein 12 kDa), has previously been show
43 ng protein-like 1 (AIPL1) is a member of the FK-506-binding protein family expressed specifically in
44 s, the calcium-binding protein S100P and the FK-506-binding protein FKBP51, was decreased following a
45 The rough endoplasmic reticulum-resident FK-506-binding protein FKBP65 can be isolated from chick
46 y-6-nitro-7-sulfonyl-benzo[f]quinoxaline) or FK-506 blocked the hypoxic seizure-induced increase in C
47 llular cAMP levels; the inhibitory effect of FK-506 but not of cyclosporin A was attenuated by rapamy
55 c immunosuppressant drugs cyclosporine A and FK-506 displayed very low background and a remarkable dy
56 ics, and in an earlier report we showed that FK-506 enhanced the fibrogenic process in in vivo and in
59 owever, at day 15 rats receiving 1 mg/day of FK 506 had a significantly lower number of apoptotic cel
61 Ca2+ current were unaltered, suggesting that FK-506 increases the fraction of SR Ca2+ released during
62 eas these two indicators represent increased FK-506-independent DNA turnover activities in thymocytes
64 The immunosuppressants cyclosporin A and FK-506 inhibited the increase in APP mRNA and holoprotei
66 yte profiles, renal function parameters, and FK 506 levels in the postoperative period up until eithe
69 yclosporine, azathioprine, 6-mercaptopurine, FK-506, methotrexate) were identified and compared with
71 mmunosuppressive agents (e.g., cyclosporine, FK-506, mycophenolate mofetil, azathioprine, OKT-3, anti
72 provide further evidence that the actions of FK-506 on cholera toxin-treated gastric chief cells are
73 on between immunophilin FKBP12 and Ry1R with FK 506 or rapamycin completely eliminates PCB 95-enhance
74 e inhibition of postsynaptic CaN activity by FK-506 or an autoinhibitory peptide induced synaptic pot
75 lls were dialyzed with either cyclosporin A, FK-506, or calcineurin autoinhibitory peptide (structura
76 PBMC proliferation was blocked in vitro with FK-506, pig-tailed macaques treated preinoculation with
77 cineurin inhibitors, cyclosporin A (CsA) and FK 506, prevent pressure-overload LVH using 2 standard r
79 ssants mycophenolic acid, cyclosporin A, and FK-506 provide a potential explanation for a reduced inc
80 neurin inhibitors, such as cyclosporin A and FK-506, rely upon binding sites on both subunits for com
83 in vivo administration of the CaN inhibitor FK-506 significantly suppressed hypoxic seizures, and po
84 he immunosuppressive drugs cyclosporin A and FK-506 suggest that it is involved in both positive and
86 udy subjects received either cyclosporine or FK-506/tacrolimus as part of their immunosuppressive reg
87 the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to inhibitors of calci
88 (P = 0.003) in the presence of anti-CD3/MMF/FK-506 treatment for liver-Tx and BM-Tx, respectively.
91 -tailed macaques treated preinoculation with FK-506 were not protected from acutely lethal disease.
92 essed by the calcineurin-dependent inhibitor FK-506, which has no effect on these activities in thymo