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1 ir relative to the translation start site of CYP2C8.
2 e substrates or time-dependent inhibitors of CYP2C8.
3 P2C family, although to a lesser degree than CYP2C8.
4 s miR-103 and miR-107 in the 3'-UTR of human CYP2C8.
5 genes and the CYP1A2-15q22-ter, CYP1B1-2p21, CYP2C8-10q23, CYP2C9-10q24, and MAOA-Xp11.4 regions as s
6       Tam metabolism was examined with human CYP2C8, 2C9, 2C18, 2C19, and 2D6 expressed in E. coli.
7 rotective against vascular dysfunction while CYP2C8*3 and 2C9*2 loss-of-function SNP, altered endothe
8  been determined, the structural features of CYP2C8 active site support its binding to anionic and bu
9                                              CYP2C8, an important member of this subfamily, metaboliz
10           Cytochrome P450 (CYP) epoxygenases CYP2C8 and CYP2J2 generate epoxyeicosatrienoic acids (EE
11 es were identified, which revealed that only CYP2C8 and CYP3A4 possess accessible cysteine residues n
12                       Proteolytic digests of CYP2C8 and CYP3A4 Supersomes revealed adducts to Cys225
13 es revealed adducts to Cys225 and Cys239 for CYP2C8 and CYP3A4, respectively.
14 10 min(-1) and 0.81 muM and 0.20 min(-1) for CYP2C8 and CYP3A4, respectively.
15 d time-dependent inhibition only occurred in CYP2C8 and CYP3A4.
16 y by CYP26A1, but other P450 enzymes such as CYP2C8 and CYP3As also contribute to atRA 4-hydroxylatio
17 nt P450, we cloned the 5'-flanking region of CYP2C8 and investigated its transcriptional regulation b
18 in rats, with very weak cytochrome P450 2C8 (CYP2C8) and cytochrome P450 2C9 (CYP2C9) inhibition, and
19 dy, we found that the full-length CYP2C8 (WT CYP2C8) and N-terminal truncated splice variant 3 ( appr
20  polymorphisms in the genes encoding UGT2B7, CYP2C8, and ABCC2 was performed and haplotypes assigned.
21                  Allelic variants of UGT2B7, CYP2C8, and ABCC2, which may predispose to the formation
22                                      CYP3A4, CYP2C8, and CYP2C9 protein levels were also increased by
23 50s, whereas enzymatic activities of CYP2C2, CYP2C8, and CYP3A4 were slightly higher in PGRMC1-defici
24 C1 with the drug-metabolizing P450s, CYP2C2, CYP2C8, and CYP3A4, in transfected cells.
25 ntified an HNF4alpha-binding site within the CYP2C8 basal promoter region that is cis-activated by co
26 e, we examine the possible downregulation of CYP2C8 by drugs capable of inducing miR107.
27 rug-drug interactions due to upregulation of CYP2C8 by PPAR activators.
28 some 10q24 within the CYP2C18-CYP2C19-CYP2C9-CYP2C8 cluster were associated with diminished clopidogr
29 led that other AA-oxidizing P450s, including CYP2C8, CYP2C9, and CYP2E1, were not expressed.
30 sponding increases in immunoreactive CYP2B6, CYP2C8, CYP2C9, and CYP3A4, all previously shown to cata
31 tivation of additional P450 enzymes (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A5).
32                         We sequenced CYP2D6, CYP2C8, CYP2C9, CYP3A4, and SLCO1B1 and tested 7 reduced
33 ented PPARalpha-mediated induction of CYP1A, CYP2C8, CYP3A4, and CYP4A11 genes, suggesting a dominant
34 (ABCB1, ABCC1, ABCC2, ABCG2, CDKN1A, CYP1B1, CYP2C8, CYP3A4, CYP3A5, MAPT, and TP53) and platinum (AB
35 nides can be ligands of human CYP2C8, making CYP2C8 distinct from the other CYP isoforms.
36 ed that both microsomal and mitochondrial WT CYP2C8 efficiently catalyzed paclitaxel 6-hydroxylation.
37 dothelial expression of the human CYP2J2 and CYP2C8 epoxygenases and mice with targeted disruption of
38 dothelial expression of the human CYP2J2 and CYP2C8 epoxygenases to increase endothelial EET biosynth
39 hat CAR, PXR, GR, and HNF4alpha can regulate CYP2C8 expression and identify specific cis-elements wit
40 hibition reversed the detrimental effects of CYP2C8 expression in Tie2-CYP2C8 Tr hearts.
41 1A, CYP2B6 and CYP3A4 (for CAR and PXR), and CYP2C8 (for PXR) gene expression.
42           However, SNPs from the IL12A, HUS, CYP2C8 genes were associated with time to anemia, allowi
43                   Although the structures of CYP2C8-glucuronide complexes have not been determined, t
44             As interaction perpetrators with CYP2C8, glucuronides of gemfibrozil and clopidogrel show
45 and enhanced DiHOME synthesis by endothelial CYP2C8 impair functional recovery and mask the beneficia
46                           ROS scavengers and CYP2C8 inhibition reversed the detrimental effects of CY
47                                              CYP2C8 is an important member of the CYP2C subfamily, wh
48                                              CYP2C8 is the most strongly inducible member of the CYP2
49        Thus, we show for the first time that CYP2C8 is transcriptionally regulated by PPARalpha, sugg
50       This review summarizes glucuronides as CYP2C8 ligands and the active-site structural features o
51 st that glucuronides can be ligands of human CYP2C8, making CYP2C8 distinct from the other CYP isofor
52 ests that mitochondrially targeted variant 3 CYP2C8 may contribute to oxidative stress in various tis
53                                Surprisingly, CYP2C8 mRNA and protein levels were induced by bezafibra
54  immunoblot analyses) did not correlate with CYP2C8 mRNA levels (measured through quantitative polyme
55         Neither precursors nor AsOs affected CYP2C8 mRNA levels, which indicated that the effect was
56        Genotypic variants of CYP3A4, CYP3A5, CYP2C8, NR1I2-206, ABCB1, ERCC1, and ERCC2 were analyzed
57 fically, overexpression of the monooxygenase CYP2C8 or genetic ablation or inhibition of the soluble
58 A 107 (miR107) and microRNA 103 downregulate CYP2C8 post-transcriptionally.
59                    Interestingly, CYP3A7 and CYP2C8 preferentially formed (4S)-OH-RA from atRA.
60                                              CYP2C8 promoter activity was increased by ectopic expres
61 ntified a distal PXR/CAR-binding site in the CYP2C8 promoter that confers inducibility of CYP2C8 via
62                                              CYP2C8 protein levels (measured through immunoblot analy
63  transfected into primary human hepatocytes, CYP2C8 protein levels were decreased, whereas AsOs incre
64 evels were decreased, whereas AsOs increased CYP2C8 protein levels.
65 118 (P < .0001), ERCC2 K751Q (P < .001), and CYP2C8 R139K (P = .01).
66  crystal structure coordinates of CYP2D6 and CYP2C8 showed that despite lacking the N-terminal 102 re
67 s and the active-site structural features of CYP2C8 that allow potential binding to glucuronides.
68 increased endothelial EET biosynthesis (Tie2-CYP2C8 Tr and Tie2-CYP2J2 Tr) or EET hydrolysis (Tie2-sE
69                                         Tie2-CYP2C8 Tr hearts also exhibited increased reactive oxyge
70           Surprisingly, compared to WT, Tie2-CYP2C8 Tr hearts had significantly reduced LVDP recovery
71 imental effects of CYP2C8 expression in Tie2-CYP2C8 Tr hearts.
72 y was significantly attenuated in CYP2J2 and CYP2C8 transgenic mice compared to wild-type controls.
73                                   CYP2J2 and CYP2C8 transgenic mice demonstrated modestly, but not si
74 e was significantly lower in both CYP2J2 and CYP2C8 transgenic mice during coadministration of N-nitr
75 y endothelial cells isolated from CYP2J2 and CYP2C8 transgenic mice.
76  to acetylcholine was observed in CYP2J2 and CYP2C8 transgenic mice.
77 ed to wild-type controls, CYP2J2 transgenic, CYP2C8 transgenic, and Ephx2(-/-) mice each exhibited a
78 CYP2C8 promoter that confers inducibility of CYP2C8 via the PXR agonist/ligand rifampicin and the CAR
79 nslation efficiency (protein/mRNA ratio) for CYP2C8 was inversely correlated with the expression of m
80                  Haplotype distributions for CYP2C8 were different in patients compared with hospital
81   When three copies of the putative MRE from CYP2C8 were inserted downstream from a luciferase expres
82 in the genes encoding the enzymes UGT2B7 and CYP2C8, which determine the formation of reactive diclof
83           Cytochrome P450 enzymes CYP3A4 and CYP2C8, which metabolically inactivate PTX in hepatic ti
84 In this study, we found that the full-length CYP2C8 (WT CYP2C8) and N-terminal truncated splice varia