ライフサイエンスコーパス: cyclosporin A

1 neration synthetic approach to cyclosporine (cyclosporin A).

2 ith the anti-psoriasis systemic therapeutic, cyclosporin A.

3 ochondrial permeability transition pore with cyclosporin A.

4 ochondrial permeability transition inhibitor cyclosporin A.

5 were inhibited by the calcineurin inhibitor cyclosporin A.

6 t, which was attenuated by pretreatment with cyclosporin A.

7 n the presence of nontoxic concentrations of cyclosporin A.

8 or for the important immunosuppressant drug, cyclosporin A.

9 mycin and was blocked by the NFAT antagonist cyclosporin A.

10 ctivation, and this response is inhibited by cyclosporin A.

11 ect was blocked by the calcineurin inhibitor cyclosporin A.

12 ation was seen when CXCR2(-/-) mice received cyclosporin A.

13 (SIV) Nef become resistant to treatment with cyclosporin A.

14 tes were mutated or following treatment with cyclosporin A.

15 cause systemic toxicity as was observed for cyclosporin A.

16 raft-versus-host disease (GVHD) consisted of cyclosporin A.

17 differ in sensitivity to the immunomodulator cyclosporin A.

18 d by some ABCG2 substrates, is unaffected by cyclosporin A.

19 tely inhibited by the calcineurin inhibitor, cyclosporin A.

20 , slightly overcoming those of verapamil and cyclosporin A.

21 uggesting a mitochondrial locus of action of cyclosporin A.

22 response to another immunosuppressive agent, cyclosporin A.

23 cluding relative resistance to inhibition by cyclosporin A.

24 of cyclophilin A with the immunosuppressant cyclosporin A.

25 gnaling antagonist, the cyclic undecapeptide cyclosporin A.

26 are only possible for the short-term use of cyclosporin A.

27 g(63) in the catalytic motif or inhibited by cyclosporin A.

28 ion by PEITC treatment was not influenced by cyclosporin A.

29 artan, 1 micromol/l), calcineurin inhibitor (cyclosporin A, 0.5 micromol/l), calcium chelator (1,2-Bi

30 Thus, like cyclosporin A, 1,25-dihydroxyvitamin D3 inhibits TCR-dri

31 y) in vivo, but not in rats pre-treated with cyclosporin A (20 mg/kg/day subcutaneously) for 3 days (

32 prevented by the calcineurin/NFAT inhibitor, cyclosporin A (25 mg/kg/day s.c.).

33 ochondrial permeability transition pore with cyclosporin A (5 microM) had no significant effect on th

34 uced permeability increase was suppressed by cyclosporin A (60%) and 1,3-dicyclohexylcarbodiimide (90

35 latonin (a non-specific antioxidant), and by cyclosporin A (a permeability transition pore blocker).

36 lear factor of activated T cells (NFAT), and cyclosporin A, a calcineurin inhibitor that reduces NFAT

37 Cyclosporin A, a competitive substrate for ABCB1, restor

38 Nonetheless, cyclosporin A, a direct mitochondrial permeability trans

39 e ability to restrict FIV in the presence of cyclosporin A, a drug that normally abolishes the intera

40 In wild-type mice, the co-administration of cyclosporin A, a known P-gp inhibitor, resulted in a 6-f

41 (2) cells transfected with ABCB4-I541F cDNA, cyclosporin A allowed a significant amount of the mutant

42 Cyclosporin A also blocked caspase-3 activation.

43 The calcineurin inhibitor cyclosporin A also blocks the dephosphorylation of TRPC6

44 Cyclosporin A also improved maturation of ABCB4-I541F in

45 rial permeability transition pore antagonist cyclosporin A also inhibited calcium-induced AIF release

46 Cyclosporin A, an inhibitor of calcineurin, increased AS

47 However, cyclosporin A, an inhibitor of calcineurin-mediated NFAT

48 Cyclosporin A, an inhibitor of cell death dependent on t

49 tive caspase-9/-3 are partially inhibited by cyclosporin A, an inhibitor of mitochondrial membrane pe

50 Accordingly, cyclosporin A, an inhibitor of T cell stimulation via th

51 However, cyclosporin A, an inhibitor of the Ca(2+)-dependent phos

52 This apoptotic cell killing was prevented by cyclosporin A, an MPT blocker, and by pancaspase and cas

53 ndrial-targeted CaMKII inhibitory protein or cyclosporin A, an mPTP antagonist with clinical efficacy

54 n competition and uses a fluorescein-labeled cyclosporin A analog and purified human CypA to quantita

55 , we predicted that the nonimmunosuppressive cyclosporin A analog valspodar would inhibit Rgg activat

56 (alisporivir, DEB025, a nonimmunosuppressive cyclosporin A analog).

57 Novel cyclosporin A analogues were synthesized utilizing the o

58 Permeability transition inhibitors cyclosporin A and aristolochic acid could inhibit mitoch

59 gimen consists of a limited 60-day course of cyclosporin A and azathioprine combined with weekly i.v.

60 partially blocked by haemoglobin, melatonin, cyclosporin A and DPQ, but was not affected by uric acid

61 g as current calcineurin inhibitors, such as cyclosporin A and FK-506, rely upon binding sites on bot

62 were sensitive to the calcineurin inhibitors cyclosporin A and FK-506, to scavengers of ROS, and to i

63 urin with either the immunosuppressant drugs cyclosporin A and FK506, or the retrovirally mediated ec

64 Cyclosporin A and FK506, which target calcineurin and th

65 duced IL-21 gene expression was inhibited by cyclosporin A and FK506.

66 e to the calcineurin-NFAT pathway inhibitors cyclosporin A and FK506.

67 rmeability transition pore with low doses of cyclosporin A and found a deficit in synaptic plasticity

68 he half-life of cyclin D1 in the presence of cyclosporin A and found no difference from control cells

69 Finally, cyclosporin A and IkappaBalpha and PI3K inhibitors but n

70 Cyclosporin A and IkBalpha inhibitor blocked TLR2-mediat

71 s-linking, and its activity was inhibited by cyclosporin A and MAPK inhibitors.

72 o cyclosporin A exposure, and the effects of cyclosporin A and mitochondrial depolarization on presyn

73 PTP), which was blocked by the PTP inhibitor cyclosporin A and MnTBAP, and reversed by L-arginine sup

74 in clinical studies and understanding of how cyclosporin A and model cyclic hexapeptides cross cell m

75 Furthermore, both cyclosporin A and NAD(+) blocked translocation of the ap

76 Both viruses were efficiently inhibited by cyclosporin A and NIM811, a nonimmunosuppressive analog

77 Calcineurin inhibitors, such as cyclosporin A and tacrolimus (FK506), have played a pivo

78 mice treated with the calcineurin inhibitor cyclosporin A and transgenic mice expressing a targeted

79 changes are inhibited by immunosuppressants cyclosporin A and triptolide.

80 PBMCs were abolished by the NFAT inhibitors cyclosporin A and VIVIT.

81 e recoupling agent 6-ketocholestanol but not cyclosporin A and were nonexistent in mitochondrial DNA-

82 in this effort, allowing access to epimeric cyclosporins A and H from a single precursor by variatio

83 Calcineurin inhibitors (FK506, cyclosporin A, and a peptide calcineurin inhibitor [CAIN

84 ning 5% IL-1Ra, 1% methylprednisolone, 0.05% cyclosporin A, and a vehicle control containing carboxym

85 or the immunosuppressants mycophenolic acid, cyclosporin A, and FK-506 provide a potential explanatio

86 However, alisporivir, cyclosporin A, and most other cyclosporins are potent in

87 ne-N,N,N',N'-tetraacetic acid, deltamethrin, cyclosporin A, and okadaic acid each alone significantly

88 dy for induction, and mycophenolate mofetil, cyclosporin A, and prednisone for maintenance.

89 we show, in diploid human fibroblasts, that cyclosporin A arrested cells in G(1) before cyclin D/cdk

90 They identify cyclosporin A as a potential novel therapeutic tool for

91 -ATG group received mycophenolate mofetile + cyclosporin A as graft-versus-host disease (GVHD) prophy

92 ansition pore inhibitors bongkrekic acid and cyclosporin A, as well as by the sulfhydryl-reducing age

93 , permeability transition pore inhibition by cyclosporin A attenuates NGF deprivation-induced loss of

94 binding immunophilins FKBP52 and FKBP51, the cyclosporin A-binding immunophilin CyP40, and protein ph

95 Cyclosporin A blockade of the mitochondrial permeability

96 Sub-micromolar concentrations of cyclosporin A blocked MPT and cell death, suggesting tha

97 Cyclosporin A blocked the inhibitory effect of JNK on mi

98 otein phosphatase 2B (calcineurin) inhibitor cyclosporin A blocked the nicotine-induced reversal.

99 osuppressor in human transplantation such as cyclosporin A blocks tissue rejection in marine sponges

100 The PTP blockers bongkrekic acid and cyclosporin A both reduced inhibition of transient K(Ca)

101 g activated rCD4s with the immunosuppressant cyclosporin, a calcineurin inhibitor, robustly inhibited

102 In multiple cell types, cyclosporin A causes a G(1) cell cycle arrest, implicati

103 Cyclosporin A coadministered for 2 weeks with ART provid

104 lerization depended on high plasma levels of cyclosporin A combined with azathioprine.

105 The complexes included the CypA-cyclosporin A complex and the BCAII-4-carboxybenzenesulf

106 Guided by the Rgg-cyclosporin A complex structure, we predicted that the n

107 were completely blocked by pretreatment with cyclosporin A, consistent with induction of the MPT.

108 utylated hydroxyanisol and the MMP inhibitor cyclosporin A (Cs A) blocked apoptosis induced by MX3350

109 Permeability of [(3)H] cyclosporin A (CsA) across SIRC cells was found at 1.74

110 Treatment with AR-C117977 or cyclosporin A (CsA) administered at a dose of 30 mg/kg s

111 Furthermore, inhibition of calcineurin with cyclosporin A (CsA) alters AQP2 localization and phospho

112 olyl cis-trans isomerase (PPIase) inhibitors cyclosporin A (CsA) and a derivative of cyclosporin A wi

113 , an effect that was prevented completely by cyclosporin A (CSA) and ATP.

114 ysteine (NAC) and Trolox (TX), as well as by cyclosporin A (CsA) and bongkrekic acid (BKA).

115 Calcineurin inhibitor cyclosporin A (CsA) and calcineurin-siRNA increase beta4

116 and necrotic cell death that were blocked by cyclosporin A (CsA) and EGTA.

117 Cyclosporin A (CsA) and tacrolimus (FK506) has been repo

118 ors of activated T cell (NFAT) activation by cyclosporin A (CsA) and VIVIT suppressed PDGF-BB-induced

119 Calcineurin inhibitors such as cyclosporin A (CsA) are the mainstay of immunosuppressiv

120 the presence of ligand is demonstrated using cyclosporin A (CsA) as a test ligand.

121 In contrast, the PTP inhibitor cyclosporin A (CsA) did not prevent priming: neither lat

122 Cyclosporin A (CsA) has been used widely to prevent reje

123 pectrometry (MS/MS) for the determination of cyclosporin A (CsA) in biological fluids in support of i

124 Although the clinical efficacy of cyclosporin A (CSA) in retinoblastoma (RB) has been attr

125 The widely used immunosuppressive drug cyclosporin A (CsA) inhibited DAF induction by VEGF in a

126 Cyclosporin A (CSA) is commonly used to prevent graft-ve

127 Cyclosporin A (CsA) is known to preserve cardiac contrac

128 The therapeutic use of cyclosporin A (CsA) is limited by nephrotoxicity that is

129 It has been proposed that cyclosporin A (CsA) may induce epithelial-to-mesenchymal

130 Hence, the authors hypothesize that cyclosporin A (CsA) may regulate TGM-2 via ROS, and this

131 myocardium, hearts were perfused with either cyclosporin A (CsA) or 4-chlorodiazepam (4-Cl-DZP) to in

132 on of calcineurin activity by treatment with cyclosporin A (CsA) or FK506 is a cornerstone of immunos

133 Current immunosuppressive strategies use cyclosporin A (CsA) or FK506 to inhibit calcineurin, whi

134 function in 170 liver transplant patients on cyclosporin A (CsA) or tacrolimus (Tac).

135 side effects of long-term corticosteroid or cyclosporin A (CsA) therapy complicate the treatment of

136 d) value) were determined for the binding of cyclosporin A (CsA) to a cyclophilin A (CypA) sample in

137 Although NC1153 acted synergistically with cyclosporin A (CsA) to prolong allograft survival, it wa

138 It has been observed that cyclosporin A (CsA) treatment, particularly in transplan

139 effects of the prototypic immunosuppressant cyclosporin A (CsA) were investigated.

140 udy, ultrafine amorphous particles (UAPs) of cyclosporin A (CsA) were prepared with synthesized ACQ d

141 n eliminated the HIV-1 stimulatory effect of cyclosporin A (CsA), a competitive inhibitor of the CypA

142 HIV-1 infectivity is increased >100-fold by cyclosporin A (CsA), a competitive inhibitor of the inte

143 pretreatment with the calcineurin inhibitor cyclosporin A (CsA), an antagonist of NFAT signaling, de

144 Treatment of kidney rudiments with Cyclosporin A (CSA), an inhibitor of Calcium/NFAT signal

145 Here, we show that cyclosporin A (CsA), an inhibitor of MPT, protects the m

146 s was caspase dependent, and a blockade with cyclosporin A (CsA), an inhibitor of the mitochondrial p

147 Although cyclosporin A (CsA), an inhibitory ligand of cyclophilin

148 the permeability transition pore inhibitor, cyclosporin A (CsA), and by the antioxidant, alpha-tocop

149 lect immunophilin ligands [FK506, rapamycin, cyclosporin A (CsA), and cyclosporin H (CsH)], which are

150 MPT inhibitors, cyclosporin A (CsA), and NIM811 temporarily decreased ne

151 ected cells with the immunosuppressive agent cyclosporin A (CsA), HIV-1 infection also is inhibited.

152 concentrations, such as tacrolimus (TaC) and cyclosporin A (CsA), is important in the outpatient foll

153 Cyclosporin A (CSA), methylprednisolone (MP), methotrexa

154 common side-effect of the administration of cyclosporin A (CSA), phenytoin, and calcium blockers.

155 actor of activated T cells (NFAT) inhibitor, cyclosporin A (CsA), suggesting that NFAT controls BCATc

156 Cyclosporin A (CsA), tacrolimus (Tac), rapamycin (Rap),

157 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of

158 Mouse embryos exposed to cyclosporin A (CsA), which inhibits calcineurin phosphat

159 ced RGC death, but this was not inhibited by cyclosporin A (CsA), which normally maintains the PTP in

160 TGM-2 and oxidative stress markers (OSMs) in cyclosporin A (CsA)-induced gingival overgrowth (GO).

161 to play a central role in the development of Cyclosporin A (CsA)-induced nephropathy.

162 dothelial growth factor (VEGF) expression in cyclosporin A (CsA)-induced rat overgrown gingival tissu

163 an antigen-independent, NF-kappaB-dependent, cyclosporin A (CsA)-resistant manner.

164 d by treatment with the proton pump modifier cyclosporin A (CsA).

165 maleate (DEM), piperonyl butoxide (PBO) and cyclosporin A (CsA).

166 ligands in a competition binding assay with cyclosporin A (CsA).

167 d the effects of the immunosuppressive agent cyclosporin A (CsA).

168 ir sensitivity to the immunosuppressive drug cyclosporin A (CsA).

169 21-day course of the immunosuppressive agent cyclosporin A (CsA).

170 1(R91W), and inhibition of calcineurin using cyclosporin A (CsA).

171 the target of immunosuppressants, FK506 and cyclosporin A (CSA).

172 the cyclophilin family of proteins that bind cyclosporin A (CsA).

173 otein targets of the immunosuppressive drug, cyclosporin A (CsA).

174 udy aims to examine the inhibitory effect of cyclosporin-A (CsA) on periodontal breakdown and to furt

175 following ischemic preconditioning (IPC) or cyclosporin-A (CsA) treatment.

176 This study compares cyclosporin A (CyA) with the pan-HDACi suberoylanilide h

177 Calcineurin inhibitors, such as the cyclosporin A-cyclophilin A and FK506-FKBP12 complexes,

178 tenuate NFATc1 activity further, we injected cyclosporin A daily.

179 Furthermore, cyclosporin A decreased protein synthesis and abolished

180 racts, and inhibitors of calcineurin such as cyclosporin A delay the destruction of cyclins, the glob

181 thermore, sensitivity to the drugs FK506 and cyclosporin A demonstrates that the RAM pathway acts in

182 porin (PSC833)-sensitive] of the fluorescent cyclosporin A derivative [N-epsilon(4-nitrobenzofurazan-

183 t, nonselective inhibition of calcineurin by cyclosporin A did not cause cardiomyocyte apoptosis afte

184 gp, but not ABCG2, was able to transport [3H]cyclosporin A directly in intact cells.

185 contrast to the reduction of cyclin D1 with cyclosporin A, ectopic expression of calcium/calmodulin-

186 Fourteen trials consistently indicate that cyclosporin A efficaciously improves clinical signs of A

187 immunosuppressant and antifungal antibiotic cyclosporin A enhances subsequent binding of cardiolipin

188 Cyclosporin A enhances the loading capacity in the prese

189 Cyclosporin A-exposed mitochondria buffered calcium more

190 when mitochondria were depolarized prior to cyclosporin A exposure, and the effects of cyclosporin A

191 ally approved immunosuppressive drugs (e.g., cyclosporin A, FK506) possess dose-dependent biphasic ef

192 eptors for immunosuppressive drugs including cyclosporin A, FK506, and rapamycin.

193 M-244769), or two inhibitors of calcineurin (cyclosporin-A, FK506).

194 cause agents that either physically compete (cyclosporin A) for or indirectly occlude (vanadate) the

195 Treatment of human platelets with cyclosporin A gave a similar phenotype.

196 In addition, cyclosporin A had no effect on the basal or prazosin-sti

197 In intact mitochondria, cyclosporin A had no effect, indicating that ATP consump

198 over, anti-IL-13 therapy in combination with cyclosporin A had profound effects on reducing murine BO

199 ients treated with xenon in combination with cyclosporin A had prolonged renal allograft survival.

200 Cyclosporin-A improved plasma membrane localization of b

201 ivity below 100 nM and are as efficacious as cyclosporin A in an in vivo mouse model of anti-CD3-indu

202 , insulin exposure was still as effective as cyclosporin A in delaying mitochondrial permeability tra

203 nt ligands (e.g., drugs such as tamoxifen or cyclosporin A) in complex protein mixtures such as cell

204 s (valproate, doxycycline, tetracycline, and cyclosporin A) in cultured hepatic cells and the livers

205 Cyclosporin-A increased expression of ABCB4(S320F) and A

206 of calcineurin (Cn) by low concentrations of cyclosporin A increases osteoblast differentiation in vi

207 iration, induced a time- and dose-dependent, cyclosporin A-independent permeability transition (PT) o

208 treated with calcineurin inhibitors such as cyclosporin A indicates that calcineurin/nuclear factor

209 ic LV seemed to be relatively insensitive to cyclosporin A, indicating that it does not require CyPA

210 d upregulated expression of renal NUPR1, and cyclosporin A induced Nupr1 expression in cultured human

211 of mutant SOD1 protects these cells against cyclosporin A-induced cell death.

212 Cyclosporin-A-induced endothelial dysfunction is related

213 scriptional signature in vivo, we found that cyclosporin A induces pathways dependent on the transcri

214 to induction of the permeability transition, cyclosporin A inhibition was less potent in striatal mit

215 mone-binding site and the mechanism by which cyclosporin A inhibits activation of the peptide pheromo

216 odamine 123 and mitoxantrone, we showed that cyclosporin A inhibits P-gp function at low micromolar c

217 Indeed, cyclosporin A injection and stereotaxic delivery of the

218 hat form "unregulated," constitutively open, cyclosporin A-insensitive permeability transition (PT) p

219 shold of unregulated (Ca(2+)-independent and cyclosporin A-insensitive) MPT pore opening induced by h

220 Together, our results suggest that cyclosporin A is neither a substrate nor an inhibitor of

221 in the absence of the immunosuppressant drug cyclosporin A is not known.

222 Cyclosporin A is recommended as first-line treatment for

223 low-dose CNI (trough tacrolimus </=5 ng/mL, cyclosporin A </=50 ng/mL) in 29 patients (18 patients w

224 Moreover, the administration of cyclosporin A markedly inhibited (99m)Tc-mebrofenin excr

225 e present at high levels in the CNS and that cyclosporin A may possess neuroprotective/neurotrophic e

226 Pore opening can be inhibited by cyclosporin A mediated via cyclophilin D.

227 In contrast, sarcomere mutation and cyclosporin A-mediated calcineurin inhibition stimulate

228 -epsilon(4-nitrobenzofurazan-7-yl)-D-Lys(8)]-cyclosporin A (NBDL-CSA) into the lumens of isolated rat

229 ot lose calcein, nor was there any effect of cyclosporin A on DeltaPsim, which ruled out a contributi

230 The effect of cyclosporin A on presynaptic calcium was abolished when

231 in humans, including dexamethasone, digoxin, cyclosporin A, ondansetron, domperidone, and loperamide.

232 or-dependent IL-4 secretion was blocked with cyclosporin A or 11R-VIVIT peptide.

233 ion was prevented by the calcineurin blocker cyclosporin A or A-285222.

234 The Ca2+-induced changes were inhibited by cyclosporin A or ADP.

235 eincubation with the calcineurin inhibitors, cyclosporin A or ascomycin, significantly reduced the ab

236 liculi, was obtained by cell treatments with cyclosporin A or C and, to a lesser extent, B, D, or H.

237 H(o) 7.4, as long as phosphatase inhibitors (cyclosporin A or endothal) were present.

238 neurin is inhibited either by the inhibitors cyclosporin A or FK506 or by small interfering RNA-targe

239 ully abrogated by the calcineurin inhibitors cyclosporin A or FK506, confirming that SrRan activates

240 udies have shown that the immunosuppressants cyclosporin A or FK506, which interact with the peptidyl

241 s blocked by specific calcineurin inhibitors cyclosporin A or FK520.

242 chondria, or if neurons were pretreated with cyclosporin A or N-methyl-4-isoleucine-cyclosporin (NIM8

243 Hearts perfused with cyclosporin A or sanglifehrin A, powerful inhibitors of

244 ating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, emphasizing the essen

245 er serum levels of IS needed higher doses of cyclosporin, a P-gp substrate, to obtain the cyclosporin

246 , 1% methylprednisolone (P < .01), and 0.05% cyclosporin A (P < .03).

247 ) prophylaxis, while the ATG groups received cyclosporin A + prednisone.

248 When endocytosis was promoted by cyclosporin A pretreatment, the dye uptake was significa

249 is mitochondrial damage was not prevented by cyclosporin A pretreatment.

250 Neither Btk deficiency nor cyclosporin A prevented FOXO1 protein phosphorylation, i

251 w that the immunophilin ligand FK506 but not cyclosporin A prevents the development of neurotoxicity

252 The MPTP inhibitor cyclosporin A protects mouse bone marrow and human cord

253 Treatment with cyclosporin A provided only a marginal and transient enh

254 The cyclosporin A receptors are referred to as cyclophilins

255 nterference had an effect similar to that of cyclosporin A: reduction of cell surface expression of C

256 In primary cultures treated with cyclosporin A, renal tubular cells isolated from Nupr1-d

257 ore opening with the cyclophilin D inhibitor cyclosporin A restored Deltapsi(m) and rescued cell viab

258 protection, but addition of the MPTP closer cyclosporin A restored protection.

259 ons with the calcineurin inhibitors FK506 or cyclosporin A resulted in nuclear accumulation of phosph

260 Furthermore, administration of cyclosporin A reversed the LPS-induced increase in podoc

261 ules known to interact with OATPs, including cyclosporin A, rifampicin, and glibenclamide, each demon

262 Cyclosporin A, sanglifehrin A, and Mg2+, inhibitors of t

263 e IL-3 gene, and included a highly inducible cyclosporin A-sensitive enhancer at -37 kb that increase

264 riggered transient, spontaneously reversible cyclosporin A-sensitive swelling closely resembling remo

265 ndria by the uniporter inhibitor RU360 or by cyclosporin A significantly prevented the OSW-1-induced

266 Treatment with cyclosporin A significantly reduced surface expression o

267 ation-induced Foxp3 binding was abrogated by cyclosporin A, suggesting a role for the phosphatase cal

268 147 is sensitive to cyclophilin-binding drug cyclosporin A, suggesting involvement of a cyclophilin i

269 The loss of pFAK is inhibited by cyclosporin A, suggesting that these Ca2+ transients exe

270 Cyclosporin A suppressed the effect of VIVIT on cardiomy

271 ncentration immediately upon incubation with cyclosporin A that correlated with the changes in synapt

272 The permeability transition pore blocker cyclosporin A, the caspase-3 inhibitor Z-DEVD-fmk (40 mi

273 e, intracellular dialysis of deltamethrin or cyclosporin A, the specific calcineurin (protein phospha

274 t versus host disease (GVHD) prophylaxis was cyclosporin A to day 180 plus mycophenolate mofetil to d

275 Furthermore, xenon works additively with cyclosporin A to preserve post-transplant renal function

276 hibition of calcineurin with either FK506 or cyclosporin A totally abolished both depolarization- and

277 nsplant when ischemia-reperfusion injury and cyclosporin A toxicity may coexist.

278 n microdissected tubules from a rat model of cyclosporin A toxicity to describe the related epithelia

279 e cyclin D1 mRNA was induced normally in the cyclosporin A-treated cells, we analyzed the half-life o

280 Cyclosporin A-treated Nfatc1(+/-) mice demonstrated rapi

281 However, cyclosporin A treatment dramatically reduced cyclin D1 p

282 A randomized, controlled trial of cyclosporin A treatment for 2 weeks was performed in per

283 Cyclosporin A treatment inhibited VA opening, implying t

284 Upon cyclosporin A treatment, Nupr1-deficient mice exhibited

285 romotion of IL-2 production was resistant to cyclosporin A treatment, suggesting that CD44 costimulat

286 1% methylprednisolone, and were absent after cyclosporin A treatment.

287 Taxol and cyclosporin A treatments also did not enhance Tx-67 perm

288 Initial and 3- to 6-month cyclosporin A trough level targets were 250 to 300 and 2

289 Indeed, we found that, like cyclosporin A, valspodar inhibits peptide pheromone acti

290 '-chlorodiazepam, an IMAC inhibitor, whereas cyclosporin A was ineffective.

291 transplanted from PVG.R8 donors and low-dose cyclosporin A was initiated.

292 inst high Ca2+ in the presence of ATP, where cyclosporin A was reported to be ineffective.

293 0)) of MDR modulators LY335979, PSC 833, and cyclosporin A were 69 nmol/L, 1 micromol/L, and 3 microm

294 involved in its interaction with the ligand cyclosporin A, were shown to be critical for CCR5-bindin

295 Both of these effects were prevented by cyclosporin A, which also decreased SHetA2-induced apopt

296 Cyclosporin A, which inhibits calcineurin upstream of NF

297 uction of the change in DeltaPsim and PCD by cyclosporin A, which inhibits mitochondrial permeability

298 Administration of cyclosporin A, which stabilizes synaptopodin, reduced LP

299 Furthermore, the combination of low dose cyclosporin A with anti-CXCL9 therapy had more profound

300 tors cyclosporin A (CsA) and a derivative of cyclosporin A with modifications in the d-Ser side chain