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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
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
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
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
36 rate that DC inhibit T cells by sequestering FK506 and continuously releasing the drug over several d
40 tetraacetic acid, the calcineurin inhibitors FK506 and cyclosporine A, or use of acinar cells from ca
42 angiogenic response to potential therapies, FK506 and Elafin, was related to reduced slit guidance l
47 s common to the immunosuppressive inhibitors FK506 and rapamycin bind to the most conserved region of
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
63 rin/NFAT binding, such as cyclosporine A and FK506, are broadly used in organ transplantation and can
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
69 ocytes, we expressed a fusion protein of the FK506 binding protein (FKBP) and caspase 8 under control
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
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
83 th are increased, and association of RyR2 by FK506 binding protein 12.6 (FKBP12.6) is decreased in PA
86 utations in the FKBP14 gene encoding FKBP22 (FK506 Binding Protein 22 kDa) cause kyphoscoliotic Ehler
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
95 d that the suggested psychiatric risk factor FK506 binding protein 51 (FKBP51) increases phosphorylat
97 f selected stress-response-associated genes (FK506 binding protein 51 [FKBP5], glucocorticoid recepto
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
103 romosome 6p21.3 at TNXB (tenascin XB)-FKBPL (FK506 binding protein like) [rs12153855/rs9391734; disco
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
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
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
122 (CnB) subunits complexed with FK506 and the FK506-binding protein (FKBP12) from human fungal pathoge
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
132 tes to BCR-mediated lytic induction and that FK506-binding protein 12 (FKBP12) binding alone is not a
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
139 e found that expression of the gene encoding FK506-binding protein 12.6/1b (FKBP1b), a small immunoph
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
156 In the quest for lead-like ligands for the FK506-binding protein 51 (FKBP51), we designed two new c
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
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.
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
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
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
190 calcineurin inhibition with cyclosporin A or FK506, both clinically approved drugs, triggers potent c
196 o have less sensitivity to oxidative stress, FK506-BP2 mutants do not live longer than wild type.
198 nt to the inhibitory effect of rapamycin and FK506 but can be blocked by the presence of mycophenolat
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
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
216 drug disk diffusion assays demonstrate that FK506 has synergistic fungicidal activity with caspofung
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
222 ined the activity of a calcineurin inhibitor FK506 in combination with caspofungin against echinocand
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.
228 activity in T cells and suggest that CsA and FK506 inhibit selected effector T cell functions via a C
231 unophilins, such as cyclosporine A (CsA) and FK506, inhibited CrkII, but not CrkI association with C3
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
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
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
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
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
251 conditional Bmpr2 deletion in ECs, low-dose FK506 prevented exaggerated chronic hypoxic PAH associat
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
259 6 h) treatment with 15 muM cyclosporine A or FK506 rescues the pre-formed immature protein trapped in
263 mouse podocytes, pre-incubation with CsA and FK506 restored the distribution of the actin cytoskeleto
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
277 them resistant to calcineurin (CN) inhibitor FK506 through retroviral transfer of a calcineurin A mut
280 sal horn neurons was profoundly increased in FK506-treated rats and was reduced by blocking NMDARs.
285 cordings in spinal cord slices revealed that FK506 treatment caused a large increase in the amplitude
291 such as activated T cells, and we found that FK506 treatment specifically decreased CSF CXCL10 from a
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
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