ライフサイエンスコーパス: CYP1A1

1 ing cytochrome P450 subfamily polypeptide 1 (CYP1A1).

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

3 tion from the mouse cytochrome P4501A1 gene (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 ocarbon receptor-mediated induction of human CYP1A1.

11 AHR activation as indicated by induction of Cyp1a1.

12 at are antimicrotubule prodrugs activated by CYP1A1.

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

14 SAL inhibited the increase in CYP1A1, -1A2, and -1B1 mRNA levels that occurs on exposu

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

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

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

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

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

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

21 49 cells by downregulating the expression of CYP1A1/1A2, at least in part.

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

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

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

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

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

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

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

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

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

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

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

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

39 er numerous biological responses mediated by CYP1A1 activity.

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

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

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

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

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

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

46 1_1A2 transgenic mouse (expressing the human CYP1A1 and CYP1A2 genes in the absence of mouse Cyp1a2 g

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

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

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

50 The Cyp1a1 and Cyp1a2 loci represent linked genes thought to

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

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

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

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

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

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

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

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

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

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

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

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

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

64 17Beta-estradiol repressed TCDD-activated Cyp1a1 and Cyp1b1 gene transcription in MCF-7 cells in t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 CYP1A1 and CYPIB1 were both inducible by dioxin in human

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

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

83 In contrast to the absence of constitutive Cyp1a1 and lacZ transgene expression in tissues of the a

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

85 fect of gene-environment interaction between CYP1A1 and serum PCB levels on breast cancer risk among

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

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

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

89 1,9(11)-dien-28-oyl]imidazole}, induced Ahr, Cyp1a1, and Cyp1b1 transcription in Nrf2+/+ MEFs but not

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

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

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

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

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

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

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

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

98 CYP1A1 bioactivates several procarcinogens and detoxifie

99 lavone derivatives can act as substrates for CYP1A1 bioactivation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

141 0 prostate tumor DNA samples have detectable CYP1A1 enhancer methylation, indicating that it is hyper

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

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

144 In the CYP1A1 enhancer, EGFR activation prevents recruitment of

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

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

147 kout mice, having the genetic absence of the CYP1A1 enzyme, with Cyp1a1(+/+) wild-type mice.

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

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

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

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

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

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

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

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

156 By inhibiting Cyp1a1 expression, chromium stimulates the formation of

157 er levels of DNA adduct formation, increased CYP1A1 expression, decreased DNA repair capacity, and in

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

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

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

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

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

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

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

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

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

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

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

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

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

171 the association of two polymorphisms in the CYP1A1 gene--the noncoding Msp I polymorphism in the 3'-

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

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

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

175 with information on both serum PCB level and CYP1A1 genotype (1999-2002).

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

177 CYP1A1 genotype was not associated with colon or rectal

178 er impact on colorectal cancer risk based on CYP1A1 genotype; this might further be modified by GSTM1

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

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

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

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

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

184 ure that have shown a participatory role for CYP1A1 in BaP toxicity, the present data indicate that,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

205 ion yet produced higher levels of endogenous CYP1A1 induction.

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

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

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

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

210 32 days, indicating that GI tract inducible CYP1A1 is absolutely required for detoxication of oral B

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

212 dicate that, in the intact animal, inducible CYP1A1 is extremely important in detoxication and protec

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

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

215 CYP1A1 is particularly well known for its ability to bio

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

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

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

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

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

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

222 We compared Cyp1a1(-/-) knockout mice, having the genetic absence of

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

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

225 In summary, the CYP1A1 m2 genetic polymorphism was associated with incre

226 ymorphisms in the cytochrome P-450 1A1 gene (CYP1A1) may affect the relation between environmental ex

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

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

229 arance was 4-fold slower in Cyp1a1(-/-) than Cyp1a1(+/+) mice.

230 s probably a major site of BaP metabolism in Cyp1a1(+/+) mice.

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

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

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

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

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

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

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

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

239 Surprisingly, CYP1A1 mRNA expression and enzymatic activities were mar

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

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

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

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

244 tissue exhibits relatively high constitutive CYP1A1 mRNA levels.

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

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

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

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

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

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

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

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

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

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

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

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

257 CYP1A1 possesses functional similarities and differences

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

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

260 cell-specific and time-dependent pattern of CYP1A1 promoter activity was observed in the embryo.

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

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

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

264 5A in Huh7 partially suppressed TCDD-induced CYP1A1 protein and enzyme activity, implicating this pro

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

266 stern blot analysis confirmed that Socs2 and Cyp1a1 protein levels were also induced in CH12.LX cells

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

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

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

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

271 16969968, CLPTM1L rs402710, CXCR2 rs1126579, CYP1A1 rs4646903, CYP2E1 rs6413432, ERCC1 rs11615, ERCC2

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

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

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

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

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

277 e rate of BaP clearance was 4-fold slower in Cyp1a1(-/-) than Cyp1a1(+/+) mice.

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

279 atically higher BaP-DNA adduct levels in all Cyp1a1(-/-) tissues assayed, with the exception of the s

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

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

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

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

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

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

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

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

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

289 olon cancer risk was observed for having any CYP1A1 variant allele and currently smoking (odds ratio

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

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

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

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

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

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

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

297 e genetic absence of the CYP1A1 enzyme, with Cyp1a1(+/+) wild-type mice.

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.