ライフサイエンスコーパス: CYP1A1

1 ing cytochrome P450 subfamily polypeptide 1 (CYP1A1).

2 tion from the mouse cytochrome P4501A1 gene (CYP1A1).

3 he canonical AhR target cytochrome P450 1a1 (Cyp1a1).

4 se that regulates mitochondrial targeting of CYP1A1.

5 fied pathway did not affect the induction of CYP1A1.

6 ieve this reflects the absence of intestinal CYP1A1.

7 d cdc37 was abolished, but not its action on CYP1A1.

8 butions nearly identical with those of human CYP1A1.

9 tics that are poor substrates for microsomal CYP1A1.

10 at are antimicrotubule prodrugs activated by CYP1A1.

11 ocarbon receptor-mediated induction of human CYP1A1.

12 AHR activation as indicated by induction of Cyp1a1.

13 Recombinant human CYPs (CYP1A1, 1A2, 1B1, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, an

14 he AHR and an ideal substrate for cytochrome CYP1A1/1A2 and 1B1, thereby also participating in an aut

15 Cigarette smoking induces CYP1A1/1A2 and is hypothesized to alter erlotinib pharma

16 eoclastogenesis induced by TCDD was lower in Cyp1a1/1a2(-/-) and Cyp1a1/1a2/1b1(-/-) cultures, indica

17 Crossing the Cyp1a1/1a2(-/-) double-knockout mouse with the Cyp1b1(-/

18 Cyp1a1(-/-) and Cyp1a1/1a2(-/-) knockouts and mice with Cyp1a1 expressio

19 enzo[a]pyrene (BaP) daily for 18 days in the Cyp1a1/1a2(-/-) produced the same degree of marked immun

20 49 cells by downregulating the expression of CYP1A1/1A2, at least in part.

21 ve stress in the lungs of wild-type mice and Cyp1a1/1a2-null mice, but the effects were markedly blun

22 -stimulated inflammatory exudates, comparing Cyp1a1/1a2/1b1((-)/(-)) C57BL/6J-background triple-knock

23 ced by TCDD was lower in Cyp1a1/1a2(-/-) and Cyp1a1/1a2/1b1(-/-) cultures, indicating that Ahr was up

24 Cyp1a1/1b1(-/-) and Cyp1a1/1a2/1b1(-/-) mice are rescued from immunosuppress

25 Oral BaP-treated Cyp1a1/1a2/1b1(-/-) mice showed the same "rescued" respo

26 -/-) single-knockout mouse, we generated the Cyp1a1/1a2/1b1(-/-) triple-knockout mouse.

27 Cyp1a1/1b1(-/-) and Cyp1a1/1a2/1b1(-/-) mice are rescued

28 l small intestine (PSI) in Cyp1a1(-/-) mice; Cyp1a1/1b1(-/-) double-knockout mice show no PSI cancer

29 same "rescued" response as that seen in the Cyp1a1/1b1(-/-) mouse; we believe this reflects the abse

30 er non-alcoholic beverages (ANXA9, AHR, POR, CYP1A1/2 and CSDC2); (iii) 10 loci for coffee; six novel

31 gests that mammalian and bird paralog pairs (CYP1A1/2 and CYP1A4/5, respectively) are the result of i

32 Prior studies of lung cancer and CYP1A1/2 in African-American and Latino populations have

33 nvestigated the haplotype block structure of CYP1A1/2 or addressed potential population stratificatio

34 ng 50 single nucleotide polymorphisms in the CYP1A1/2 region and 184 ancestry informative markers sel

35 To investigate haplotypes in the CYP1A1/2 region and lung cancer in African-Americans and

36 es, that is, ethoxyresorufin O-deethylation (CYP1A1/2), between five donors.

37 eplicated (in/near GCKR, ABCG2, AHR, POR and CYP1A1/2).

38 medium is also revealed by the induction of CYP1A1, a downstream target of AhR activation.

39 the regulation of CAR mRNA mimicked that of Cyp1A1, a known AhR target gene.

40 Thus, modulation of CYP1A1 activity may represent a promising alternative st

41 In concordance, total CYP1A1 activity, as measured by the ethoxyresorufin O-de

42 er numerous biological responses mediated by CYP1A1 activity.

43 obe selective activation by cells expressing CYP1A1 and 2W1, CYPs known to be expressed in high frequ

44 ersistently perturbed patterns (AHRR, MYO1G, CYP1A1 and CNTNAP2).

45 This study showed that the expression of CYP1A1 and CYP1A2 are cell specific and CYP2E1 and GSTM1

46 The human CYP1A genes CYP1A1 and CYP1A2 are in a head-to-head orientation on c

47 n Ahr null mice, these results indicate that Cyp1a1 and Cyp1a2 do not play a dominant role in AHR-med

48 for normal up-regulation by dioxin, whereas Cyp1a1 and Cyp1a2 do not.

49 1_1A2 transgenic mouse (expressing the human CYP1A1 and CYP1A2 genes in the absence of mouse Cyp1a2 g

50 controls the adaptive up-regulation of both Cyp1a1 and Cyp1a2 genes in vivo.

51 d in the 14-kb intergenic region between the Cyp1a1 and Cyp1a2 genes.

52 and cynomolgus monkey and up to 45-fold for CYP1A1 and CYP1A2 in vitro in rat and human hepatocytes

53 The Cyp1a1 and Cyp1a2 loci represent linked genes thought to

54 ed cytochrome P450 (CYP) enzyme activity and CYP1A1 and CYP1A2 mRNA expression.

55 arallel toxicologic studies using individual Cyp1a1 and Cyp1a2 null mice support the observation that

56 Thus, chimeric constructs of CYP1A1 and CYP1A2 were created, and their localization w

57 Most human P450 enzymes, including CYP1A1 and CYP1A2, exhibit a high preference for estradi

58 RCA1 is recruited to the promoter regions of CYP1A1 and CYP1B1 along with ARNT and/or AhR following x

59 l control of the xenobiotic metabolism genes Cyp1a1 and Cyp1b1 and (ii) inhibition of adipogenesis in

60 nd BaP metabolism was similar to BaP-induced Cyp1A1 and Cyp1B1 and molecular clock gene expression in

61 Although the TCDD-responsive enhancers for CYP1A1 and CYP1B1 are well characterized, a similar CYP1

62 ocarbon receptor (AhR) mediates induction of CYP1A1 and CYP1B1 by 2,3,7,8-tetrachlorodibenzo-rho-diox

63 As expected, the CYP1A1 and CYP1B1 enhancers bind AhR in TCDD-treated cel

64 gland tissue demonstrated that TCDD-induced Cyp1A1 and Cyp1B1 expression in Per1(ldc) and Per1(ldc)/

65 The structure-dependent induction of CYP1A1 and CYP1B1 gene expression in Ah-responsive MDA-M

66 Analysis of CYP1A1 and CYP1B1 gene expression showed the maximum enz

67 17Beta-estradiol repressed TCDD-activated Cyp1a1 and Cyp1b1 gene transcription in MCF-7 cells in t

68 blocked PAH and dioxin-mediated induction of CYP1A1 and CYP1B1 in cell lines derived from the human a

69 BaP-induced Cyp1a1 and Cyp1b1 mRNA levels were higher 4 hours after

70 was 0.0001 and 0.0032, based on induction of CYP1A1 and CYP1B1 mRNA, respectively.

71 Ligand-induced recruitment of the AhR to the CYP1A1 and CYP1B1 promoters was inhibited when HDAC6 was

72 We have also found that the inducibility of CYP1A1 and CYP1B1 transcripts following xenobiotic stres

73 fects of TCDD on mammary gland expression of Cyp1A1 and Cyp1B1 vary over time and are significantly g

74 he contrary, no change in gene expression of CYP1A1 and CYP1B1 was observed when the cells were expos

75 An additive induction of CYP1A1 and CYP1B1 was observed with cotreatment of SRM 1

76 Furthermore, we showed that expression of CYP1A1 and CYP1B1 was reduced significantly in an indepe

77 -characterized AhR-regulated genes including Cyp1a1 and Cyp1b1 were corroborated.

78 The tamoxifen-metabolizing enzymes CYP1A1 and CYP1B1 were detected by immunohistochemistry

79 stance polypeptide, as well as expression of Cyp1a1 and Cyp1b1, both AhR target genes.

80 r of HDAC6, also suppressed the induction of CYP1A1 and CYP1B1.

81 e transcription of numerous genes, including CYP1A1 and CYP1B1.

82 nes was observed in response to BP exposure (CYP1A1 and CYP1B1; signal log ratio of 4.7 and 2.5, resp

83 (PBDEs) and induction of cytochrome's P450 (CYP1A1 and CYP2B isoforms) were evaluated.

84 CYP1A1 and CYPIB1 were both inducible by dioxin in human

85 The transcription correlation between CYP1A1 and hTERT may suggest a possible new mechanism fo

86 Expression of Cyp1a1 and its related enzyme activity have long been us

87 vivo experiments examined the expression of Cyp1a1 and other AhR-regulated genes in liver, kidney, a

88 should explore possible interactions between CYP1A1 and sources of polycyclic aromatic hydrocarbons,

89 Cyp1a1(-/-) and Cyp1a1/1a2(-/-) knockouts and mice with

90 aired expression of AhR-regulated genes (eg, CYP1A1) and an upregulation of the corresponding proinfl

91 hypermethylation in the cytochrome P450 1A1 (CYP1A1) and cytochrome P450 1B1 (CYP1B1) promoters of bl

92 1,9(11)-dien-28-oyl]imidazole}, induced Ahr, Cyp1a1, and Cyp1b1 transcription in Nrf2+/+ MEFs but not

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

94 We replicated findings for CpGs in AHRR, CYP1A1, and GFI1 at strict Bonferroni-corrected statisti

95 We conclude that small intestine CYP1A1, and not liver CYP1A1, is critically important in

96 us knock-out) identified 171 genes unique to Cyp1a1-/- and 119 unique to Cyp1a2-/- mice.

97 Wild type (WT), Cyp1a1-/- and Cyp1a2-/- (8-10 wk, C57BL/6J background) m

98 behind the differences in susceptibility of Cyp1a1-/- and Cyp1a2-/- mice to HLI and suggest novel pa

99 at were differentially regulated between WT, Cyp1a1-/- and Cyp1a2-/- mice.

100 the absence of downstream signals (COX-2 and CYP1A1) as well as regulatory T-lymphocytes and by compu

101 rs, suggesting that dysregulation of the AHR/CYP1A1 axis may play a role in inflammatory skin disease

102 ction of TCDD to induce cytochrome P450 1A1 (CYP1A1) because blocking this newly identified pathway d

103 CYP1A1 bioactivates several procarcinogens and detoxifie

104 lavone derivatives can act as substrates for CYP1A1 bioactivation.

105 Inversely, exposure to AhR ligands induces Cyp1a1 but not Ccno and impeded ciliogenesis.

106 As a result, induction of Cyp1a1 by pharmaceutical drug candidates or environmenta

107 diates the expression of target genes (e.g., CYP1A1) by binding to dioxin response element (DRE) sequ

108 On the other hand, CYP1A1 can also produce highly carcinogenic intermediate

109 luding those implicated for caffeine (ARID3B/CYP1A1), carbohydrate metabolism (FGF21), schizophrenia

110 es in seven gene regions (AHRR, MYO1G, GFI1, CYP1A1, CNTNAP2, KLF13 and ATP9A) was associated with ma

111 Mouse MT-CYP1A1 consists of two NH2-terminal-truncated molecular

112 nificantly from that in the Nrf1(flox/flox)::CYP1A1-Cre control.

113 a rat CYP1A1-Cre transgene (Nrf1(flox/flox)::CYP1A1-Cre mice).

114 als harboring an Nrf1(flox) allele and a rat CYP1A1-Cre transgene (Nrf1(flox/flox)::CYP1A1-Cre mice).

115 hrene (3-MC) to these mice (Nrf1(flox/flox)::CYP1A1-Cre+3MC mice) resulted in loss of hepatic Nrf1 ex

116 ly upregulated in livers of Nrf1(flox/flox)::CYP1A1-Cre+3MC mice, suggesting that Nrf1 normally suppr

117 d dramatically in livers of Nrf1(flox/flox)::CYP1A1-Cre+3MC mice.

118 synergistically enhanced AhR ligand-induced Cyp1a1/CYP1A1 in these cells with comparable enhancement

119 ed expression of Ah-responsive genes such as Cyp1a1/CYP1A1 in YAMC mouse colonocytes and Caco-2 human

120 el, enzymatically active, spliced variant of CYP1A1 (CYP1A1v) formed by excision of an 84-bp cryptic

121 in dioxin-induced teratogenesis, we compared Cyp1a1(-/-), Cyp1a2(-/-), and Cyp1b1(-/-) knock-out mice

122 The Cyp1a1, Cyp1a2, and Cyp1b1 genes are up-regulated by the

123 Finally, deletion of the Cyp1a1, Cyp1a2, and Cyp1b1 in triple knockout mice resul

124 otein and messenger RNA (mRNA) expression of CYP1A1, CYP1A2, and CYP1B1.

125 aryl hydrocarbon hydroxylase (Ah) receptor (Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1).

126 s (SNP) in genes involved in HCA metabolism (CYP1A1, CYP1A2, CYP1B1, GSTA1, GSTM1, GSTM3, GSTP1, NAT1

127 g transcription of multiple genes, including CYP1A1, CYP1A2, CYP1B1, UGT1A1, UGT1A6, IL6, and SAA1.

128 revious associations between SNPs in AHR and CYP1A1-CYP1A2 and caffeine and coffee consumption from G

129 tivity of CYP1A2 was higher than that of the CYP1A1-CYP1A2 chimera containing the N-terminal end of C

130 eptor (AHR) and cytochrome P450 1A1 and 1A2 (CYP1A1-CYP1A2) genes that are associated with habitual c

131 er these SNPs (AHR: rs6968865 and rs4410790; CYP1A1-CYP1A2: rs2472297 and rs2470893) and 6 additional

132 difference in constitutive or ligand-induced CYP1A1; CYP1A2; UDP glucuronosyltransferase 1A2; NAD(P)H

133 not significantly different in fetuses from Cyp1a1(-/-), Cyp1b1(-/-), and Cyp1(+/+) wild-type mice.

134 Standard AhR-mediated stimulations (Cyp1a1, Cyp1b1, Ahrr) were similar for each PAH and for

135 xenobiotic-metabolizing AhR targets such as Cyp1a1, Cyp1b1, and Nqo1 were regulated by both ligand a

136 Most increased in expression (>=5-FC) were CYP1A1, CYP1B1, and USP17L9P; most decreased (>=6-FC) we

137 Other cytochromes P450, including CYP1A1, CYP1B1, CYP1A2, and CYP3A4, were also able to ep

138 Multiple cytochrome P450 (CYP1A1, CYP2A19 and CYP2C36) genes displayed different t

139 These mice exhibited increased CYP1A1, CYP2E1, and CYP2U1 expression and abundant level

140 associated with an AhR-dependent increase of CYP1A1 (cytochrome P4501A1).

141 pressor (AhRR) and AhR-mediated induction of CYP1A1, cytokines, and acute toxicity.

142 that SIN3A is necessary for the induction of CYP1A1-dependent ethoxyresorufin-o-deethylase (EROD) enz

143 Mice constitutively expressing Cyp1a1 displayed increased CYP1A1 enzymatic activity in

144 ls within the adult small intestine, using a CYP1A1-driven Cre-Lox approach.

145 are present together at the same time on the Cyp1a1 enhancer during transrepression.

146 NA sequencing shows that the TCDD-responsive CYP1A1 enhancer is highly methylated in LNCaP cells but

147 We do not detect CYP1A1 enhancer methylation in 30 DNA samples isolated f

148 We also analyzed CYP1A1 enhancer methylation in human prostate tissue DNA

149 0 prostate tumor DNA samples have detectable CYP1A1 enhancer methylation, indicating that it is hyper

150 s have shown that ER alpha is present at the Cyp1a1 enhancer only after co-treatment with E2 and TCDD

151 )-activated aryl hydrocarbon receptor to the CYP1A1 enhancer sequence; additionally, NO-aspirin 2 sup

152 In the CYP1A1 enhancer, EGFR activation prevents recruitment of

153 xenobiotic metabolizing enzymes UGT1A10 and CYP1A1, enhancing carcinogen detoxification.

154 Inhibition of CYP1A1 enzymatic activity ameliorated the skin immunopat

155 In this study, we identify CYP1A1 enzymatic activity as a critical regulator of ben

156 activation of the AHR pathway and increased CYP1A1 enzymatic activity compared with healthy donors,

157 tively expressing Cyp1a1 displayed increased CYP1A1 enzymatic activity in the skin, which resulted in

158 y-4'-nitroflavone all inhibited induction of CYP1A1 enzyme activity by FICZ or 2,3,7,8-tetrachlorodib

159 ral CPI-based compounds were pM-nM potent in CYP1A1 expressing cells.

160 be a novel regulatory system for whole-body CYP1A1 expression by a factor originating in the gut.

161 and Cyp1a1/1a2(-/-) knockouts and mice with Cyp1a1 expression deleted in gastrointestinal (GI) tract

162 or Cyp1a2/1b1(-/-) knockouts, and mice with Cyp1a1 expression deleted in hepatocytes can ingest larg

163 ; compound 8n is not reliant on induction of CYP1A1 expression for antitumor activity.

164 study, we demonstrate that the induction of CYP1A1 expression in Huh.8 cells by TCDD but not by beta

165 Indirubin was also a more potent inducer of Cyp1a1 expression in transgenic hAHR mouse hepatocytes c

166 is tailored to the characteristic pattern of CYP1A1 expression observed in a large percentage of huma

167 By inhibiting Cyp1a1 expression, chromium stimulates the formation of

168 stimulate canonical DRE-driven AHR-mediated CYP1A1 expression, thus eliminating the potential for AH

169 AhR activation and, downstream of AhR, lung Cyp1A1 expression.

170 vation was evaluated with reporter cells and Cyp1A1 expression.

171 sm of dietary CYP1A1 inducers and whole-body CYP1A1 expression.

172 enin is indispensable for Cyp1b1 but not for Cyp1a1 expression.

173 CV infection on hepatic cytochrome P450 1A1 (CYP1A1) expression and function, we used a human hepatom

174 ith the enhancer but not the promoter of the CYP1A1 gene after TCDD treatment with similar kinetics a

175 YP1A1 under control of the full-length human CYP1A1 gene and 9 kb of flanking regulatory DNA.

176 th the proximal promoter and enhancer of the Cyp1a1 gene and demonstrate that increased binding to th

177 ish that SIN3A physically interacts with the CYP1A1 gene and extends the transcriptional role of SIN3

178 -type BRCA1 affect xenobiotic stress-induced CYP1A1 gene expression.

179 t nuclear translocation, followed by induced CYP1A1 gene expression.

180 Four CYP1A1 gene polymorphisms (3801T --> C, Ile462Val, 3205T

181 the xenobiotic response element of the mouse CYP1A1 gene, an AHR-responsive gene.

182 contrast to TCDD, CA is unable to induce the CYP1A1 gene, thus revealing an AhR agonist-specific mutu

183 ation of AhR as assessed by transcription of CYP1A1 gene.

184 dioxin activation of the cytochrome P4501A1 (CYP1A1) gene.

185 ve effects of variants in the fetal NAT2 and CYP1A1 genes were observed in both the Iowan and the Dan

186 The SLCO2A1 and CYP1A1 genes, which were upregulated at the forearm of n

187 istent association between breast cancer and CYP1A1 genotype was found.

188 CYP1A1 genotype was not associated with colon or rectal

189 This lab has previously shown that Cyp1a1(-/-) global knockout mice treated by oral adminis

190 meters were therefore compared in wild-type, Cyp1a1(-/-) global knockout, intestinal epithelial cell-

191 ays was found in the order CYP1B1 > CYP1A2 > CYP1A1 > CYP2E1 > myoglobin, the same as the order of th

192 taining a 206-302-residue peptide segment of CYP1A1 had less affinity to bind to ordered microdomains

193 The purified protease processed CYP1A1 in a sequence-specific manner, leading to its mit

194 of chimeric signals and bimodal targeting of CYP1A1 in different species.

195 by chemically inducing the transcription of CYP1A1 in four cell lines: control normal lung cells (CC

196 tored the expression of AhR and induction of CYP1A1 in MEF RelA null cells.

197 Here we show that dysregulated expression of Cyp1a1 in mice depletes the reservoir of natural AHR lig

198 ver occurred at 12 h, whereas highly induced CYP1A1 in small intestine persisted throughout the 30-da

199 ibenzo-p-dioxin (TCDD)-mediated induction of CYP1A1 in thymus of B6 mice.

200 linical specimens revealed overexpression of CYP1A1 in various types of ovarian cancers compared with

201 compounds were found to significantly induce Cyp1a1 in vivo but were not verified to bind or activate

202 Fold changes in mRNA up to 10,000-fold for CYP1A1 in vivo in rat and cynomolgus monkey and up to 45

203 on of estrogen-metabolizing enzymes, such as CYP1A1, in breast cells.

204 genes, notably cytochrome P4501A1 encoded by CYP1A1, in response to the exogenous prototypical ligand

205 Expression of AHR-regulated gene CYP1A1 increased up to 41-fold and most Nrf2-pathway gen

206 nduced by 1,25-dihydroxyvitamin D(3), and of CYP1A1, induced by benzo(a)pyrene.

207 e in regulation of the metabolism of dietary CYP1A1 inducers and whole-body CYP1A1 expression.

208 In distinct contrast, we show here that CYP1A1 inducibility is essential in the detoxication of

209 lend further support to the hypothesis that Cyp1a1 induction and/or AhR activation is not synonymous

210 e current study evaluates the specificity of Cyp1a1 induction as a marker for AhR affinity and activa

211 HCV subgenomic replicon (Huh.8) to evaluate CYP1A1 induction by the aryl hydrocarbon receptor (AhR)

212 However, TCDD-mediated Cyp1A1 induction in the mammary glands of Per1(ldc) and

213 the long-term actions of TCDD except that on CYP1A1 induction, indicating that the influence of the n

214 on SAA1 expression and partial DRE-mediated CYP1A1 induction.

215 ion yet produced higher levels of endogenous CYP1A1 induction.

216 e SIN3A, thus validating a role for SIN3A in CYP1A1 induction.

217 the N terminus of CYP1A2 partially directed CYP1A1 into ordered regions.

218 These data demonstrate that induction of Cyp1a1 is a nonspecific biomarker of direct AhR affinity

219 This is the first report that shows that CYP1A1 is aberrantly hypermethylated in human prostate c

220 32 days, indicating that GI tract inducible CYP1A1 is absolutely required for detoxication of oral B

221 The mouse MT-CYP1A1 is an extrinsic membrane protein, which exhibited

222 Transcription of CYP1A1 is highly induced by 2,3,7,8-tetrachlorodibenzo-p

223 Thus, for oral BaP, CYP1A1 is more important in detoxication than in metabol

224 CYP1A1 is particularly well known for its ability to bio

225 Cytochrome P450 1A1 (CYP1A1) is one of the most important detoxification enzy

226 e that small intestine CYP1A1, and not liver CYP1A1, is critically important in oral BaP detoxication

227 fic Cyp1a1 knockout, and hepatocyte-specific Cyp1a1 knockout mice as a function of long-term oral exp

228 pe mice; intestinal epithelial cell-specific Cyp1a1 knockout mice behaved like Cyp1a1(-/-) mice, dyin

229 Hepatocyte-specific Cyp1a1 knockout mice remained as healthy as wild-type mi

230 nockout, intestinal epithelial cell-specific Cyp1a1 knockout, and hepatocyte-specific Cyp1a1 knockout

231 days of oral BaP, we found surprisingly low CYP1A1 levels in liver, compared with that in small inte

232 The CYP1A1 m1 and m4 genotypes were not associated with brea

233 Induced CYP1A1 message, protein, and enzyme activity were partia

234 Cyp1a1(-/-) mice died within 30 days whereas Cyp1a1(+/+) mice displayed no outward signs of toxicity.

235 At an oral BaP dose of 125 mg/kg/day, Cyp1a1(-/-) mice died within 30 days whereas Cyp1a1(+/+)

236 The cause of death in Cyp1a1(-/-) mice receiving oral BaP seemed to be immunot

237 on of the bone marrow; some toxic effects in Cyp1a1(-/-) mice were noted at a BaP dose as low as 1.25

238 l-specific Cyp1a1 knockout mice behaved like Cyp1a1(-/-) mice, dying with immunosuppression approxima

239 oma of the proximal small intestine (PSI) in Cyp1a1(-/-) mice; Cyp1a1/1b1(-/-) double-knockout mice s

240 e of marked immunosuppression as seen in the Cyp1a1(-/-) mouse; we believe this reflects the absence

241 culture medium are sufficient to up-regulate CYP1A1 mRNA and enzyme activity.

242 r SIN3A decreased TCDD-mediated induction of CYP1A1 mRNA and EROD activity in human hepatoma cell lin

243 Surprisingly, CYP1A1 mRNA expression and enzymatic activities were mar

244 of DNA methylation, increases TCDD-inducible CYP1A1 mRNA expression in cancerous LNCaP cells but not

245 Suppression of CYP1A1 mRNA expression in TCDD-treated Huh.8 cells was p

246 Whereas in vivo Cyp1a1 mRNA expression is a sensitive marker for AhR act

247 EROD activity and CYP1A1 mRNA levels were correlated with TK MF, supportin

248 tissue exhibits relatively high constitutive CYP1A1 mRNA levels.

249 In this study, we showed overexpression of CYP1A1 mRNA, but not CYP1B1 transcripts, in ovarian canc

250 The peak of CYP1A1 (mRNA, protein) expression in liver occurred at 1

251 cytochrome P450, subfamily I, polypeptide 1 (Cyp1A1) mRNA regardless of genotype.

252 The authors conclude that the CYP1A1 MspI and EPHX1 genotypes modified the association

253 confidence interval (CI): -283.6, -29.0) for CYP1A1 MspI and with Tyr/His113 (93.8 g, 95% CI: -188.6,

254 ernal metabolic genes, cytochrome P-450 1A1 (CYP1A1) MspI and epoxide hydrolase 1 (EPHX1) Tyr113His,

255 P1A2, containing the N-terminal regions from CYP1A1, no longer localized in ordered domains, whereas

256 In contrast, neither CYP1A1 nor CYP1B1 appears to play a role in dioxin-media

257 these data provided the first evidence that CYP1A1 overexpression and alternative splicing could con

258 ufort Sea to determine the concentrations of CYP1A1 phase I metabolites of polycyclic aromatic hydroc

259 AHRR and CYP1A1 play a key role in the aryl hydrocarbon receptor

260 azolidin-1-yl)benzenesulfonates (PIB-SOs) in CYP1A1-positive cancer cells, both in vitro and in vivo.

261 CYP1A1 possesses functional similarities and differences

262 As a result, it is widely accepted that CYP1A1 potentiates the toxicity of this class of chemica

263 strain (CYPLucR) carries a functional human CYP1A1 promoter (-1612 to +293)-luciferase reporter gene

264 g the interaction of these proteins with the Cyp1a1 promoter and allowing histone acetylation to proc

265 thyltransferase 1 (HDAC1-DNMT1) complexes to Cyp1a1 promoter chromatin and inhibits histone marks ind

266 cence protein (CYP-GFP) construct, driven by CYP1A1 promoter.

267 5A in Huh7 partially suppressed TCDD-induced CYP1A1 protein and enzyme activity, implicating this pro

268 SIN3A is required for TCDD induction of the CYP1A1 protein in Hepa-1 cells but not for expression of

269 for 2008 and 2009) and cytochrome P450 1A1 (Cyp1a1) (r(2) = 0.20, p < 0.001 for 2008 and 2009; r(2)

270 H3 lysine 4, a mark of active genes, on the CYP1A1 regulatory region, whereas this histone modificat

271 ranks were attributed to NRAMP, MX, CXC, and Cyp1a1 responses.

272 CYP1A to the corresponding residues of human CYP1A1 resulted in TCB pose distributions nearly identic

273 xpression of its negative feedback regulator CYP1A1, results in reduced peristaltic activity of the c

274 16969968, CLPTM1L rs402710, CXCR2 rs1126579, CYP1A1 rs4646903, CYP2E1 rs6413432, ERCC1 rs11615, ERCC2

275 Interestingly, the upregulation was CYP1A1 selective and lost upon administration of a synth

276 Notably, the expression FAM5C, PLA2G4E and CYP1A1 showed an increased expression in females compare

277 eus and transcription of the AhR target gene Cyp1a1, showing that the AhR pathway is functional in B

278 n, we have studied the mechanism of mouse MT-CYP1A1 targeting to gain insight into the regulatory fea

279 Asp or induced cellular PKC caused increased CYP1A1 targeting to MT and correspondingly lower levels

280 ser to the heme in ensembles of rat or human CYP1A1 than of killifish CYP1A.

281 Constitutive expression of Cyp1a1 throughout the body or restricted specifically to

282 homeodomain genes); (2) cell survival (e.g., CYP1A1 to degrade aromatic genotoxic compounds); (3) cyc

283 asmic reticular protein, cytochrome P4501A1 (CYP1A1), to mitochondria involves activation of a crypti

284 resulted in greater than 55% suppression of CYP1A1 transcription compared with the parent cell line

285 In addition, siRNA was used to silence CYP1A1 transcription in A549 observing a decrease in the

286 at a significant component of TCDD-inducible Cyp1a1 transcription is the result of recruitment of est

287 n environmental procarcinogen that activates Cyp1a1 transcriptional responses mediated by the aryl hy

288 r (DREC), are located 1.4 kb upstream of the Cyp1a1 transcriptional start site and 12.6 kb upstream o

289 ne, and the other strain (CYP1A1N) expresses CYP1A1 under control of the full-length human CYP1A1 gen

290 tallothionein-A), and xenobiotic metabolism (Cyp1a1) utilizing quantitative polymerase chain reaction

291 pite the high degree of sequence similarity, CYP1A1 was found to localize to disordered regions, wher

292 However, only CYP1A1 was inducible in human HepG2 cells.

293 Furthermore, expression of its close homolog Cyp1a1 was inhibited by beta-catenin.

294 lation of the prototypic AHR responsive gene Cyp1a1 was negatively regulated by PMA and IL-1beta trea

295 hR expression and TCDD-mediated induction of CYP1A1 was significantly reduced in RelA-deficient MEF c

296 endothelial cells, whereas its close homolog Cyp1a1 was upregulated in an aryl hydrocarbon receptor-d

297 ay plays an active role in the activation of CYP1A1 which subsequently activates hTERT transcription.

298 A novel co-transcription of CYP1A1 with hTERT, the active subunit of telomerase has

299 1A2 chimera containing the N-terminal end of CYP1A1 with subsaturating CPR concentrations, but it was

300 We determined a 2.6 A structure of human CYP1A1 with the inhibitor alpha-naphthoflavone.