ライフサイエンスコーパス: CYP2D6

1 tic metabolizing enzyme cytochrome P450 2D6 (CYP2D6).

2 ntibody type 1 targeting cytochrome P4502D6 (CYP2D6).

3 l as non-MHC genes (IL-1RA, IL-6, IL-10, and CYP2D6).

4 potentiation of HNF4alpha transactivation of CYP2D6.

5 tion of HNF4alpha-induced transactivation of CYP2D6.

6 s and also in cells expressing mitochondrial CYP2D6.

7 predominantly endoplasmic reticulum-targeted CYP2D6.

8 ferentiated neurons expressing mitochondrial CYP2D6.

9 nd replace it with allelic variants of human CYP2D6.

10 ght be in strong linkage disequilibrium with CYP2D6.

11 tions of P-glycoprotein, villin, CYP1A1, and CYP2D6.

12 predominantly endoplasmic reticulum-targeted CYP2D6.

13 ferentiated neurons expressing mitochondrial CYP2D6.

14 uration in clinically relevant genes such as CYP2D6.

15 sing the two frequent human protein isoforms CYP2D6.1 and CYP2D6.2 and an as yet undescribed variant

16 frequent human protein isoforms CYP2D6.1 and CYP2D6.2 and an as yet undescribed variant of this enzym

17 Immune responses to CYP2D6(245-254) were the strongest both at diagnosis and

18 CD8 T cell targets on CYP2D6-in particular CYP2D6(245-254)-may be the focus of novel immune interve

19 g for cytochromes P450 (CYPs) 2D6 (CYP2D6*4, CYP2D6*3, CYP2D6*5, and CYP2D6*6) and 2E1 (cl/c2), multi

20 CYP2D6 (*4 and *6) and CYP3A5 (*3) genotypes were determ

21 Women with the CYP2D6 *4/*4 genotype had worse relapse-free time (RF-ti

22 In the multivariate analysis, women with the CYP2D6 *4/*4 genotype still tended to have worse RFS (ha

23 n tamoxifen-treated patients, women with the CYP2D6 *4/*4 genotype tend to have a higher risk of dise

24 Significant within-family association of CYP2D6*4 alleles and AS was demonstrated.

25 r the most frequent poor metabolizer allele (CYP2D6*4) was not associated with increased susceptibili

26 enes coding for cytochromes P450 (CYPs) 2D6 (CYP2D6*4, CYP2D6*3, CYP2D6*5, and CYP2D6*6) and 2E1 (cl/

27 chromes P450 (CYPs) 2D6 (CYP2D6*4, CYP2D6*3, CYP2D6*5, and CYP2D6*6) and 2E1 (cl/c2), multidrug resis

28 CYPs) 2D6 (CYP2D6*4, CYP2D6*3, CYP2D6*5, and CYP2D6*6) and 2E1 (cl/c2), multidrug resistance 1 (MDR1

29 Cytochrome P450 2D6 (CYP2D6), a major drug-metabolizing enzyme, is responsibl

30 For CYP2D6, a clear relationship between polar surface area

31 rectly position a range of substrates in the CYP2D6 active site with the known sites of metabolism ab

32 The measured CYP3A4 and CYP2D6 activities also failed to predict the susceptible

33 A higher percentage of patients with reduced CYP2D6 activity (hereafter referred to as phenotypic int

34 s compared with patients with normal or high CYP2D6 activity (phenotypic normal metabolizers [pNMs] a

35 P2D6 activity, and 15 709 had normal or high CYP2D6 activity based on genotype and inhibitors.

36 CYP2D6 activity can also be reduced by concomitant use o

37 yb5 can be a major determinant of CYP3A4 and CYP2D6 activity in vivo, with a potential impact on the

38 xylase activity and that HNF4alpha regulates CYP2D6 activity in vivo.

39 ky had genotypes associated with extremes in CYP2D6 activity that may have affected their response to

40 P2D6-metabolized opioids, 15 960 had reduced CYP2D6 activity, and 15 709 had normal or high CYP2D6 ac

41 es, and phenotype assignment was impacted by CYP2D6 allele-specific CNVs in 2% of all patients.

42 gest that women who carry one or two variant CYP2D6 alleles that encode enzymes with null or reduced

43 ent ways: (1) rapid discrimination of common CYP2D6 alleles, (2) high-resolution haplotyping for asso

44 e or more of the numerous drugs sensitive to CYP2D6 allelic composition.

45 ust approach for the expression of different CYP2D6 allelic variants in transgenic mice and thus can

46 We also show that WBC express CYP2D6, an enzyme capable of synthesizing morphine from

47 rphisms in the drug-metabolizing enzyme gene CYP2D6 and a number of linked microsatellites that is bo

48 of seven simple nucleotide polymorphisms in CYP2D6 and also to assay repeat number variation at five

49 Weak linkage was also demonstrated between CYP2D6 and AS.

50 achieved different effects in patients with CYP2D6 and beta1-receptor polymorphisms.

51 yrosol formation and supported findings that CYP2D6 and CYP2A6 mediated this reaction.

52 omic testing, 65% had potentially actionable CYP2D6 and CYP2C19 phenotypes, and phenotype assignment

53 n the x-ray crystal structure coordinates of CYP2D6 and CYP2C8 showed that despite lacking the N-term

54 Human breast CYP2D6 and CYP2D7P (from a pseudogene) mRNAs were previo

55 s of blood THMs, including factors affecting CYP2D6 and CYP2E1 activity.

56 man CYP450 proteins CYP1A2, CYP2C9, CYP2C19, CYP2D6 and CYP3A4 are the major drug-metabolizing isofor

57 s with baculosomes further demonstrated that CYP2D6 and CYP3A4 could transform tyrosol into hydroxyty

58 out affinity for the major drug-metabolizing CYP2D6 and CYP3A4 enzymes and CYP21A2, with the latter r

59 2A6 and CYP2E1) or this region and alpha2-3 (CYP2D6 and CYP3A4) and suggested variation in the affini

60 imilarity and genetic recombinations between CYP2D6 and evolutionarily related pseudogenes CYP2D7 and

61 phase clinically important haplotypes at the CYP2D6 and HLA loci.

62 cation, deletion and fusion events involving CYP2D6 and its evolutionarily related cousin CYP2D7.

63 s no association between any polymorphism of CYP2D6 and Parkinson's disease, but two of 10 dinucleoti

64 ic cationic form by mitochondrially directed CYP2D6 and result in neuronal degradation in mice.

65 egulation of P450 expression (especially for CYP2D6) and more complex trans-regulation of P450 activi

66 compounds and their metabolites from CYP1A2, CYP2D6, and CYP3A4 and a mixture of the three P450s desi

67 P enzymes including CYP1A2, CYP2C9, CYP2C19, CYP2D6, and CYP3A4 and the crucial steroidogenic enzymes

68 major enzymes detected were CYP1B1, CYP2B6, CYP2D6, and CYP3A4 with mean values of 2.5, 2.6, 2.7, an

69 not inhibited by an anti-CYP2C11 or an anti-CYP2D6 antibody.

70 opaminergic neurons expressing mitochondrial CYP2D6 are fully capable of activating the pro-neurotoxi

71 Genetic variations in CYP2D6 are responsible for interindividual heterogeneity

72 had identified a region 115 kb downstream of CYP2D6 as enhancer for CYP2D6, containing two completely

73 riate HLA-DR molecule and recognition of the CYP2D6 autoantigenic sequence were critical to the syner

74 HO-1*P450 complexes with CYP1A2, CYP1A1, and CYP2D6, but not all P450s.

75 y, we show that the mitochondrially targeted CYP2D6 can efficiently catalyze MPTP-mimicking compounds

76 Tam metabolism by CYP2D6 coexpressed with P450 reductase in a baculovirus

77 115 kb downstream of CYP2D6 as enhancer for CYP2D6, containing two completely linked single nucleoti

78 so analyzed commercial DNA samples for their CYP2D6 copy numbers and confirmed that our results were

79 n-metabolizing enzymes GSTT1, GSTM1, CYP1A1, CYP2D6, CYP2C19, SULT1A1, and NQO1 were previously deter

80 We sequenced CYP2D6, CYP2C8, CYP2C9, CYP3A4, and SLCO1B1 and tested 7

81 n metabolizing-enzyme genes (such as CYP3A4, CYP2D6, CYP2C9, CYP1A2, CYP2E1 and UGT1A4) in THLE-2 cel

82 , membrane-associated, P450 isoforms CYP3A4, CYP2D6, CYP2C9, CYP2C19, CYP2E1, and CYP1A2 are responsi

83 ot only a mixed inhibitor of CYP2B6, CYP2C9, CYP2D6, CYP2E1 and CYP3A4, but also a non-competitive in

84 ha-thujone by human CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 occurs with up to 80% C-4 met

85 50 enzymes (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A5).

86 enzymes analysed in these three groups were: CYP2D6, CYP2E1, NAD(P)H-menadione reductase, glutathione

87 o detectable effect on expression of CYP1A1, CYP2D6, cytochrome b5, liver or intestinal fatty acid bi

88 to, or within, the cytochrome P450 2D6 gene (CYP2D6, debrisoquine hydroxylase) located at chromosome

89 The patients with CYP2D6 deficiency also appeared more likely to experienc

90 Twelve of the patients were CYP2D6 deficient, and four carried the *1Xn or *2Xn alle

91 ct in representative cytochromes (CYP3A4 and CYP2D6) demonstrated insignificant inhibitory activity,

92 it is difficult to predict pathways of human CYP2D6-dependent drug metabolism on the basis of animal

93 mice and thus can help to evaluate potential CYP2D6-dependent interindividual differences in drug res

94 ene (GSTM1) or the cytochrome P450 2D6 gene (CYP2D6) did not show a significant association with the

95 bstrates of a major drug-metabolizing enzyme CYP2D6 display increased elimination during pregnancy, b

96 sessment of the consequences of differential CYP2D6 drug metabolism, we have developed a novel straig

97 CYP2D6 gene, could affect the disposition of CYP2D6 drug substrates.

98 To characterize the CYP2D6 enhancer element, we applied chromatin conformati

99 cause large inter-individual variability in CYP2D6 enzyme activity and are currently used as biomark

100 ed due to competition and/or blockage of the CYP2D6 enzyme by Amphetamine; We also found that the syn

101 molecule was exclusively metabolized by the CYP2D6 enzyme, and options to address the issue are desc

102 s highly polymorphic gene which encodes the (CYP2D6) enzyme, involved in the metabolism of 20-25% of

103 to have a strong DDI through the CYP3A4 and CYP2D6 enzymes, respectively.

104 rongly associated with a higher abundance of CYP2D6 exon 3 skipping junctions.

105 Mitochondrial CYP2D6 expressing Neuro-2A cells produced higher levels

106 sed SHP (by approximately 50%) and decreased CYP2D6 expression (by 1.5-fold) in Tg-CYP2D6 mice, the m

107 Several novel SNPs associated with CYP2D6 expression and enzyme activity were validated in

108 uced cholestasis increases SHP and represses CYP2D6 expression in Tg-CYP2D6 mice in part through ERal

109 The rate of deficiency in CYP2D6 expression in these Caucasian state psychiatric h

110 YP2D6) mice as an animal model where hepatic CYP2D6 expression is increased during pregnancy.

111 However, the enhancer effect on CYP2D6 expression, and the causative variant, remained t

112 the previously identified enhancer region in CYP2D6 expression, expanding the number of candidate var

113 th the enhancer element and SNP rs5758550 on CYP2D6 expression, supporting consideration of rs5758550

114 P knockdown led to a significant increase in CYP2D6 expression.

115 alpha), a known transcriptional activator of CYP2D6 expression.

116 a high dose led to 2- to 3-fold decreases in CYP2D6 expression.

117 e effects of estrogen-induced cholestasis on CYP2D6 expression.

118 Patients found to be CYP2D6 extensive metabolizers (EM) remained on 20 mg and

119 coadministered with tamoxifen interfere with CYP2D6 function, thereby reducing endoxifen concentratio

120 6 substrates, a mouse line carrying both the CYP2D6 gene and the HNF4alpha conditional mutation was g

121 Single nucleotide polymorphisms in the CYP2D6 gene are not uncommon, and some alleles code for

122 ple, we tested an 890 kb region flanking the CYP2D6 gene associated with poor drug-metabolizing activ

123 abolism of a natural toxin or antigen by the CYP2D6 gene may increase susceptibility to AS.

124 Association of alleles of the CYP2D6 gene was examined by both case-control and within

125 a transgenic mouse line expressing the human CYP2D6 gene was generated.

126 Allelic variants of the CYP2D6 gene, a member of the cytochrome P450 gene superf

127 known to regulate in vitro expression of the CYP2D6 gene, could affect the disposition of CYP2D6 drug

128 The complete wild-type CYP2D6 gene, including its regulatory sequence, was micr

129 to extensively characterize variation in the CYP2D6 gene.

130 rated tissues, all of which showed excellent CYP2D6 genotype agreement.

131 demiology studies on the association between CYP2D6 genotype and breast cancer recurrence report wide

132 no clinically important association between CYP2D6 genotype and breast cancer survival in tamoxifen-

133 nalyses were conducted by drug and isolating CYP2D6 genotype and inhibitors.

134 n addition, no association was found between CYP2D6 genotype and RFSt (adjusted hazard ratio, 0.929;

135 the first algorithm to computationally infer CYP2D6 genotype at basepair resolution from HTS data.

136 CYP2D6 genotype did not predict treatment outcome for ei

137 Accounting for CYP2D6 genotype status did not change these estimates.

138 Thirty-one studies of the association of CYP2D6 genotype with breast cancer survival have yielded

139 Endoxifen clearance was unaffected by CYP2D6 genotype.

140 ociation between endoxifen concentrations or CYP2D6 genotypes and clinical outcome in patients with e

141 CYP2D6 genotypes and phenotypes of 550 service personnel

142 genic metabolite, are reduced in women whose CYP2D6 genotypes confer poor enzyme function.

143 Endoxifen concentrations and CYP2D6 genotypes were associated with relapse-free survi

144 Seventy-six CYP2D6 genotypes were characterized for 530 service pers

145 as to associate endoxifen concentrations and CYP2D6 genotypes with clinical outcome in patients with

146 better predictor of tamoxifen efficacy than CYP2D6 genotypes.

147 ata on the frequency of cytochrome P450-2D6 (CYP2D6) genotypes in state psychiatric hospital patients

148 Blood samples were retrieved for CYP2D6 genotyping and endoxifen measurements by Amplichi

149 CYP2D6 genotyping is recommended prior to treatment deci

150 We argue that a recommendation for CYP2D6 genotyping of candidates for tamoxifen therapy, a

151 n, supporting consideration of rs5758550 for CYP2D6 genotyping panels to yield more accurate phenotyp

152 We examined the feasibility of using CYP2D6 genotyping to determine optimal tamoxifen dose an

153 s of specific sequences of p53, p16, CYP1A1, CYP2D6, GSTM1 and GSTM3 were performed independently on

154 We find that Hubble.2D6 predicts CYP2D6 haplotype functional status with 88% accuracy in

155 ural network to predict functional status of CYP2D6 haplotypes, called Hubble.2D6.

156 nal studies to assign a functional status to CYP2D6 haplotypes.

157 olizing enzymes such as cytochrome P450 2D6 (CYP2D6) has been postulated to underlie antidepressant i

158 CYP2D6 have been intensively studied, but the role of CY

159 Associations with CYP2D6 have either been absent altogether or have involv

160 d debrisoquine were significantly altered in CYP2D6-HBN mice, the AUC0-8 h being increased approximat

161 olol alpha-hydroxylation were observed using CYP2D6-HBN microsomes, indicating a significant role for

162 expression of a known positive regulator of CYP2D6, hepatocyte nuclear factor 4alpha (HNF4alpha), di

163 DRD3, DRD2, CYP2D6, HTR2A, COMT, HSPG2 and SOD2 genes have variants

164 data presented in this study show that only CYP2D6 humanized mice but not wild-type mice display sig

165 fe significantly reduced (6.9 +/- 1.6 h), in CYP2D6 humanized mice compared with wild-type animals (1

166 of HNF4alpha, DEB 4-hydroxylase activity in CYP2D6 humanized mice decreased more than 50%.

167 The CYP2D6 humanized mice represent an attractive model for

168 e liver, intestine, and kidney from only the CYP2D6 humanized mice.

169 Here, we introduce CYP2D6-humanized (Tg-CYP2D6) mice as an animal model whe

170 in the livers of pregnant versus nonpregnant CYP2D6-humanized (tg-CYP2D6) mice was compiled via micro

171 In CYP2D6-humanized transgenic (Tg-CYP2D6) mice, cholestasi

172 d to investigate whether T-regs specific for CYP2D6 immunodominant regions and restricted by the appr

173 We genotyped CYP2D6 in 1,309 patients with breast cancer who were tre

174 uide for the use of medications that inhibit CYP2D6 in patients administered tamoxifen.

175 s, provides further evidence for the role of CYP2D6 in radical cure.

176 se in the expression and activity of hepatic CYP2D6 in Tg-CYP2D6 mice.

177 knockout mice, indicating a possible role of CYP2D6 in the metabolism of these compounds both in vivo

178 CD8 T cell targets on CYP2D6-in particular CYP2D6(245-254)-may be the focus of

179 CYP2D6 status, whilst OH-PQm display direct, CYP2D6-independent, activity.

180 d KLF9 expression is in part responsible for CYP2D6 induction during pregnancy via the potentiation o

181 cription factors potentially responsible for CYP2D6 induction during pregnancy, a panel of genes diff

182 e probability of treatment weighting, use of CYP2D6-inhibiting (versus CYP2D6-neutral) antidepressant

183 owing high in vitro permeability and lacking CYP2D6 inhibition as main optimization parameters.

184 ico ADMET models for Caco-2 permeability and CYP2D6 inhibition were also successfully applied for thi

185 prove compound aqueous solubility and reduce CYP2D6 inhibition, which led to the discovery of compoun

186 achieve the therapeutic effect regardless of CYP2D6 inhibition.

187 amage, which is effectively prevented by the CYP2D6 inhibitor quinidine.

188 imary dopaminergic neurons was attenuated by CYP2D6 inhibitor, quinidine, and also partly by monoamin

189 re frequent among the individuals prescribed CYP2D6 inhibitors (inverse probability-weighted odds rat

190 ffects were minimized in the presence of two CYP2D6 inhibitors, quinidine and ajmalicine.

191 patients taking strong cytochrome P450 2D6 (CYP2D6) inhibitors).

192 Preliminary evaluation of the CYP3A4 and CYP2D6 inhibitory activity in optimized ligands evidence

193 CYP2D6 is a highly polymorphic human gene responsible fo

194 CYP2D6 is expressed on the hepatocyte surface, and it ca

195 CYP2D6 is highly polymorphic gene which encodes the (CYP

196 onsistent with our previous observation that CYP2D6 is responsible for the metabolic activation of ta

197 Among the genes, CYP2D6 is significantly associated with SCZ SNPs in eGen

198 data-driven enrichment analysis showed that CYP2D6 is significantly involved in drug metabolism of c

199 CYP2D6 is the key enzyme responsible for the conversion

200 CYP2D6 is the key enzyme responsible for the generation

201 Cytochrome P450 2D6 (CYP2D6) is a highly polymorphic gene whose protein produ

202 t the hepatic isoenzyme cytochrome P450 2D6 (CYP2D6) is the key enzyme required to convert PQ into it

203 Caco-2 penetration and did not block CYP3A4, CYP2D6 isoenzymes, or P-glycoprotein.

204 ports of associations between alleles of the CYP2D6 locus (nearby on 22q13) and IPD, although inconsi

205 vided informed consent were genotyped at the CYP2D6 locus during their hospital stay.

206 se toxins in WT mice but remain unchanged in Cyp2d6 locus knockout mice, indicating a possible role o

207 ification from loss of heterozygosity at the CYP2D6 locus.

208 on of CYP3A4-mediated triazolam turnover and CYP2D6-mediated bufuralol and debrisoquine turnover on a

209 insights into mechanisms underlying altered CYP2D6-mediated drug metabolism during pregnancy, laying

210 pharmacology, toxicology, and physiology of CYP2D6-mediated metabolism.

211 and showed greatly reduced susceptibility to CYP2D6-mediated metabolism.

212 ity that may have affected their response to CYP2D6 medications.

213 ly to experience side effects in response to CYP2D6 medications.

214 ecule containing deuterium, which attenuates CYP2D6 metabolism and increases active metabolite half-l

215 tudies demonstrated that women with impaired CYP2D6 metabolism have lower endoxifen concentrations an

216 ides substantial drug exposure unaffected by CYP2D6 metabolism, acceptable toxicity, and promising an

217 moxifen dosing in patients with intermediate CYP2D6 metabolism.

218 king its metabolic liability associated with CYP2D6 metabolism.

219 -neutral) antidepressants concomitantly with CYP2D6-metabolized opioids was associated with a higher

220 , 51.2 [15.4] years; 66.5% women) prescribed CYP2D6-metabolized opioids, 15 960 had reduced CYP2D6 ac

221 d are currently used as biomarker to predict CYP2D6 metabolizer phenotype.

222 nes cover a wide spectrum of different human CYP2D6 metabolizer phenotypes.

223 A U-shaped association was found between CYP2D6 metabolizer status and breast cancer-specific mor

224 Both poor and ultrarapid CYP2D6 metabolizers of tamoxifen have a worse prognosis

225 g poor, intermediate, normal, and ultrarapid CYP2D6 metabolizers were -0.8 cm(2), -4.5 cm(2), -4.1 cm

226 g poor, intermediate, normal, and ultrarapid CYP2D6 metabolizers were 7.1%, 7.6%, 6.7%, and 18.8%, re

227 4.52 (95% CI, 1.42 to 14.37) for ultrarapid CYP2D6 metabolizers.

228 as poor, intermediate, normal, or ultrarapid CYP2D6 metabolizers.

229 CYP2D6 metabolizes nearly 25% of clinically used drugs.

230 KLF9 to CYP2D6 promoter in the livers of tg-CYP2D6 mice during pregnancy.

231 es SHP and represses CYP2D6 expression in Tg-CYP2D6 mice in part through ERalpha transactivation of S

232 In transgenic (Tg)-CYP2D6 mice, SHP knockdown led to a significant increase

233 reased CYP2D6 expression (by 1.5-fold) in Tg-CYP2D6 mice, the magnitude of differences being much sma

234 ression and activity of hepatic CYP2D6 in Tg-CYP2D6 mice.

235 reased hepatic levels during pregnancy in Tg-CYP2D6 mice.

236 Here, we introduce CYP2D6-humanized (Tg-CYP2D6) mice as an animal model where hepatic CYP2D6 exp

237 nant versus nonpregnant CYP2D6-humanized (tg-CYP2D6) mice was compiled via microarray experiments fol

238 In CYP2D6-humanized transgenic (Tg-CYP2D6) mice, cholestasis triggered by administration of

239 on-functional alleles of the cytochrome P450 CYP2D6 might be poor candidates for adjuvant tamoxifen t

240 rgeting suspected enhancer regions decreased CYP2D6 mRNA expression by 70%, only upon deletion of the

241 weighting, use of CYP2D6-inhibiting (versus CYP2D6-neutral) antidepressants concomitantly with CYP2D

242 ith dinucleotide repeat markers mapping near CYP2D6 on ch22q13.

243 The cytochrome P450 mono-oxygenase gene, CYP2D6 on chromosome 22q13 (ch22q13), has been inconsist

244 g toxicity and ineffective treatment, making CYP2D6 one of the most important pharmacogenes.

245 address this, we crossed mice humanized for CYP2D6 or CYP3A4 with mice carrying a hepatic Cyb5 delet

246 mely, cytochrome P450 (CYP) 3A4, CYP2C9, and CYP2D6, organic anion transporting polypeptide (OATP) 1B

247 y the polymorphic cytochrome P-450 2D6 gene (CYP2D6), oxidizes tamoxifen to its most active metabolit

248 city was obtained by coculturing T-regs with CYP2D6-peptide-loaded semimature dendritic cells (smDCs)

249 Binding affinity of CYP2D6 peptides to HLA-A2 was predicted by the algorithm

250 Seven CYP2D6 peptides with high HLA-A2 binding affinity coloca

251 Prediction of CYP2D6 phenotype relies on curation of literature-derive

252 We examined the association between CYP2D6 polymorphisms and Parkinson's disease in a case-c

253 ot occur at concentrations observed in human CYP2D6 poor metabolizers.

254 sults from deletion and mutation analysis of CYP2D6 promoter activity identified a KLF9 putative bind

255 that KLF9 itself is a weak transactivator of CYP2D6 promoter but significantly enhances CYP2D6 promot

256 ssay showed increased recruitment of KLF9 to CYP2D6 promoter in the livers of tg-CYP2D6 mice during p

257 However, HNF4alpha recruitment to CYP2D6 promoter increased at term pregnancy, accompanied

258 f CYP2D6 promoter but significantly enhances CYP2D6 promoter transactivation by hepatocyte nuclear fa

259 , SHP repressed HNF4alpha transactivation of CYP2D6 promoter.

260 decreases in the recruitment of HNF4alpha to CYP2D6 promoter.

261 the transactivation of cytochrome P450 2D6 (CYP2D6) promoter by hepatocyte nuclear factor (HNF) 4alp

262 si-synthetic data set in which data from the CYP2D6 region are embedded within simulated data on 100K

263 In-depth examination of the CYP2D6 region revealed that a nonsynonymous single nucle

264 effectors targeting identical or overlapping CYP2D6 regions.

265 rder to probe the potential for differential CYP2D6 regulation in lung normal tissue and tumors.

266 We investigated CYP2D6-specific CD8 T cell human leukocyte antigen (HLA)

267 Conclusion: HLA-A2-restricted, CYP2D6-specific CD8 T cell immune responses vary accordi

268 CYP2D6-specific CD8 T cell reactivity was tested at diag

269 Intensity of CYP2D6-specific CD8 T cell responses correlated with dis

270 nd frequency of circulating and intrahepatic CYP2D6-specific CD8 T cells via tetramer staining.

271 y, IFN-gamma production, and cytotoxicity of CYP2D6-specific CD8 T cells were higher at diagnosis tha

272 T-regs generated under CYP2D6-specific conditions and cocultured with smDCs are

273 Conclusion: T-regs generated under CYP2D6-specific conditions and cocultured with smDCs are

274 CYP2D6-specific protein expression was detected in the l

275 CYP2D6-specific regulatory T cells (CYP2D6 T-regs) were

276 moxifen metabolism and the evidence relating CYP2D6 status to breast cancer outcomes in tamoxifen-tre

277 le studies have examined the relationship of CYP2D6 status to breast cancer outcomes in tamoxifen-tre

278 y of PQ against liver stages depends on host CYP2D6 status, whilst OH-PQm display direct, CYP2D6-inde

279 or preclinical pharmacological evaluation of CYP2D6 substrates because of marked species differences

280 inical evidence indicates that metabolism of CYP2D6 substrates is increased during pregnancy, but the

281 a gene modulates in vivo pharmacokinetics of CYP2D6 substrates, a mouse line carrying both the CYP2D6

282 ficant individual differences in response to CYP2D6 substrates.

283 P2C19, and CYP17A1 but not that of CYP2E1 or CYP2D6, suggesting that the b(5) interaction varies amon

284 hondrion-targeted human cytochrome P450 2D6 (CYP2D6), supported by mitochondrial adrenodoxin and adre

285 ndrially targeted human cytochrome P450 2D6 (CYP2D6), supported by mitochondrial adrenodoxin and adre

286 quence were critical to the synergistic smDC-CYP2D6 T-reg immunoregulatory functions, and lack of eit

287 semimature dendritic cells (smDCs), and smDC-CYP2D6 T-regs also expressed high levels of FOXP3 (forkh

288 CYP2D6-specific regulatory T cells (CYP2D6 T-regs) were obtained from peptide-pulsed monocyt

289 ificantly boosted the suppressive ability of CYP2D6 T-regs.

290 thin four genes (SNX19, ARL6IP4, APOPT1, and CYP2D6) that potentially contribute to SCZ susceptibilit

291 ell immune responses to cytochrome P450IID6 (CYP2D6), the autoantigen of autoimmune hepatitis type 2

292 ell immune responses to cytochrome P450IID6 (CYP2D6), the autoantigen of autoimmune hepatitis type 2

293 orphic dinucleotide repeat markers linked to CYP2D6 to determine whether the association was present

294 ceptor agonist, which utilizes inhibition of CYP2D6 to increase its bioavailability.

295 ts demonstrate a significant contribution by CYP2D6 to the catalysis of tam-4-hydroxylation by human

296 aplotypes for investigating the evolution of CYP2D6 variation.

297 on results that Hosking et al. obtained near CYP2D6 were almost identical before and after marker sel

298 of 10 dinucleotide repeat markers linked to CYP2D6 were associated with the disease.

299 ressing predominantly mitochondrion-targeted CYP2D6 were more sensitive to MPTP-mediated mitochondria

300 ssing predominantly mitochondrially targeted CYP2D6 were more sensitive to toxin-mediated respiratory

301 mes (cytochrome P450 3A4 and 2D6 [CYP3A4 and CYP2D6]) were also measured in these 17 patients.

302 Moreover, docking into the CYP2D6 X-ray structure provided a reliable alignment for