ライフサイエンスコーパス: FK506

1 ant drug cyclosporine A (CsA) or tacrolimus (FK506).

2 (dexamethasone) and a calcineurin inhibitor (FK506).

3 wo inhibitors of calcineurin (cyclosporin-A, FK506).

4 ssed the effects of a calcineurin inhibitor, FK506.

5 her CNA12 or eGFP in the presence/absence of FK506.

6 eurin-specific inhibitors cyclosporine A and FK506.

7 ding protein for the immunosuppressant drug, FK506.

8 g in the high-affinity ligands rapamycin and FK506.

9 ) or alphaCD3 is inhibited by CsA or related FK506.

10 PGC1-alpha mRNA was down-regulated by FK506.

11 e complex with the structurally related drug FK506.

12 ymetrix 430A chips, and CN was inhibited via FK506.

13 atic growth and strongly inhibited (>99%) by FK506.

14 the immunosuppressive calcineurin inhibitor FK506.

15 the immunosuppressive drugs cyclosporine and FK506.

16 hibited by dexamethasone but was enhanced by FK506.

17 i-IgE Ab in the presence of dexamethasone or FK506.

18 but not by the calcineurin pathway inhibitor FK506.

19 ent and proteinuria, which were prevented by FK506.

20 ion but blocked by the calcineurin inhibitor FK506.

21 ded more than eGFP-CTLs in mice treated with FK506.

22 ycin (RAPA; 0.1-0.5-1 mg/kg ip), tacrolimus (FK506; 0.1-0.5-1 mg/kg ip), mycophenolate mofetil (MMF;

23 y, we showed that systemic administration of FK506 (1.5 mg kg(-1) day(-1)) for 7 days in rats led to

24 (CaSR) blocker NPS2390 (0.1 and 10 mum) nor FK506 (10 mum), a drug which displaces FKBP12.6 from rya

25 FK506 (2 mg/kg) significantly prolonged graft survival (

26 FK506 (50 ng/mL) and cyclosporine A (800 ng/mL) had comp

27 d by the Ca(2)(+) chelator, EGTA, as well as FK506, a specific inhibitor of Ca(2)(+)-calmodulin-depen

28 nderlie clinical arrhythmias associated with FK506 administration.

29 xhibits in vitro synergy with caspofungin or FK506 against drug susceptible or resistant C. albicans

30 tor caspofungin or the calcineurin inhibitor FK506 against the human fungal pathogen Candida albicans

31 Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, wh

32 Low-dose FK506 also reversed severe PAH in rats with medial hyper

33 We noted that FK506 altered nuclear localization of the GR and inhibit

34 Recently FK506, an inhibitor of the FKBP family of peptidyl proly

35 Using FK506, an inhibitor of the FKBP51 isomerase activity, we

36 er transfection, the addition of AP20187 (an FK506 analog) induced regulated dimerization of Fv-SLK 1

37 Next, the effect of two small molecules, FK506 and (-)-epigallocatechin-3-gallate (EGCG), known t

38 rate that DC inhibit T cells by sequestering FK506 and continuously releasing the drug over several d

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

40 Calcineurin inhibitors (FK506 and cyclosporine A) and the cathepsin L inhibitor

41 inhibited 20-30% by calcineurin inhibitors (FK506 and cyclosporine A).

42 tetraacetic acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from ca

43 ungi and is a target of the natural products FK506 and Cyclosporine A.

44 angiogenic response to potential therapies, FK506 and Elafin, was related to reduced slit guidance l

45 ed rat islets were incubated with vehicle or FK506 and harvested at 24-hr intervals.

46 was not prevented by immunosuppression with FK506 and mycophenolate mofetil.

47 FK506 and okadaic acid also inhibited the increase, impl

48 Importantly, pretreatment with FK506 and overexpression of the GluR1 mutants, S845D (ph

49 ICI values showed an additive effect between FK506 and PHMB, AMB, or VCZ.

50 s common to the immunosuppressive inhibitors FK506 and rapamycin bind to the most conserved region of

51 wo inexpensive and widely available ligands, FK506 and rapamycin, functioned similarly to Shld1, with

52 rolide structure of the natural FKBP binders FK506 and Rapamycin.

53 atalytic domain that binds to the inhibitors FK506 and rapamycin.

54 ich is inhibitable by the immunosuppressants FK506 and rapamycin.

55 get of the immunosuppresive antifungal drugs FK506 and rapamycin.

56 lified alpha-ketoamide analogue derived from FK506 and the first structure-activity relationship anal

57 reporter to evaluate the effects of DEX and FK506 and the overexpression of GRbeta and FKBP51 on glu

58 ls were treated with dexamethasone (DEX) and FK506 and transfected with GRbeta and FKBP51 expression

59 1 is abolished by the calcineurin inhibitor (FK506) and by knocking out the calcineurin target, prz1.

60 ty of the calcineurin inhibitors tacrolimus (FK506) and cyclosporine A (CSA) to enhance the activity

61 (2+)-sensing domain of STIM1 with the 12-kDa FK506- and rapamycin-binding protein (FKBP12, also known

62 neurin inhibitors such as cyclosporine A and FK506 are effective immunosuppressants but produce sever

63 Rapamycin and FK506 are two macrocyclic natural products that bind to

64 Rapamycin and FK506 are two macrocyclic natural products, which tightl

65 rin/NFAT binding, such as cyclosporine A and FK506, are broadly used in organ transplantation and can

66 The critical role of CsA/FK506 as an immunosuppressant following transplantation

67 FK506 augmented the intracellular acidification of VSMCs

68 neal injections of the calcineurin inhibitor FK506 before and after infusion of the radiocontrast age

69 the tip of the beta4-beta5 loop in the first FK506 binding domain (FK1) of the FKBP51 and FKBP52 prot

70 lin production, whereas the immunomodulatory FK506 binding protein (FK506BP) was up-regulated.

71 ocytes, we expressed a fusion protein of the FK506 binding protein (FKBP) and caspase 8 under control

72 rapamycin-inducible interaction between the FK506 binding protein (FKBP) and the FKBP-rapamycin bind

73 The FK506 binding protein (FKBP) family of proteins provide

74 Expression of FK506 binding protein (FKBP)-clathrin light chain chimer

75 Our data revealed that both the FK506 binding protein (FKBP)-like domain and the tetratr

76 Members of this family, and notably FK506 binding protein (FKBP12), are thought to be involv

77 t involving an endogenous ER-localized 13-kD FK506 binding protein (FKBP13) competing with the FKBP12

78 and bronchial epithelial gene expression of FK506 binding protein (FKBP5), an indicator of steroid r

79 The 52 kDa FK506 binding protein (FKBP52) is an important positive

80 Through insertion of a modified FK506 binding protein (insertable FKBP12, iFKBP) into th

81 entrapped in the core of ELP nanoparticles, FK506 binding protein 12 (FKBP), which is the cognate pr

82 in mice in the context of rapamycin-induced FK506 binding protein 12 (FKBP12)-FKBP12 rapamycin bindi

83 h genotype shows similar expression of RyR1, FK506 binding protein 12 kDa, and Ca(2+)-ATPase, but RyR

84 Dissociation of the small FK506 binding protein 12 subunit (FKBP12) increases RyR1

85 FKBP12 (FK506 binding protein 12) is a prolyl cis-trans isomeras

86 Calstabin2, also named FK506 binding protein 12.6 (FKBP12.6), is a subunit of r

87 We previously identified the FK506 binding protein 38 (FKBP38) as a negative regulato

88 that PA competes with the mTORC1 inhibitor, FK506 binding protein 38 (FKBP38), for mTOR binding at a

89 ine methylation within the gene encoding for FK506 binding protein 5 (FKBP5) was measured in Holocaus

90 ylase, brain-derived neurotrophic factor and FK506 binding protein 5.

91 Single nucleotide polymorphisms of the FK506 binding protein 51 (FKBP51) gene have been repeate

92 d that the suggested psychiatric risk factor FK506 binding protein 51 (FKBP51) increases phosphorylat

93 FK506 binding protein 51 (FKBP51, also called FKBP5) bel

94 FK506 binding protein 51 kDa (FKBP51, encoded by FKBP5)

95 eased the relative association of Hsp90 with FK506 binding protein 51 versus FK506 binding protein 52

96 f Hsp90 with FK506 binding protein 51 versus FK506 binding protein 52 and inhibited hormone-induced G

97 ations in lysyl hydroxylase 2 (LH2/PLOD2) or FK506 binding protein 65 (FKBP65/FKBP10).

98 S107 (a stabilizer of RyR1-FK506 binding protein coupling that reduces Ca(2+) leak)

99 romosome 6p21.3 at TNXB (tenascin XB)-FKBPL (FK506 binding protein like) [rs12153855/rs9391734; disco

100 The recognition protein (FK506 binding protein) is inserted into functionally-ina

101 2-rapamycin-binding domain (FRB) and FKBP12 (FK506 binding protein), the interaction of hypoxia-induc

102 ocorticoid-induced leucine zipper (GILZ) and FK506 binding protein-51 (FKBP51)].

103 opsis thaliana lines (BP12) expressing yeast FK506 Binding Protein12 were developed.

104 re shown to require the functionality of the FK506 binding protein42 TWISTED DWARF1 (TWD1), although

105 ted the molecular events associated with the FK506 binding proteins (FKBP) -52 and -51 response to co

106 FKBP5) belongs to a family of immunophilins, FK506 binding proteins (FKBPs).

107 This methodology relies on a mutated FK506-binding protein (FKBP) destabilizing domain (dd) f

108 The FK506-binding protein (FKBP) family of peptidyl-prolyl i

109 Mips are part of the FK506-binding protein (FKBP) family, whose members typic

110 , a cell-permeable molecule used to dimerize FK506-binding protein (FKBP) fusion proteins and initiat

111 between five single-cysteine variants of the FK506-binding protein (FKBP) labeled with a donor probe,

112 the chemically inducible dimerization domain FK506-binding protein (FKBP) or to the hexameric protein

113 chimeric molecule by fusing a domain of the FK506-binding protein (FKBP) to the C terminus of APP.

114 asmic reticulum membranes with a fluorescent FK506-binding protein (FKBP), and FRET was determined fo

115 the scattering data features two independent FK506-binding protein (FKBP)-like and tetratricopeptide

116 and with FRET measurements involving RyR and FK506-binding protein (FKBP).

117 ity for the abundant, cytoplasmic chaperone, FK506-binding protein (FKBP).

118 how that the SPRY1 domain is located next to FK506-binding protein (FKBP).

119 One chimera consists of a FK506-binding protein (FKBP12) fused to a cellular 'addr

120 onstants were determined for those amides of FK506-binding protein (FKBP12), ubiquitin, and chymotryp

121 phatase calcineurin when bound to the 12 kDa FK506-binding protein (FKBP12).

122 dependent on its interaction with the 12-kDa FK506-binding protein (FKBP12).

123 on of the 12-kDa cis-trans proline isomerase FK506-binding protein (FKBP12).

124 Calmodulin (CaM) and FK506-binding protein (FKBP12.6) bind to RyR2 and stabil

125 ucocorticoid receptors (GRs), and (4) 51 kDa FK506-binding protein (FKBP5).

126 shock protein 47 (Hsp47/SERPINH1) and 65-kDa FK506-binding protein (FKBP65/FKBP10), have been shown t

127 eby a chimeric PrP(C) composed of a modified FK506-binding protein (Fv) fused with PrP(C) and termed

128 FK506-binding protein 10 (FKBP10) is a collagen chaperon

129 Loss of function mutations in FK506-binding protein 10 (FKBP10), encoding the FKBP65 p

130 tes to BCR-mediated lytic induction and that FK506-binding protein 12 (FKBP12) binding alone is not a

131 The FK506-binding protein 12 (FKBP12) is a cytoplasmic prote

132 n transgenic plants deficient in Arabidopsis FK506-binding protein 12 (FKP12), whereas FKP12 overexpr

133 a(2+) channel (dihydropyridine receptor) and FK506-binding protein 12 as well as in "hot spot" region

134 labeled CaM binding near donor-labeled FKBP (FK506-binding protein 12.6) on the cytoplasmic domain of

135 we found that hippocampal overexpression of FK506-binding protein 12.6/1b (FKBP1b), a negative regul

136 Hippocampal overexpression of FK506-binding protein 12.6/1b (FKBP1b), a negative regul

137 e found that expression of the gene encoding FK506-binding protein 12.6/1b (FKBP1b), a small immunoph

138 Recently, we found that FK506-binding protein 12.6/1b (FKBP1b), a small protein

139 In cardiomyocytes, FK506-binding protein 1b/12.6 (FKBP1b) binds and stabili

140 FK506-binding protein 38 (FKBP38), a membrane-anchored,

141 e response regions of progesterone-regulated FK506-binding protein 5 (FKBP5) immunophilin and small R

142 evels of the glucocorticoid-responsive genes FK506-binding protein 5 (Fkbp5), Period 1 (Per1), and se

143 The FKBP5 gene codes for a co-chaperone, FK506-binding protein 5, that exerts negative feedback o

144 portant modulator of stress responses is the FK506-binding protein 51 (FKBP5/FKBP51).

145 The FK506-binding protein 51 (FKBP51) is a key regulator of

146 The FK506-binding protein 51 (FKBP51) is a promising drug ta

147 FK506-binding protein 51 (FKBP51) is gaining increased r

148 In the quest for lead-like ligands for the FK506-binding protein 51 (FKBP51), we designed two new c

149 Here, we show that the Hsp90 cochaperone, FK506-binding protein 51 (FKBP51), which possesses both

150 ic antigen, transmembrane protease serine 2, FK506-binding protein 51 and fatty acid synthase.

151 FK506-binding protein 51 is involved in hypothalamic-pit

152 Immunophilin FK506-binding protein 52 (FKBP52) is a cochaperone that

153 We have now examined the role of FK506-binding protein 8 (FKBP8), a component of the CFTR

154 protein 90 (Hsp90)-associated co-chaperones: FK506-binding protein 8 (FKBP8), activator of Hsp90 ATPa

155 a by dimerizing rapamycin-binding domain and FK506-binding protein domains that are attached to ciste

156 e Ca(2+) channel CaV1.1, calmodulin, and the FK506-binding protein FKBP12, as well as in "hot spot" r

157 ncrease) and unaltered RyR2 affinity for the FK506-binding protein FKBP12.6 (Kd~0.8 nmol/L).

158 The large FK506-binding protein FKBP52 has been characterized as a

159 mall-molecule drug discovery, as engineering FK506-binding protein into intracellular sites within Ca

160 Mutation of the immunophilin-like FK506-binding protein TWISTED DWARF1 (FKBP42/TWD1) cause

161 Here, we assess the impact of FK506-binding protein with a molecular mass of approxima

162 lyses demonstrated CG17282 is a noncanonical FK506-binding protein with an inactive peptide prolyl-is

163 t into two moieties that were fused to FKBP (FK506-binding protein) and FRB (rapamycin-binding domain

164 ation of receptor function by FKBP52 (52-kDa FK506-binding protein), which acts at a later stage of t

165 gh-resolution X-ray structures of ubiquitin, FK506-binding protein, chymotrypsin inhibitor 2, and rub

166 domain) was fused with a cDNA for a modified FK506-binding protein, Fv (Fv-SLK 1-373).

167 the immunophilins, cyclophilin A, and 12-kDa FK506-binding protein, in resting human Jurkat T cells.

168 Phosphatidic acid (PA) interacts with the FK506-binding protein-12-rapamycin-binding (FRB) domain

169 own that male mice with targeted ablation of FK506-binding protein-52 (Fkbp52) develop hypospadias, m

170 Heat shock protein 47 (HSP47) and FK506-binding protein-65 (FKBP65) defects cause types X

171 The FK506-binding proteins (FKBP) 51 and 52 are cochaperones

172 FK506-binding proteins (FKBP) 51 and 52 are cochaperones

173 The 12-kDa FK506-binding proteins (FKBP12 and FKBP12.6) are regulat

174 some amino acid sequence similarity to human FK506-binding proteins (FKBPs) in residues 166 to 252 lo

175 Immunophilins, including FK506-binding proteins (FKBPs), are protein chaperones w

176 ) are a chaperone superfamily comprising the FK506-binding proteins (FKBPs), cyclophilins, and parvul

177 FK506-binding proteins FKBP12.6 and FKBP12 are associate

178 FKBP38 is a member of the family of FK506-binding proteins that acts as an inhibitor of the

179 is in many ways an exceptional member of the FK506-binding proteins.

180 iphosphate-binding cassette transporters and FK506-binding proteins.

181 CN inhibitor FK506 blocked expression of 38 genes, as confirmed by qu

182 Calcineurin inhibition by FK506 blocks M. circinelloides transition to hyphae and

183 e inhibition of calcineurin with tacrolimus (FK506) blocks both cellular processes.

184 ine in motor function in Drosophila requires FK506-BP2 function within the muscle.

185 Muscle expression of FK506-BP2 in FK506-BP2 mutants completely restores the s

186 Although FK506-BP2 mutant flies are found to have less sensitivit

187 Interestingly, FK506-BP2 mutant flies have reduced sensitivity to the e

188 Muscle expression of FK506-BP2 in FK506-BP2 mutants completely restores the sensitivity of

189 o have less sensitivity to oxidative stress, FK506-BP2 mutants do not live longer than wild type.

190 this effect of S107 is absent in calstabin (FK506-BP2) mutants.

191 nt to the inhibitory effect of rapamycin and FK506 but can be blocked by the presence of mycophenolat

192 L4, and CCL18 was significantly inhibited by FK506 but, with the exception of CCL1, was enhanced by d

193 The MMF/FK506 combination proved the best balance with less toxi

194 e observations that a calcineurin inhibitor, FK506, completely abrogated the dephosphorylation, and m

195 s recognized by the cyclophilin-CsA and FKBP-FK506 complexes.

196 the calcineurin inhibitors cyclosporin A or FK506, confirming that SrRan activates NFATc1 signaling

197 Our studies indicate that low-dose FK506 could be useful in the treatment of PAH.

198 FK506 crosses the blood brain barrier, is well tolerated

199 Thus, FK506, CSA, and A238L all prevent "LxVP"-mediated substr

200 Calcineurin inhibitors (FK506, cyclosporin A, and a peptide calcineurin inhibito

201 or the three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide

202 t pharmacologically relevant concentrations, FK506 decreases insulin secretion and reduces mitochondr

203 FK506 did not affect Na(+),HCO3(-) cotransport activity

204 FK506 did not prevent the generation and proliferation o

205 FK506 does not prevent DC survival, maturation, or costi

206 selective genetic and pharmacological tools (FK506) does the same.

207 ptidylprolyl isomerase FKBP12 interacts with FK506 forming a complex that inhibits the protein phosph

208 RAPA >/=0.5 mg/Kg, FK506 >/=0.5 mg/Kg, and MMF >/=120 mg/kg had detrimental

209 drug disk diffusion assays demonstrate that FK506 has synergistic fungicidal activity with caspofung

210 Cyclosporin A (CsA) and tacrolimus (FK506) has been reported to reduce proteinuria in patien

211 itors, such as cyclosporin A and tacrolimus (FK506), have played a pivotal role in the preservation o

212 m3:Fpr1 interaction by the immunosuppressant FK506, illustrating the assay's capacity to identify che

213 FK506 immunosuppression facilitated the establishment of

214 cells by pretreatment with cyclosporine A or FK506, implicating the calcium-dependent phosphatase cal

215 of ER luminal FKBP10 was almost as potent as FK506 in attenuating expression of PrP(C).

216 ined the activity of a calcineurin inhibitor FK506 in combination with caspofungin against echinocand

217 In vitro studies: FK506 in combination with PHMB, VCZ, or AMB enhanced fun

218 However, FK506 increased the association of FKBP51 with GRbeta an

219 ests were performed with PHMB, AMB, VCZ, and FK506, individually and in combination against Aspergill

220 In conclusion, CsA and FK506 inhibit proteinuria by protecting against PAN-indu

221 activity in T cells and suggest that CsA and FK506 inhibit selected effector T cell functions via a C

222 Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signaling, there

223 FK506 inhibited the observed alphaSYN oligomerization bo

224 unophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not CrkI association with C3

225 Treatment with the FK506 inhibitor of FKBP-FRB interaction prevented the fo

226 FK506 inhibits retrograde trafficking of H-Ras from the

227 ity by treatment with cyclosporin A (CsA) or FK506 is a cornerstone of immunosuppressive therapies.

228 Tacrolimus (FK506) is one of the most widely used immunosuppressive

229 Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and T

230 that posttransplantation diabetes induced by FK506 may be mediated by its effects on mitochondrial fu

231 of the microarray data identified potential FK506-mediated pathways and regulatory motifs.

232 Here, we show that AMD3100 and FK506 mobilization of endogenous stem cells immediately

233 Pathway analysis of microarray data showed FK506 modification of pathways involving ATP metabolism,

234 y treatment with substrates (cyclosporine A, FK506), modulators (tariquidar), or small corrector mole

235 of this study was to determine the effect of FK506 on CSF chemokine levels in PND patients.

236 tigated the protective mechanisms of CsA and FK506 on proteinuria in a rat model of MCD induced by pu

237 cts of TPR ligands, cyclosporine A (CsA) and FK506, on AR activity were not observed, indicating that

238 atment as well as cyclosporine A, but not by FK506 or bile acids, suggesting that Gly(50) is involved

239 t of neurons with the calcineurin inhibitors FK506 or cyclosporin A resulted in nuclear accumulation

240 eurin; inhibition of calcineurin with either FK506 or cyclosporin A totally abolished both depolariza

241 In vivo, mice that received FK506 or were deficient in the calcineurin isoform Abeta

242 ytic site, antagonism with cyclosporine A or FK506, or intracellular perfusion with a peptide mimicki

243 ytotoxicity in the presence of cyclosporine, FK506, or rapamycin.

244 onstrated previously that a 12-day course of FK506 permits the induction of tolerance to fully MHC-mi

245 mmunosuppressive drugs (e.g., cyclosporin A, FK506) possess dose-dependent biphasic effects that caus

246 r calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of NF-kappaB and acinar cell

247 The calcineurin inhibitor FK506 prevented contrast-induced activation of NF-kappaB

248 conditional Bmpr2 deletion in ECs, low-dose FK506 prevented exaggerated chronic hypoxic PAH associat

249 Treatment with FK506 produced a synergistic effect in the grafts from A

250 tors of the PI activity of FKBP12, including FK506, rapamycin, and cycloheximide, increase steady-sta

251 les, macrocyclic natural products, including FK506, rapamycin, and cyclosporin, bind PPIases with nan

252 imilarly, administration of the CN inhibitor FK506 reduced proteinuria and tubular injury but had mor

253 d in response to cell treatment with CsA and FK506, reflecting increased trans-to-cis conversion of C

254 FK506 released FKBP12 from type I receptors activin rece

255 6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature protein trapped in

256 We confirmed their FK506 resistance and anti-PTLD activity in vivo using a

257 or the calcineurin cnbR or cnaA genes confer FK506 resistance and restore hyphal growth.

258 and found that FKBP12-silenced EBV-CTLs are FK506 resistant.

259 Here we examined whether or not FK506-resistant EBV-CTLs control EBV-driven tumor progre

260 FK506-resistant epimutants readily reverted to the drug-

261 Cyp40 and FKBP51 are the targets of CsA and FK506, respectively.

262 mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cytoskeleto

263 from patients with idiopathic PAH, low-dose FK506 reversed dysfunctional BMPR2 signaling.

264 FK506 significantly decreased mitochondrial content and

265 other hand, MMF alone or in association with FK506 significantly prolonged the time to islet rejectio

266 vation of BMP pathway activity with low-dose FK506, suggesting an approach to management of human bla

267 coincubation with the calcineurin inhibitor FK506, suggesting involvement of DYRK1A and nuclear fact

268 Combination of dexamethasone and FK506 suppressed production of all chemokines by anti-Ig

269 Mice receiving CNA12-CTLs and treated with FK506 survived significantly longer than control-treated

270 en, and treatment with the immunosuppressant FK506 (tacrolimus) decreases CSF white blood cell counts

271 FK506 (Tacrolimus) is a potent inhibitor of calcineurin

272 The calcineurin inhibitor FK506 (tacrolimus) reduced cell death and lateral transf

273 pontaneous resistance to the antifungal drug FK506 (tacrolimus) via two distinct mechanisms.

274 The best response was achieved with FK506 (tacrolimus), via a dual mechanism of action as a

275 them resistant to calcineurin (CN) inhibitor FK506 through retroviral transfer of a calcineurin A mut

276 that can be selectively targeted by CsA and FK506 to achieve inhibition of androgen-induced cell pro

277 Binding of FK506 to the FKBP domain causes the target domain to fir

278 man transplant recipients, LCMV infection of FK506-treated mice resulted in a lethal disease characte

279 sal horn neurons was profoundly increased in FK506-treated rats and was reduced by blocking NMDARs.

280 of miniature EPSCs in dorsal horn neurons of FK506-treated rats.

281 ciceptive and mechanical hypersensitivity in FK506-treated rats.

282 rn neurons was also significantly greater in FK506-treated than in vehicle-treated rats.

283 Both FK506 treatment and FKBP10 depletion were effective in r

284 cordings in spinal cord slices revealed that FK506 treatment caused a large increase in the amplitude

285 Our results showed that CsA and FK506 treatment decreased proteinuria via a mechanism as

286 FK506 treatment of dendritic cells (FKDC) limits their c

287 FK506 treatment prior to IR prevented Drp1-S637 dephosph

288 We show that FK506 treatment results in a profound reduction in PrP(C

289 such as activated T cells, and we found that FK506 treatment specifically decreased CSF CXCL10 from a

290 CSF samples before and after FK506 treatment were tested by multiplex assay for the p

291 s nor spine density changes were affected by FK506 treatment, suggesting that calcineurin acts via a

292 mobilization is resistant to cyclosporine or FK506 treatment, while de novo CD40L and cytokine expres

293 2-, and 1.43-fold, respectively, after 48-hr FK506 treatment.

294 lanted into B6 AID(-/-) mice with or without FK506 treatment.

295 ive strategy inspired by the natural product FK506, we have synthetically modified an HIV protease in

296 RAPA and/or FK506 were inefficient in preventing rejection, even whe

297 lymphoma regression despite the presence of FK506, whereas eGFP-CTLs did not.

298 aft recipients treated with cyclosporine and FK506, whereas there was a significant decrease in NK ce

299 ted with cyclosporine A (CsA) or tacrolimus (FK506), which not only often causes severe adverse effec

300 the alpha-ketoamide moiety of rapamycin and FK506 with a sulfonamide was envisaged with the retentio