PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19786111-9 2010 We conclude that the combination of tacrolimus/sirolimus+/-MTX for GVHD prophylaxis in the setting of RIC HCT for MF appears to reduce the incidence of severe aGVHD and NRM, and leads to improved OS compared to CSA/MMF+/-MTX. Tacrolimus 36-46 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 211-214 21680259-9 2012 We detected multiple reaction monitoring (MRM) transitions of m/z 1220>1203 and 1231.9>1215.1 for CsA and d12 CsA respectively which co-eluted at 1.30min, and 821.6>768.5 and 809.6>756.5 for tacrolimus and ascomycin respectively which co-eluted at 1.17 min. Tacrolimus 203-213 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 104-107 21680259-9 2012 We detected multiple reaction monitoring (MRM) transitions of m/z 1220>1203 and 1231.9>1215.1 for CsA and d12 CsA respectively which co-eluted at 1.30min, and 821.6>768.5 and 809.6>756.5 for tacrolimus and ascomycin respectively which co-eluted at 1.17 min. Tacrolimus 203-213 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 116-119 19481021-4 2009 The aim of this prospective study was to evaluate the safety and efficacy of conversion to tacrolimus and atorvastatin in CsA-treated heart transplant recipients and dyslipidemia refractory to fluvastatin. Tacrolimus 91-101 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 122-125 19481021-11 2009 CONCLUSIONS: Conversion to tacrolimus and atorvastatin appears to be a safe and effective lipid-lowering therapy in CsA-treated heart transplant recipients with dyslipidemia refractory to fluvastatin. Tacrolimus 27-37 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 116-119 16877482-13 2006 CONCLUSION: Our results suggest that in patients with CAN and deteriorating allograft function, CsA-to-tacrolimus conversion or CsA minimization achieved comparable efficacies in retarding the decline of graft function. Tacrolimus 103-113 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 96-99 17889206-2 2007 The objective of this study was to prospectively assess the impact of conversion from cyclosporine (CsA) to tacrolimus on lung function in patients who developed BOS while receiving CsA-based immunosuppressive therapy. Tacrolimus 108-118 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 182-185 11956176-6 2002 In contrast, aldosterone-stimulated hMR transcriptional activity was reduced to 53 +/- 11.2% (P < 0.03) after pretreatment of M cells for 3 d with CsA and to 71 +/- 9.6% (P < 0.05) after pretreatment with FK506. Tacrolimus 211-216 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 150-153 12570836-6 2003 Disappointingly, CSA and the other molecules as FK506, sharing the capacity to inhibit calcineurin, should be administered for all patient life, as tolerance to alloantigens is not achieved by these molecules. Tacrolimus 48-53 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 17-20 16120063-9 2005 CONCLUSIONS: Our study supplies supportive clinical evidence that inhibition of the enterohepatic cycle in case of CsA co-administration explains some of the differences observed in PK of MMF when co-administered with either TACR or CsA. Tacrolimus 225-229 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 115-118 16008701-15 2005 Topical tacrolimus is a promising alternative to topical CsA for treatment of KCS and may be beneficial in patients with less than optimal response to topical CsA. Tacrolimus 8-18 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 159-162 12207006-2 2002 Data regarding the role of cyclosporine (CsA) and FK-506 in AMT have shown that CsA is less effective than FK-506. Tacrolimus 50-56 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 80-83 12115224-7 2002 The suppressive action of CSA on VEGF synthesis was calcineurin dependent, as evidenced by a comparable inhibition by FK-506. Tacrolimus 118-124 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 26-29 10465413-8 1999 The first stage of constructing this model consisted of using conformational comparison of CsA and FK506, GRID and GROUP analysis and restrained molecular dynamics to dock CsA into the FK506 binding site of the FK506-FKBP12-CN structure. Tacrolimus 185-190 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 172-175 11605779-1 2001 Like cyclosporine (CsA), tacrolimus acts through the inhibition of renal phosphatase calcineurin. Tacrolimus 25-35 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 19-22 10798763-6 2000 FK506 and MMF were also able to upregulate IL-8, although the effect was less dramatic than observed for CsA. Tacrolimus 0-5 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 105-108 10708116-2 2000 As a result, serious adverse effects, such as nephrotoxicity and neurotoxicity, have been observed under CsA/tacrolimus therapy. Tacrolimus 109-119 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 105-108 10465413-8 1999 The first stage of constructing this model consisted of using conformational comparison of CsA and FK506, GRID and GROUP analysis and restrained molecular dynamics to dock CsA into the FK506 binding site of the FK506-FKBP12-CN structure. Tacrolimus 185-190 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 172-175 1707162-1 1991 Like Cyclosporin A (CsA), the macrolide FK 506 is a potent immunosuppressive that inhibits early steps of T cell activation, including the synthesis of Interleukin 2 (II-2) and numerous other lymphokines. Tacrolimus 40-46 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 20-23 9709036-1 1998 The immunosuppressive fungal products cyclosporin A (CsA) and FK506 bind with high affinity to intracellular receptor proteins: cyclophilin (CYP) is one of the receptors for CsA and FK506-binding protein (FKBP) is one of the receptors for FK506. Tacrolimus 62-67 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 174-177 9709036-1 1998 The immunosuppressive fungal products cyclosporin A (CsA) and FK506 bind with high affinity to intracellular receptor proteins: cyclophilin (CYP) is one of the receptors for CsA and FK506-binding protein (FKBP) is one of the receptors for FK506. Tacrolimus 182-187 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 53-56 8757216-5 1996 The effects of CSA and FK-506 on SCF-dependent release of histamine were dose-dependent (IC50: CSA, 1 to 10 ng/ml; FK-506, 0.3 to 3 ng/ml). Tacrolimus 23-29 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 95-98 8757216-5 1996 The effects of CSA and FK-506 on SCF-dependent release of histamine were dose-dependent (IC50: CSA, 1 to 10 ng/ml; FK-506, 0.3 to 3 ng/ml). Tacrolimus 115-121 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 15-18 8894806-9 1996 Both CSA and M17 synergized more strongly with FK 506 than they did between themselves. Tacrolimus 47-53 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 5-8 9453019-5 1998 We also measured ADO plasma level in two KTR treated with FK506, a CsA analog. Tacrolimus 58-63 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 67-70 7693684-3 1993 CsA and FK506 inhibited depolarization-induced glucagon gene transcription, FK506 being more potent than CsA. Tacrolimus 76-81 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 0-3 7693684-4 1993 CsA/FK506 responsiveness was mediated by the glucagon CRE and also by well characterized CREs of the choriogonadotropin and somatostatin genes. Tacrolimus 4-9 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 0-3 7693684-5 1993 Rapamycin antagonized the inhibitory effect of FK506 but not CsA, suggesting that FK506 and CsA may act through complex formation with distinct intracellular immunophilins. Tacrolimus 47-52 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 92-95 7693684-8 1993 The interference with CRE-mediated gene transcription represents a novel mechanism of CsA/FK506 action, which may underlie pharmacological effects and toxic manifestations of these potent immunosuppressive drugs. Tacrolimus 90-95 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 86-89 3291267-3 1988 The introduction of new drugs such as FK 506, some of which are clearly synergistic with CsA, could ameliorate past problems with drug toxicity. Tacrolimus 38-44 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 89-92 33896035-9 2021 CONCLUSION: Our data support the quick conversion to tacrolimus in the condition of persistent low CSA levels with acceptable efficacy and safety. Tacrolimus 53-63 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 99-102 28405602-12 2017 After drug conversion of a twice-daily CNI formulation to a once-daily tacrolimus formulation, CSA-treated patients needed longer to improve their cognitive functioning. Tacrolimus 71-81 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 95-98 28405602-14 2017 CONCLUSIONS: Patients with once-daily tacrolimus formulation had a better psychomotor speed than CSA-treated patients. Tacrolimus 38-48 ERCC excision repair 8, CSA ubiquitin ligase complex subunit Homo sapiens 97-100