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1 wo inhibitors of calcineurin (cyclosporin-A, FK506).
2 ide effects and worse clinical outcomes than FK506.
3 ent and proteinuria, which were prevented by FK506.
4 ion but blocked by the calcineurin inhibitor FK506.
5 ded more than eGFP-CTLs in mice treated with FK506.
6 ssed the effects of a calcineurin inhibitor, FK506.
7 her CNA12 or eGFP in the presence/absence of FK506.
8 eurin-specific inhibitors cyclosporine A and FK506.
9 ding protein for the immunosuppressant drug, FK506.
10 g in the high-affinity ligands rapamycin and FK506.
11 ) or alphaCD3 is inhibited by CsA or related FK506.
12        PGC1-alpha mRNA was down-regulated by FK506.
13 e complex with the structurally related drug FK506.
14 ymetrix 430A chips, and CN was inhibited via FK506.
15 t peptide completely reversed the effects of FK506.
16 ydrazine substitution of the C22-carbonyl of FK506.
17 ycin (RAPA; 0.1-0.5-1 mg/kg ip), tacrolimus (FK506; 0.1-0.5-1 mg/kg ip), mycophenolate mofetil (MMF;
18 y, we showed that systemic administration of FK506 (1.5 mg kg(-1) day(-1)) for 7 days in rats led to
19  (CaSR) blocker NPS2390 (0.1 and 10 mum) nor FK506 (10 mum), a drug which displaces FKBP12.6 from rya
20                                              FK506 (2 mg/kg) significantly prolonged graft survival (
21                                              FK506 (50 ng/mL) and cyclosporine A (800 ng/mL) had comp
22 8 is a pharmacological target of tacrolimus (FK506), a macrolide immunosuppressant with several clini
23 d by the Ca(2)(+) chelator, EGTA, as well as FK506, a specific inhibitor of Ca(2)(+)-calmodulin-depen
24 tor antagonist CNQX or calcineurin inhibitor FK506 abolished the S-SCAM overexpression-induced loss o
25 nderlie clinical arrhythmias associated with FK506 administration.
26 xhibits in vitro synergy with caspofungin or FK506 against drug susceptible or resistant C. albicans
27 tor caspofungin or the calcineurin inhibitor FK506 against the human fungal pathogen Candida albicans
28                       Treatment with CsA and FK506 also inhibited PAN-induced podocytes apoptosis, wh
29                                     Low-dose FK506 also reversed severe PAH in rats with medial hyper
30                                     Recently FK506, an inhibitor of the FKBP family of peptidyl proly
31                                        Using FK506, an inhibitor of the FKBP51 isomerase activity, we
32 er transfection, the addition of AP20187 (an FK506 analog) induced regulated dimerization of Fv-SLK 1
33 nable us to develop a less immunosuppressive FK506 analog, APX879, with an acetohydrazine substitutio
34     Next, the effect of two small molecules, FK506 and (-)-epigallocatechin-3-gallate (EGCG), known t
35                                The inhibitor FK506 and an isoform-selective inhibitor of GSK3alpha, B
36 rate that DC inhibit T cells by sequestering FK506 and continuously releasing the drug over several d
37 hatase and the target of immunosuppressants, FK506 and cyclosporin A (CSA).
38                      Calcineurin inhibitors (FK506 and cyclosporine A) and the cathepsin L inhibitor
39  inhibited 20-30% by calcineurin inhibitors (FK506 and cyclosporine A).
40 tetraacetic acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from ca
41 ungi and is a target of the natural products FK506 and Cyclosporine A.
42  angiogenic response to potential therapies, FK506 and Elafin, was related to reduced slit guidance l
43 ed rat islets were incubated with vehicle or FK506 and harvested at 24-hr intervals.
44  was not prevented by immunosuppression with FK506 and mycophenolate mofetil.
45                                              FK506 and okadaic acid also inhibited the increase, impl
46 ICI values showed an additive effect between FK506 and PHMB, AMB, or VCZ.
47 s common to the immunosuppressive inhibitors FK506 and rapamycin bind to the most conserved region of
48 rolide structure of the natural FKBP binders FK506 and Rapamycin.
49 atalytic domain that binds to the inhibitors FK506 and rapamycin.
50 ich is inhibitable by the immunosuppressants FK506 and rapamycin.
51 e seen in FKBP12 ternary complexes formed by FK506 and rapamycin.
52 get of the immunosuppresive antifungal drugs FK506 and rapamycin.
53 lified alpha-ketoamide analogue derived from FK506 and the first structure-activity relationship anal
54 and regulatory (CnB) subunits complexed with FK506 and the FK506-binding protein (FKBP12) from human
55 nd the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluorocytosine (5FC) were found when Crypto
56 ty of the calcineurin inhibitors tacrolimus (FK506) and cyclosporine A (CSA) to enhance the activity
57  Calcineurin inhibitors, such as tacrolimus (FK506) and cyclosporine, are widely used as standard imm
58 neurin inhibitors such as cyclosporine A and FK506 are effective immunosuppressants but produce sever
59                                Rapamycin and FK506 are macrocyclic natural products with an extraordi
60                                Rapamycin and FK506 are two macrocyclic natural products that bind to
61                                Rapamycin and FK506 are two macrocyclic natural products, which tightl
62          Cyclosporin A (CsA) and tacrolimus (FK506) are valuable immunosuppressants for a range of cl
63 rin/NFAT binding, such as cyclosporine A and FK506, are broadly used in organ transplantation and can
64 but compounds targeting calcineurin, such as FK506, are immunosuppressive.
65                                              FK506 augmented the intracellular acidification of VSMCs
66 neal injections of the calcineurin inhibitor FK506 before and after infusion of the radiocontrast age
67 the tip of the beta4-beta5 loop in the first FK506 binding domain (FK1) of the FKBP51 and FKBP52 prot
68 lin production, whereas the immunomodulatory FK506 binding protein (FK506BP) was up-regulated.
69 ocytes, we expressed a fusion protein of the FK506 binding protein (FKBP) and caspase 8 under control
70                                          The FK506 binding protein (FKBP) family of proteins provide
71                                Expression of FK506 binding protein (FKBP)-clathrin light chain chimer
72              Our data revealed that both the FK506 binding protein (FKBP)-like domain and the tetratr
73          Members of this family, and notably FK506 binding protein (FKBP12), are thought to be involv
74 t involving an endogenous ER-localized 13-kD FK506 binding protein (FKBP13) competing with the FKBP12
75  and bronchial epithelial gene expression of FK506 binding protein (FKBP5), an indicator of steroid r
76                                   The 52 kDa FK506 binding protein (FKBP52) is an important positive
77              Through insertion of a modified FK506 binding protein (insertable FKBP12, iFKBP) into th
78  entrapped in the core of ELP nanoparticles, FK506 binding protein 12 (FKBP), which is the cognate pr
79  in mice in the context of rapamycin-induced FK506 binding protein 12 (FKBP12)-FKBP12 rapamycin bindi
80 h genotype shows similar expression of RyR1, FK506 binding protein 12 kDa, and Ca(2+)-ATPase, but RyR
81                    Dissociation of the small FK506 binding protein 12 subunit (FKBP12) increases RyR1
82                                      FKBP12 (FK506 binding protein 12) is a prolyl cis-trans isomeras
83 th are increased, and association of RyR2 by FK506 binding protein 12.6 (FKBP12.6) is decreased in PA
84                       Calstabin2, also named FK506 binding protein 12.6 (FKBP12.6), is a subunit of r
85 oform (RyR1) interaction with calmodulin and FK506 binding protein 12.6.
86 utations in the FKBP14 gene encoding FKBP22 (FK506 Binding Protein 22 kDa) cause kyphoscoliotic Ehler
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 ocaust survivors showed lower methylation of FK506 binding protein 5 (FKBP5) intron 7, site 6 compare
90 ine methylation within the gene encoding for FK506 binding protein 5 (FKBP5) was measured in Holocaus
91 ved in regulating the stress system, such as FK506 binding protein 5 (FKBP5), interact with early-lif
92 ding of Raf1-tr to the cytoplasmic chaperone FK506 binding protein 5.
93 ylase, brain-derived neurotrophic factor and FK506 binding protein 5.
94       Single nucleotide polymorphisms of the FK506 binding protein 51 (FKBP51) gene have been repeate
95 d that the suggested psychiatric risk factor FK506 binding protein 51 (FKBP51) increases phosphorylat
96                                              FK506 binding protein 51 (FKBP51, also called FKBP5) bel
97 f selected stress-response-associated genes (FK506 binding protein 51 [FKBP5], glucocorticoid recepto
98                                              FK506 binding protein 51 kDa (FKBP51, encoded by FKBP5)
99 eased the relative association of Hsp90 with FK506 binding protein 51 versus FK506 binding protein 52
100 f Hsp90 with FK506 binding protein 51 versus FK506 binding protein 52 and inhibited hormone-induced G
101 ations in lysyl hydroxylase 2 (LH2/PLOD2) or FK506 binding protein 65 (FKBP65/FKBP10).
102                   S107 (a stabilizer of RyR1-FK506 binding protein coupling that reduces Ca(2+) leak)
103 romosome 6p21.3 at TNXB (tenascin XB)-FKBPL (FK506 binding protein like) [rs12153855/rs9391734; disco
104                     The recognition protein (FK506 binding protein) is inserted into functionally-ina
105 ocorticoid-induced leucine zipper (GILZ) and FK506 binding protein-51 (FKBP51)].
106 opsis thaliana lines (BP12) expressing yeast FK506 Binding Protein12 were developed.
107 re shown to require the functionality of the FK506 binding protein42 TWISTED DWARF1 (TWD1), although
108 e of each immunophilin family, cyclophilins, FK506 binding proteins (FKBPs), and parvulins in bacteri
109 FKBP5) belongs to a family of immunophilins, FK506 binding proteins (FKBPs).
110 old that wrapped over a helix, typical of an FK506-binding domain.
111 ically inactive Cas9 (dCas9) in complex with FK506-binding protein (FKBP) and a CEM consisting of FK5
112 imerization system composed of the canonical FK506-binding protein (FKBP) and circular permutants of
113                                          The FK506-binding protein (FKBP) family of peptidyl-prolyl i
114                         Mips are part of the FK506-binding protein (FKBP) family, whose members typic
115 , a cell-permeable molecule used to dimerize FK506-binding protein (FKBP) fusion proteins and initiat
116 between five single-cysteine variants of the FK506-binding protein (FKBP) labeled with a donor probe,
117 the chemically inducible dimerization domain FK506-binding protein (FKBP) or to the hexameric protein
118 on, in which they form binary complexes with FK506-binding protein (FKBP) through a shared FKBP-bindi
119 the scattering data features two independent FK506-binding protein (FKBP)-like and tetratricopeptide
120 how that the SPRY1 domain is located next to FK506-binding protein (FKBP).
121 and with FRET measurements involving RyR and FK506-binding protein (FKBP).
122  (CnB) subunits complexed with FK506 and the FK506-binding protein (FKBP12) from human fungal pathoge
123                  WDB002, in complex with the FK506-binding protein (FKBP12), potently and selectively
124 on of the 12-kDa cis-trans proline isomerase FK506-binding protein (FKBP12).
125 phatase calcineurin when bound to the 12 kDa FK506-binding protein (FKBP12).
126                         Calmodulin (CaM) and FK506-binding protein (FKBP12.6) bind to RyR2 and stabil
127 d shield-1 (S1), AgDD, an engineered variant FK506-binding protein (FKBP1A), rapidly (t (1/2) ~5 min)
128 shock protein 47 (Hsp47/SERPINH1) and 65-kDa FK506-binding protein (FKBP65/FKBP10), have been shown t
129 eby a chimeric PrP(C) composed of a modified FK506-binding protein (Fv) fused with PrP(C) and termed
130                                              FK506-binding protein 10 (FKBP10) is a collagen chaperon
131                Loss of function mutations in FK506-binding protein 10 (FKBP10), encoding the FKBP65 p
132 tes to BCR-mediated lytic induction and that FK506-binding protein 12 (FKBP12) binding alone is not a
133                                          The FK506-binding protein 12 (FKBP12) is a cytoplasmic prote
134 n transgenic plants deficient in Arabidopsis FK506-binding protein 12 (FKP12), whereas FKP12 overexpr
135 a(2+) channel (dihydropyridine receptor) and FK506-binding protein 12 as well as in "hot spot" region
136 labeled CaM binding near donor-labeled FKBP (FK506-binding protein 12.6) on the cytoplasmic domain of
137  we found that hippocampal overexpression of FK506-binding protein 12.6/1b (FKBP1b), a negative regul
138                Hippocampal overexpression of FK506-binding protein 12.6/1b (FKBP1b), a negative regul
139 e found that expression of the gene encoding FK506-binding protein 12.6/1b (FKBP1b), a small immunoph
140                      Recently, we found that FK506-binding protein 12.6/1b (FKBP1b), a small protein
141                           In cardiomyocytes, FK506-binding protein 1b/12.6 (FKBP1b) binds and stabili
142                                              FK506-binding protein 38 (FKBP38), a membrane-anchored,
143             FKBP4, encoding the immunophilin FK506-binding protein 4, was identified as a plausible c
144 f microRNA (miRNA) expression related to the FK506-binding protein 5 (FKBP5) gene may contribute to t
145 e response regions of progesterone-regulated FK506-binding protein 5 (FKBP5) immunophilin and small R
146 evels of the glucocorticoid-responsive genes FK506-binding protein 5 (Fkbp5), Period 1 (Per1), and se
147 lves the interaction of IFI44L with cellular FK506-binding protein 5 (FKBP5), which in turn interacts
148     Corticosteroid-mediated transactivation (FK506-binding protein 5 induction by FLU) increased in t
149 or alpha and corticosteroid transactivation (FK506-binding protein 5) and transrepression markers (IL
150     The FKBP5 gene codes for a co-chaperone, FK506-binding protein 5, that exerts negative feedback o
151 portant modulator of stress responses is the FK506-binding protein 51 (FKBP5/FKBP51).
152                                          The FK506-binding protein 51 (FKBP51) is a key regulator of
153                                          The FK506-binding protein 51 (FKBP51) is a promising drug ta
154                                              FK506-binding protein 51 (FKBP51) is gaining increased r
155                             The immunophilin FK506-binding protein 51 (FKBP51), in conjunction with t
156   In the quest for lead-like ligands for the FK506-binding protein 51 (FKBP51), we designed two new c
157 ic antigen, transmembrane protease serine 2, FK506-binding protein 51 and fatty acid synthase.
158                                              FK506-binding protein 51 is involved in hypothalamic-pit
159             We have now examined the role of FK506-binding protein 8 (FKBP8), a component of the CFTR
160 protein 90 (Hsp90)-associated co-chaperones: FK506-binding protein 8 (FKBP8), activator of Hsp90 ATPa
161 AIPL1 and PDE6 are known to interact via the FK506-binding protein domain of AIPL1, the contribution
162 a by dimerizing rapamycin-binding domain and FK506-binding protein domains that are attached to ciste
163 e Ca(2+) channel CaV1.1, calmodulin, and the FK506-binding protein FKBP12, as well as in "hot spot" r
164 ncrease) and unaltered RyR2 affinity for the FK506-binding protein FKBP12.6 (Kd~0.8 nmol/L).
165                                    The large FK506-binding protein FKBP52 has been characterized as a
166 mall-molecule drug discovery, as engineering FK506-binding protein into intracellular sites within Ca
167 ion between a novel anti-angiogenic protein, FK506-binding protein like (FKBPL), and these diseases.
168            Mutation of the immunophilin-like FK506-binding protein TWISTED DWARF1 (FKBP42/TWD1) cause
169                Here, we assess the impact of FK506-binding protein with a molecular mass of approxima
170 lyses demonstrated CG17282 is a noncanonical FK506-binding protein with an inactive peptide prolyl-is
171 rtance of simultaneous interactions of AIPL1-FK506-binding protein with the prenyl moieties of PDE6 a
172 t into two moieties that were fused to FKBP (FK506-binding protein) and FRB (rapamycin-binding domain
173 ation of receptor function by FKBP52 (52-kDa FK506-binding protein), which acts at a later stage of t
174 domain) was fused with a cDNA for a modified FK506-binding protein, Fv (Fv-SLK 1-373).
175 the immunophilins, cyclophilin A, and 12-kDa FK506-binding protein, in resting human Jurkat T cells.
176    Phosphatidic acid (PA) interacts with the FK506-binding protein-12-rapamycin-binding (FRB) domain
177            Heat shock protein 47 (HSP47) and FK506-binding protein-65 (FKBP65) defects cause types X
178                        CID tools such as the FK506-binding protein-FKBP-rapamycin-binding- (FKBP-FRB)
179                                              FK506-binding protein-like (FKBPL) has previously been s
180                                          The FK506-binding proteins (FKBP) 51 and 52 are cochaperones
181                                              FK506-binding proteins (FKBP) 51 and 52 are cochaperones
182 some amino acid sequence similarity to human FK506-binding proteins (FKBPs) in residues 166 to 252 lo
183 ) are a chaperone superfamily comprising the FK506-binding proteins (FKBPs), cyclophilins, and parvul
184                                              FK506-binding proteins FKBP12.6 and FKBP12 are associate
185      FKBP53 is one of the seven multi-domain FK506-binding proteins present in Arabidopsis thaliana,
186 iphosphate-binding cassette transporters and FK506-binding proteins.
187 is in many ways an exceptional member of the FK506-binding proteins.
188                    Calcineurin inhibition by FK506 blocks M. circinelloides transition to hyphae and
189 e inhibition of calcineurin with tacrolimus (FK506) blocks both cellular processes.
190 calcineurin inhibition with cyclosporin A or FK506, both clinically approved drugs, triggers potent c
191 ine in motor function in Drosophila requires FK506-BP2 function within the muscle.
192                         Muscle expression of FK506-BP2 in FK506-BP2 mutants completely restores the s
193                                     Although FK506-BP2 mutant flies are found to have less sensitivit
194                               Interestingly, FK506-BP2 mutant flies have reduced sensitivity to the e
195            Muscle expression of FK506-BP2 in FK506-BP2 mutants completely restores the sensitivity of
196 o have less sensitivity to oxidative stress, FK506-BP2 mutants do not live longer than wild type.
197  this effect of S107 is absent in calstabin (FK506-BP2) mutants.
198 nt to the inhibitory effect of rapamycin and FK506 but can be blocked by the presence of mycophenolat
199               Here we show that CsA, but not FK506, causes activation of the integrated stress respon
200                                      The MMF/FK506 combination proved the best balance with less toxi
201           Our studies indicate that low-dose FK506 could be useful in the treatment of PAH.
202                                              FK506 crosses the blood brain barrier, is well tolerated
203                                        Thus, FK506, CSA, and A238L all prevent "LxVP"-mediated substr
204                      Calcineurin inhibitors (FK506, cyclosporin A, and a peptide calcineurin inhibito
205 or the three specific calcineurin inhibitors FK506, cyclosporine A, or calcineurin inhibitory peptide
206 t pharmacologically relevant concentrations, FK506 decreases insulin secretion and reduces mitochondr
207                                              FK506 did not affect Na(+),HCO3(-) cotransport activity
208                                              FK506 does not prevent DC survival, maturation, or costi
209 selective genetic and pharmacological tools (FK506) does the same.
210 n alpha2delta-1 gene KO mice, treatment with FK506 failed to increase the frequency of NMDAR-mediated
211 s, and mutations of the A. fumigatus CnA/CnB-FK506-FKBP12-complex identify a Phe88 residue, not conse
212 ptidylprolyl isomerase FKBP12 interacts with FK506 forming a complex that inhibits the protein phosph
213 sistent with these data and as compared with FK506, GNF362 had favorable acute GVHD and GVL propertie
214                                Compared with FK506, GNF362 more selectively deleted donor alloreactiv
215                           RAPA >/=0.5 mg/Kg, FK506 >/=0.5 mg/Kg, and MMF >/=120 mg/kg had detrimental
216  drug disk diffusion assays demonstrate that FK506 has synergistic fungicidal activity with caspofung
217          Cyclosporin A (CsA) and tacrolimus (FK506) has been reported to reduce proteinuria in patien
218 itors, such as cyclosporin A and tacrolimus (FK506), have played a pivotal role in the preservation o
219 m3:Fpr1 interaction by the immunosuppressant FK506, illustrating the assay's capacity to identify che
220                                              FK506 immunosuppression facilitated the establishment of
221 of ER luminal FKBP10 was almost as potent as FK506 in attenuating expression of PrP(C).
222 ined the activity of a calcineurin inhibitor FK506 in combination with caspofungin against echinocand
223                            In vitro studies: FK506 in combination with PHMB, VCZ, or AMB enhanced fun
224 PS, we found that systemic administration of FK506 in male and female mice significantly increased th
225 ests were performed with PHMB, AMB, VCZ, and FK506, individually and in combination against Aspergill
226 lpha2delta-1 genetic KO similarly attenuated FK506-induced thermal and mechanical hypersensitivity.
227                       In conclusion, CsA and FK506 inhibit proteinuria by protecting against PAN-indu
228 activity in T cells and suggest that CsA and FK506 inhibit selected effector T cell functions via a C
229        Further studies revealed that CsA and FK506 inhibited PAN-induced p38 and JNK signaling, there
230                                              FK506 inhibited the observed alphaSYN oligomerization bo
231 unophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not CrkI association with C3
232                                              FK506 inhibits retrograde trafficking of H-Ras from the
233 ity by treatment with cyclosporin A (CsA) or FK506 is a cornerstone of immunosuppressive therapies.
234 rs of alphaS toxicity, including tacrolimus (FK506), isradipine, nilotinib, nortriptyline, and triflu
235                 Co-application of HpSlyD and FK506 led to significant reductions in CDX2, VIL1, and T
236 nding protein (FKBP) and a CEM consisting of FK506 linked to a molecule that interacts with cellular
237 that posttransplantation diabetes induced by FK506 may be mediated by its effects on mitochondrial fu
238  of the microarray data identified potential FK506-mediated pathways and regulatory motifs.
239               Here, we show that AMD3100 and FK506 mobilization of endogenous stem cells immediately
240   Pathway analysis of microarray data showed FK506 modification of pathways involving ATP metabolism,
241 y treatment with substrates (cyclosporine A, FK506), modulators (tariquidar), or small corrector mole
242 of this study was to determine the effect of FK506 on CSF chemokine levels in PND patients.
243 tigated the protective mechanisms of CsA and FK506 on proteinuria in a rat model of MCD induced by pu
244 atment as well as cyclosporine A, but not by FK506 or bile acids, suggesting that Gly(50) is involved
245 t of neurons with the calcineurin inhibitors FK506 or cyclosporin A resulted in nuclear accumulation
246 eurin; inhibition of calcineurin with either FK506 or cyclosporin A totally abolished both depolariza
247                  In vivo, mice that received FK506 or were deficient in the calcineurin isoform Abeta
248 ytic site, antagonism with cyclosporine A or FK506, or intracellular perfusion with a peptide mimicki
249 r calcineurin with BAPTA, cyclosporine A, or FK506 prevented activation of NF-kappaB and acinar cell
250                    The calcineurin inhibitor FK506 prevented contrast-induced activation of NF-kappaB
251  conditional Bmpr2 deletion in ECs, low-dose FK506 prevented exaggerated chronic hypoxic PAH associat
252                               Treatment with FK506 produced a synergistic effect in the grafts from A
253 e to 5FOA and the antifungal drugs rapamycin/FK506 (rap/FK506) and 5-fluorocytosine (5FC) were found
254 tors of the PI activity of FKBP12, including FK506, rapamycin, and cycloheximide, increase steady-sta
255 les, macrocyclic natural products, including FK506, rapamycin, and cyclosporin, bind PPIases with nan
256 imilarly, administration of the CN inhibitor FK506 reduced proteinuria and tubular injury but had mor
257 d in response to cell treatment with CsA and FK506, reflecting increased trans-to-cis conversion of C
258                                              FK506 released FKBP12 from type I receptors activin rece
259 6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature protein trapped in
260 or the calcineurin cnbR or cnaA genes confer FK506 resistance and restore hyphal growth.
261              Here we examined whether or not FK506-resistant EBV-CTLs control EBV-driven tumor progre
262                                              FK506-resistant epimutants readily reverted to the drug-
263 mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cytoskeleto
264                 Inhibition of calcineurin by FK506 results in an increase in the net phosphorylation
265  from patients with idiopathic PAH, low-dose FK506 reversed dysfunctional BMPR2 signaling.
266                                              FK506 significantly decreased mitochondrial content and
267                               Treatment with FK506 significantly increased the frequency of mEPSCs an
268 other hand, MMF alone or in association with FK506 significantly prolonged the time to islet rejectio
269 vation of BMP pathway activity with low-dose FK506, suggesting an approach to management of human bla
270  coincubation with the calcineurin inhibitor FK506, suggesting involvement of DYRK1A and nuclear fact
271   Mice receiving CNA12-CTLs and treated with FK506 survived significantly longer than control-treated
272 en, and treatment with the immunosuppressant FK506 (tacrolimus) decreases CSF white blood cell counts
273                                              FK506 (Tacrolimus) is a potent inhibitor of calcineurin
274                    The calcineurin inhibitor FK506 (tacrolimus) reduced cell death and lateral transf
275 pontaneous resistance to the antifungal drug FK506 (tacrolimus) via two distinct mechanisms.
276          The best response was achieved with FK506 (tacrolimus), via a dual mechanism of action as a
277 them resistant to calcineurin (CN) inhibitor FK506 through retroviral transfer of a calcineurin A mut
278                                   Binding of FK506 to the FKBP domain causes the target domain to fir
279 d thermal and mechanical hypersensitivity in FK506-treated mice.
280 sal horn neurons was profoundly increased in FK506-treated rats and was reduced by blocking NMDARs.
281 of miniature EPSCs in dorsal horn neurons of FK506-treated rats.
282 ciceptive and mechanical hypersensitivity in FK506-treated rats.
283 rn neurons was also significantly greater in FK506-treated than in vehicle-treated rats.
284                                         Both FK506 treatment and FKBP10 depletion were effective in r
285 cordings in spinal cord slices revealed that FK506 treatment caused a large increase in the amplitude
286              Our results showed that CsA and FK506 treatment decreased proteinuria via a mechanism as
287                               FKBP12.6 KO or FK506 treatment enhances CH-induced PH, while S107 (a sp
288                                              FK506 treatment of dendritic cells (FKDC) limits their c
289                                              FK506 treatment prior to IR prevented Drp1-S637 dephosph
290                                 We show that FK506 treatment results in a profound reduction in PrP(C
291 such as activated T cells, and we found that FK506 treatment specifically decreased CSF CXCL10 from a
292                 CSF samples before and after FK506 treatment were tested by multiplex assay for the p
293 s nor spine density changes were affected by FK506 treatment, suggesting that calcineurin acts via a
294 mobilization is resistant to cyclosporine or FK506 treatment, while de novo CD40L and cytokine expres
295 lanted into B6 AID(-/-) mice with or without FK506 treatment.
296 2-, and 1.43-fold, respectively, after 48-hr FK506 treatment.
297                                  RAPA and/or FK506 were inefficient in preventing rejection, even whe
298  lymphoma regression despite the presence of FK506, whereas eGFP-CTLs did not.
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

 
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