ライフサイエンスコーパス: CYP1B1

1 utations in the gene for cytochrome P4501B1 (CYP1B1).

2 also suppressed the induction of CYP1A1 and CYP1B1.

3 n pathways that are potentially regulated by CYP1B1.

4 tion of numerous genes, including CYP1A1 and CYP1B1.

5 RNA (mRNA) expression of CYP1A1, CYP1A2, and CYP1B1.

6 size within 20 days but not when mice lacked Cyp1b1.

7 pressed tumor multiplicity in the absence of Cyp1b1.

8 reased the stability of enzymatically active CYP1B1.

9 actor(s) critical to the cAMP stimulation of CYP1B1.

10 to, respectively, the FUER and AP-1 sites of CYP1B1.

11 the lower efficiency of GSTP1 compared with CYP1B1.

12 bolism) of cytochrome P-450 (CYP) 1A1 and/or CYP1B1.

13 bited the basal level of CYP1A1 mRNA but not CYP1B1.

14 fier locus that is not linked genetically to CYP1B1.

15 tutively expressed low levels of bone marrow CYP1B1.

16 n is required for constitutive expression of CYP1B1.

17 ted in repression of its downstream effector CYP1B1.

18 ct sequencing of the entire coding region of CYP1B1.

19 resides between residues 37 and 41 of human CYP1B1.

20 uals carrying the CYP1B1*4 compared with the CYP1B1*1 haplo-type.

21 CYP1B1.4 was distinctly faster than that of CYP1B1.1.

22 1.4 was a mere 1.6 h compared with 4.8 h for CYP1B1.1.

23 DCT, and TYR genes and the CYP1A2-15q22-ter, CYP1B1-2p21, CYP2C8-10q23, CYP2C9-10q24, and MAOA-Xp11.4

24 dometrial cancer in individuals carrying the CYP1B1*4 compared with the CYP1B1*1 haplo-type.

25 me P450 reductase, the cellular level of the CYP1B1.4 allelic variant (containing a Ser at the amino

26 hase analysis revealed that the half-life of CYP1B1.4 was a mere 1.6 h compared with 4.8 h for CYP1B1

27 of immunodetectable and enzymatically active CYP1B1.4 was distinctly faster than that of CYP1B1.1.

28 ion, biochemistry and functional analysis of CYP1B1, a member of the cytochrome p450 family of mono-o

29 CYP1B1 activates polycyclic aromatic hydrocarbon carcino

30 are consistent with the idea that CYP1A1 and CYP1B1 activation leads to 5F-203 toxicity through DNA d

31 a is not a simple monogenic disease and that CYP1B1 activity levels could influence the phenotype.

32 genotypes, and therefore complete absence of CYP1B1 activity, frequently lead to severe phenotypes.

33 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2, whereas CYP1B1 additionally demethylated 4-MeOE2 to 4-OHE2.

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

35 ruited to the promoter regions of CYP1A1 and CYP1B1 along with ARNT and/or AhR following xenobiotic e

36 f the xenobiotic metabolism genes Cyp1a1 and Cyp1b1 and (ii) inhibition of adipogenesis in mouse embr

37 catalytic activity and coupling efficiency; CYP1B1 and 1D1 had coupling efficiencies under 4%.

38 The Cyp1b1 and Ahrr genes require AIP expression for normal

39 n of potential regulators of retinal growth, Cyp1b1 and Cx43, and the topographic guidance molecule e

40 e activation of estrogen-metabolizing enzyme CYP1B1 and formation of reactive estrogen metabolites an

41 Incubation of E(2) with CYP1B1 and GSTP1 resulted in the formation of 4-OHE(2),

42 is setting, we prepared recombinant purified CYP1B1 and GSTP1 to examine their individual and combine

43 When CYP1B1 and GSTP1 were added together, the rate of conjug

44 ferences in promoter sequence for two genes, CYP1B1 and GSTP1, were then explored across four human t

45 inherited cause of childhood glaucoma after CYP1B1 and juvenile open-angle glaucoma after MYOC.

46 d with the causal genes, viz., SCGB1D2, MET, CYP1B1 and MMP9 in terms of expression similarity and pa

47 bolism was similar to BaP-induced Cyp1A1 and Cyp1B1 and molecular clock gene expression in mouse mamm

48 y, therefore, depend on activation of PAH by Cyp1b1 and on offsetting suppression by Cyp1b1 of endoge

49 The severe dysgenesis in eyes lacking both CYP1B1 and TYR was alleviated by administration of the t

50 Male Apoe(-/-)/Cyp1b1(+/+) and Apoe(-/-)/Cyp1b1(-/-) mice were infused

51 antly different in fetuses from Cyp1a1(-/-), Cyp1b1(-/-), and Cyp1(+/+) wild-type mice.

52 1 (GLC3A), for which the responsible gene is CYP1B1, and 1p36 (GLC3B) and 14q24 (GLC3C), for which th

53 Three of the genes, QPCT, CYP1B1, and LXN, are densely methylated in >95% of uncul

54 tic-metabolizing AhR targets such as Cyp1a1, Cyp1b1, and Nqo1 were regulated by both ligand and suspe

55 n hydroxylase (Ah) receptor (Cyp1a1, Cyp1a2, Cyp1b1, and Nqo1).

56 l other genes implicated in glaucoma (PITX2, CYP1B1, and optineurin) were also represented.

57 ncreased in expression (>=5-FC) were CYP1A1, CYP1B1, and USP17L9P; most decreased (>=6-FC) were IL36A

58 results suggest that DMBA activates p53 in a CYP1B1- and mEH-dependent manner in vivo but is not AhR-

59 at DMBA-induced splenic immunosuppression is CYP1B1- and microsomal epoxide hydrolase (mEH)-dependent

60 In contrast, neither CYP1A1 nor CYP1B1 appears to play a role in dioxin-mediated teratog

61 aise the possibility that elevated CHIT1 and CYP1B1 are early indicators of COPD development in HIV-i

62 Allelic variations in CYP1B1 are reported to modulate the incidence of several

63 Both CYP1A genes and CYP1B1 are transcriptionally induced by the aryl hydroca

64 the TCDD-responsive enhancers for CYP1A1 and CYP1B1 are well characterized, a similar CYP1A2 enhancer

65 oma-related genes, such as PITX2, FOXC1, and CYP1B1, are enabling a better understanding of anterior

66 Hence, we propose Cyp1b1 as a target of beta-catenin indirectly influencin

67 TYR is not a modifier of the CYP1B1-associated PCG phenotype in the Saudi Arabian pop

68 e that these data provide strong support for CYP1B1 being one of the RALDH-independent components by

69 The recently identified cytochrome P4501B1 (CYP1B1) bioactivates PAHs but is also a physiological re

70 tochrome P450 family 1 subfamily B member 1 (CYP1B1), both previously associated with COPD, were amon

71 peptide, as well as expression of Cyp1a1 and Cyp1b1, both AhR target genes.

72 ating that beta-catenin is indispensable for Cyp1b1 but not for Cyp1a1 expression.

73 d the stability not only of immunodetectable CYP1B1, but also--unexpectedly given the size of the pro

74 eptor (AhR) mediates induction of CYP1A1 and CYP1B1 by 2,3,7,8-tetrachlorodibenzo-rho-dioxin (dioxin)

75 rans-retinol (t-ROH), but unlike the CYP26s, CYP1B1 cannot degrade t-RA.

76 Cytochrome P450 1A1 (CYP1A1) and 1B1 (CYP1B1) catalyze the oxidative metabolism of 17 beta-est

77 Cytochrome P450 1B1 (CYP1B1) catalyzes estrogen hydroxylation and activation

78 fected individuals from five families had no CYP1B1 coding mutations, and each family had a unique SN

79 ified with tagging SNPs in TMCO1, CAV1/CAV2, CYP1B1, COL1A2, COL5A1, CDKN2B/CDKN2BAS-1, SIX1/SIX6 or

80 at the observed cell-specific differences in CYP1B1 constitutive expression are not mediated by DNA p

81 CYP1B1 contributed to the development of Ang II-induced

82 Expression of CHIT1 and CYP1B1 correlated with the expression of genes involved

83 Cyp1b1 could also generate 20-hydroxyeicosatetraenoic ac

84 Functionally, Cyp1b1 could generate retinoic acid from retinol leading

85 ause of its microsomal location in the cell, CYP1B1 could not be measured directly by existing method

86 suggested that one residue, Val395 in human CYP1B1, could account for the differential hydroxylation

87 Other cytochromes P450, including CYP1A1, CYP1B1, CYP1A2, and CYP3A4, were also able to epoxidize

88 ffects of butyrate on enhancing induction of Cyp1b1/CYP1B1, AhR repressor (Ahrr/AhRR) and TCDD-induci

89 The major enzymes detected were CYP1B1, CYP2B6, CYP2D6, and CYP3A4 with mean values of 2

90 taxanes (ABCB1, ABCC1, ABCC2, ABCG2, CDKN1A, CYP1B1, CYP2C8, CYP3A4, CYP3A5, MAPT, and TP53) and plat

91 ated with glaucoma, optineurin, cochlin, and CYP1B1 (cytochrome P450, family 1, subfamily B, polypept

92 ogical regulator, as evidenced by linkage of CYP1B1 deficiency to congenital human glaucoma.

93 We show that CYP1B1-deficient (CYP1B1(-/-)) mice fail to elicit a neo

94 We generated Cyp1b1-deficient mice carrying the Min allele of the ade

95 These Cyp1b1-deficient Min mice developed twice as many tumors

96 Tumors from older (130 days) Cyp1b1-deficient Min mice selectively exhibited focal ar

97 Cyp1b1 deletion did not affect circulating DMBA and meta

98 Both CYP1A1 and CYP1B1 demethylated 2-MeOE2 and 2-OH-3-MeOE2 to 2-OHE2,

99 Importantly, CYP1B1 depletion decreased the invasive potential of the

100 CYP1B1 depletion in endometrial carcinoma cells leads to

101 A TSP2 knockdown in CYP1B1(-/-) ECs also restored capillary morphogenesis.

102 CYP1B1(-/-) ECs exhibited increased oxidative stress and

103 Reexpression of CYP1B1 in CYP1B1(-/-) ECs resulted in down-regulation of TSP2 expr

104 licate a putative causal missense variant in CYP1B1, encoding the homonymous xenobiotic- and hormone-

105 ding protein-associated factor (PCAF) to the CYP1B1 enhancer in HepG2 cells but failed to induce recr

106 As expected, the CYP1A1 and CYP1B1 enhancers bind AhR in TCDD-treated cells.

107 CYP1B1 enzymatic activity was evaluated using an ethoxyr

108 on of the human, monkey, dog, rat, and mouse CYP1B1 enzymes yields active proteins that differ in the

109 rities and differences with human CYP1A2 and CYP1B1 enzymes, but the structural basis for this has be

110 cytochrome P4501 family (CYP1A1, CYP1A2 and CYP1B1) enzymes are most active in hydroxylating a varie

111 ncing of the promoter (-1 to -867) and the 3 CYP1B1 exons.

112 ubjects, and CD163 inversely correlated with CYP1B1 expression in AMs.

113 Attenuation of CYP1B1 expression in endometrial carcinoma cells induces

114 In addition, TCDD-induced Cyp1B1 expression in Per1(ldc) and Per1(ldc)/Per2(ldc) m

115 ue demonstrated that TCDD-induced Cyp1A1 and Cyp1B1 expression in Per1(ldc) and Per1(ldc)/Per2(ldc) m

116 Thus, increased CYP1B1 expression is central to and seems to be responsi

117 and post-transcriptional mechanisms and that CYP1B1 expression is not susceptible to the same post-tr

118 Cyp1b1 expression was higher in the tumors compared with

119 and used to capture and specifically detect CYP1B1 from samples in solution.

120 onally regulating the cytochrome P450 enzyme Cyp1b1 Furthermore, expression of its close homolog Cyp1

121 veral unexpected genes such as Expi (Wdnm1), Cyp1b1, Gelsolin, Ramp2 and class I MHC genes.

122 We hypothesize that polymorphisms of CYP1B1 gene can predict higher incidence of endometrial

123 t stable recruitment of p300 and PCAF to the CYP1B1 gene does not require their tethering to the prom

124 structure-dependent induction of CYP1A1 and CYP1B1 gene expression in Ah-responsive MDA-MB-468 breas

125 Analysis of CYP1A1 and CYP1B1 gene expression showed the maximum enzyme-induced

126 DF 203, did not show drug-induced CYP1A1 and CYP1B1 gene expression.

127 ere observed in methylation patterns for the CYP1B1 gene from MCF-7 and HepG2 cells, treatment with t

128 rare polymorphisms at codons 119 and 432 of CYP1B1 gene have higher risk for endometrial cancer, and

129 , the genetic distributions of six different CYP1B1 gene polymorphisms were investigated, by sequence

130 stradiol repressed TCDD-activated Cyp1a1 and Cyp1b1 gene transcription in MCF-7 cells in the presence

131 moxifen, whereas promoter methylation of the CYP1B1 gene, encoding a tamoxifen- and estradiol-metabol

132 oxide on an oligonucleotide representing the CYP1B1 gene.

133 e P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene are a common cause of human primary congeni

134 Functionally, Cyp1b1 generated retinoic acid as well as 20-hydroxyeico

135 The mammalian CYP1A1, CYP1A2, and CYP1B1 genes (encoding cytochromes P450 1A1, 1A2, and 1B

136 The Cyp1a1, Cyp1a2, and Cyp1b1 genes are up-regulated by the aryl hydrocarbon re

137 ndicates that the plaice CYP1B and mammalian CYP1B1 genes share a common ancestry.

138 moking, family history of breast cancer, and CYP1B1 genotype were significant predictors of the level

139 study demonstrated that the distributions of CYP1B1 genotypes at codons 119 and 432 were significantl

140 ndrogen receptor genes are influenced by the CYP1B1 genotypes in endometrial cancer.

141 Our data show that null CYP1B1 genotypes, and therefore complete absence of CYP1

142 Our results support that CYP1B1 glaucoma is not a simple monogenic disease and th

143 nce for estradiol 2-hydroxylation, but human CYP1B1 greatly favors 4-hydroxylation.

144 involved in HCA metabolism (CYP1A1, CYP1A2, CYP1B1, GSTA1, GSTM1, GSTM3, GSTP1, NAT1, NAT2, SULT1A1,

145 R assays for seven target gene (AhR, CYP1A1, CYP1B1, GSTM1, GSTM3, GSTP1, and GSTT1) and three refere

146 e associated with the level of expression of CYP1B1, GSTP1, and other transcripts on a gene-specific

147 damage in the arrays was found in the order CYP1B1 > CYP1A2 > CYP1A1 > CYP2E1 > myoglobin, the same

148 Whereas extant human CYP1B1 has one molecule of alpha-naphthoflavone in a clo

149 The Phase I enzyme cytochrome p450 1B1 (CYP1B1) has been postulated to play a key role in estrog

150 and dioxin-mediated induction of CYP1A1 and CYP1B1 in cell lines derived from the human aerodigestiv

151 Reexpression of CYP1B1 in CYP1B1(-/-) ECs resulted in down-regulation of

152 Here we explored the role of CYP1B1 in endometrial carcinogenesis.

153 terfering RNA-mediated approach to knockdown CYP1B1 in endometrial carcinoma cell line followed by fu

154 nderstand the molecular basis of the role of CYP1B1 in endometrial carcinomas, we profiled the expres

155 The role of CYP1B1 in estradiol carcinogenicity thus depends on the

156 due to absent metabolic activation of BaP by CYP1B1 in immune cells.

157 use; we believe this reflects the absence of CYP1B1 in immune tissues.

158 These results confirm a role for CYP1B1 in inducing PAH-mediated mitochondrial dysfunctio

159 revealing differences from the extant human CYP1B1 in ligand binding, metabolism, and potential mole

160 n glioma endothelia, potentially implicating Cyp1b1 in other brain pathologies.

161 also reveal a direct role for mitochondrial CYP1B1 in PAH-mediated oxidative and chemical damage to

162 investigated the putative pathogenic role of CYP1B1 in PAH.

163 tream tobacco smoke resulted in induction of CYP1B1 in serially collected buccal samples from the one

164 arise from generation of DMBA metabolites by Cyp1b1 in the developing tumors.

165 BaP-metabolizing CYP1B1 in the PSI and CYP3A59 in the PGD are the most li

166 Finally, deletion of the Cyp1a1, Cyp1a2, and Cyp1b1 in triple knockout mice resulted in reduced bone

167 ein may explain the strong overexpression of CYP1B1 in tumors compared with nondiseased tissues.

168 utive and inducible expression of Cyp1a1 and Cyp1b1 in vascular smooth muscle cells (VSMCs) from Ahr(

169 pyrene (BP), which is similarly activated by Cyp1b1 in vitro, did not affect tumorigenesis in Min mic

170 Inhibition of Cyp1b1 in vivo increased BBB permeability being in line

171 n mice in vivo pharmacological inhibition of Cyp1b1 increased BBB permeability for small molecular tr

172 table to the presence of LC were revealed as CYP1B1 independent.

173 romoter, restored polII and TBP binding, and CYP1B1 inducibility.

174 Thus, the deficiency of CYP1B1 induction in HepG2 cells is ascribable to cytosin

175 We speculate that CYP1B1 inhibition in endometrial carcinomas could be a u

176 -/-)/Cyp1b1(+/+) mice was coadministered the CYP1B1 inhibitor 2,3',4,5'-tetramethoxystilbene (TMS) ev

177 tenuated in CYP1B1(-/-) mice, and the potent CYP1B1 inhibitor 2,3',4,5'-tetramethoxystilbene (TMS; 3

178 istry, data are presented demonstrating that CYP1B1 is capable of eliciting responses that are consis

179 at in murine VSMCs, expression of Cyp1al and Cyp1b1 is differentially influenced by Ahr phenotype and

180 and in situ analysis revealed that pulmonary CYP1B1 is increased in hypoxic PAH, hypoxic+SU5416 PAH,

181 CYP1B1 is overexpressed in a wide variety of human disea

182 ly charged domain at residues 41-48 of human CYP1B1 is part of the mitochondrial (mt) import signal.

183 LC expression of p450 enzyme CYP1B1 is required for maximal rapid induction of DNA-da

184 data presented herein also demonstrate that CYP1B1 is targeted for its polymorphism-dependent degrad

185 ycyclic aromatic hydrocarbon (PAH)-inducible CYP1B1 is targeted to mitochondria by sequence-specific

186 aining of endometrial carcinomas showed that CYP1B1 is up-regulated in endometrial cancers.

187 phase I enzyme known as cytochrome P450 1B1 (CYP1B1) is involved in the metabolism of many endogenous

188 gen-metabolizing enzyme cytochrome P450 1B1 (CYP1B1) is reported in idiopathic PAH and murine models

189 s, we compared Cyp1a1(-/-), Cyp1a2(-/-), and Cyp1b1(-/-) knock-out mice with Cyp1(+/+) wild-type mice

190 Significantly, CYP1B1 knockdown leads to down-regulated expression of c

191 This study analyzed CYP1B1, LTBP2, and MYOC mutations in a cohort of primary

192 Mutations in three genes (CYP1B1, LTBP2, TEK) have been reported in PCG patients.

193 A 27-fold cAMP stimulation of the CYP1B1-luciferase reporter in Y-1 adrenal cells depends

194 Thus, CYP1B1 may serve as a target for therapeutic agents for

195 Increased CYP1B1-mediated estrogen metabolism promotes the develop

196 These PAH suppressions depend on Cyp1b1-mediated metabolism.

197 active quinones were produced as part of the CYP1B1-mediated oxidation reaction, the adduct formation

198 ens exert feedback inhibition on CYP1A1- and CYP1B1-mediated oxidative estrogen metabolism, thereby r

199 The results present direct proof of CYP1B1-mediated, E2-induced adduct formation and provide

200 Cyp1b1 metabolism of DMBA and endogenous oxygenation pro

201 Cytochrome P450 1B1 (Cyp1b1) metabolism contributes to physiologic functions

202 Finally, administration of the CYP1B1 metabolite 16alpha-hydroxyestrone (1.5 mg . kg(-1

203 Thus, CYP1B1 metabolizes cell products that modulate intracell

204 These effects were minimized in Apoe(-/-)/Cyp1b1(+/+) mice treated with TMS and in Apoe(-/-)/Cyp1b

205 icle for 4 weeks; another group of Apoe(-/-)/Cyp1b1(+/+) mice was coadministered the CYP1B1 inhibitor

206 Ang II produced AAAs in Apoe(-/-)/Cyp1b1(+/+) mice; mice treated with TMS or Apoe(-/-)/Cyp

207 (+/+) mice treated with TMS and in Apoe(-/-)/Cyp1b1(-/-) mice and by concurrent treatment with the su

208 and TSP2 were both observed in retinas from CYP1B1(-/-) mice and were reversed by administration of

209 etinal endothelial cells (ECs) prepared from CYP1B1(-/-) mice are less adherent, less migratory, and

210 /+) mice; mice treated with TMS or Apoe(-/-)/Cyp1b1(-/-) mice had reduced AAAs.

211 Male Apoe(-/-)/Cyp1b1(+/+) and Apoe(-/-)/Cyp1b1(-/-) mice were infused with Ang II or its vehicle

212 Hypoxic PAH was attenuated in CYP1B1(-/-) mice, and the potent CYP1B1 inhibitor 2,3',4

213 ed in mice treated with TMS and in Apoe(-/-)/Cyp1b1(-/-) mice.

214 We show that CYP1B1-deficient (CYP1B1(-/-)) mice fail to elicit a neovascular response

215 Here we show that Cyp1b1-/- mice have ocular drainage structure abnormalit

216 age structure/ocular dysgenesis phenotype of Cyp1b1-/- mice, suggesting that Tyr is a modifier of the

217 Using Cyp1b1-/- mice, we identified the tyrosinase gene (Tyr)

218 In contrast, Cyp1b1 mRNA and protein were expressed under constitutiv

219 lls B[a]P induced CYP1A1 mRNA by 23-fold and CYP1B1 mRNA by 3.9-fold.

220 dine (10 microM for 6 days) did not activate CYP1B1 mRNA expression in HepG2 cells.

221 ealed an increased expression of p450 family CYP1B1 mRNA in Ikkbeta(-/-) cells compared with wild-typ

222 BaP-induced Cyp1a1 and Cyp1b1 mRNA levels were higher 4 hours after dosing at n

223 he degradation of CYP1A1 mRNA, while leaving CYP1B1 mRNA unaffected.

224 and 0.0032, based on induction of CYP1A1 and CYP1B1 mRNA, respectively.

225 ramatic increase in the amount of CYP1A1 and CYP1B1 mRNA, the two major isoforms involved in carcinog

226 was a dose-dependent decrease in CYP1A1 and CYP1B1 mRNA.

227 cted child or more than 1 subject carrying 2 CYP1B1 mutant alleles.

228 CYP1B1 mutation screening of 52 patients with PCG was pe

229 Our results indicate that CYP1B1 mutations may be responsible for half of cases of

230 This is the largest analysis of CYP1B1 mutations performed in European patients with PCG

231 CYP1B1 mutations were twice as frequent in affected indi

232 G-T-A-3' was associated with the majority of CYP1B1 mutations.

233 anifested disease phenotypes attributable to CYP1B1 mutations.

234 This investigation demonstrates that CYP1B1 null mice are almost completely protected from th

235 ce, but the effects were markedly blunted in Cyp1b1-null mice.

236 n WT, p53-null, and AhR-null mice but not in CYP1B1-null or mEH-null mice.

237 R-null mice after DMBA treatment, but not in CYP1B1-null or mEH-null mice.

238 ant enzymes, we demonstrated that CYP1A1 and CYP1B1 O-demethylated the methoxyestrogens to catechol e

239 H by Cyp1b1 and on offsetting suppression by Cyp1b1 of endogenous tumor-enhancing substrates.

240 Cytochrome P450 1 wild-type, Cyp1a2(-/-), Cyp1b1(-/-), or Cyp1a2/1b1(-/-) knockouts, and mice with

241 tration was elevated in PAH, consistent with CYP1B1 overexpression and activity.

242 nsistent with this hypothesis, we found that CYP1B1 overexpression potentiates RGC survival.

243 CYP1B1 oxidized E2 to the catechol 4-OHE2 and the labile

244 se-related genes AHRR (P = 1.13 x 10-62) and CYP1B1 (P < 2.49 x 10-61).

245 ; P = 2.9 x 10(-6) ) and 2p22 (rs232542 near CYP1B1; P = 4.1 x 10(-6) ).

246 based on visual field loss had enrichment of CYP1B1 pathogenic variants and a more severe phenotype c

247 Individuals with CYP1B1 pathogenic variants, whether heterozygous or homo

248 were homozygous or compound heterozygous for CYP1B1 pathogenic variants, which provided a likely basi

249 = .008; etap2 = 0.06) than patients without CYP1B1 pathogenic variants.

250 aforementioned histone modifications at the CYP1B1 promoter and for induction of CYP1B1 transcriptio

251 ced recruitment of the AhR to the CYP1A1 and CYP1B1 promoters was inhibited when HDAC6 was inactivate

252 e P450 1A1 (CYP1A1) and cytochrome P450 1B1 (CYP1B1) promoters of bladder cancer tissues by bisulfite

253 levels and post-translational regulation of CYP1B1 protein.

254 d lower compared with the other four allelic CYP1B1 proteins (containing Asn453), as analyzed by both

255 The estradiol metabolites by CYP1B1 received particular attention because of their ca

256 In this study, we showed that CYP1A1 and CYP1B1 recognized as substrates both the parent hormone

257 Inhibition of CYP1B1 reduced both oxidative stress and arsenic-stimula

258 of the -2296 to +25 region examined with the CYP1B1 reporter constructs.

259 Results demonstrate that an anti-CYP1B1 scFv-QCM immunosensor could be used to detect P45

260 Three anti-CYP1B1 scFvs (designated B-66, D-23, and L-21) were biot

261 Identification and characterization of CYP1B1 sequence variants.

262 Analysis of the CYP1B1 sequences in light of these findings suggested th

263 erved in response to BP exposure (CYP1A1 and CYP1B1; signal log ratio of 4.7 and 2.5, respectively).

264 p1a1/1a2(-/-) double-knockout mouse with the Cyp1b1(-/-) single-knockout mouse, we generated the Cyp1

265 s, and mtDNA damage that was attenuated by a CYP1B1-specific inhibitor, 2,3,4,5-tetramethoxystilbene.

266 In support, the mitochondrial CYP1B1 supported by mitochondrial ferredoxin (adrenodoxi

267 cyclin E-binding protein (CEBP1) as a novel CYP1B1 target.

268 The metabolism of endogenous substrates by Cyp1b1, therefore, suppresses tumor initiation but also

269 We assessed the contribution of CYP1B1 to angiotensin (Ang) II-induced abdominal aortic

270 n particular, we focussed on the capacity of CYP1B1 to regulate the molecular mechanisms associated w

271 In fact, mutation of this valine in human CYP1B1 to the leucine present in the rat enzyme produces

272 ripheral blood three-gene assay (KLF6, BNC2, CYP1B1) to detect the state of operational tolerance by

273 at the CYP1B1 promoter and for induction of CYP1B1 transcription (in MCF-7 cells), the recruitments

274 -28-oyl]imidazole}, induced Ahr, Cyp1a1, and Cyp1b1 transcription in Nrf2+/+ MEFs but not in Nrf2-/-

275 strate here that DF 203 increases CYP1A1 and CYP1B1 transcription in sensitive MCF-7 cells, accompani

276 dothelial metabolic barrier function through Cyp1b1 transcription.

277 so found that the inducibility of CYP1A1 and CYP1B1 transcripts following xenobiotic stress was signi

278 howed overexpression of CYP1A1 mRNA, but not CYP1B1 transcripts, in ovarian cancer cell lines when co

279 of multiple genes, including CYP1A1, CYP1A2, CYP1B1, UGT1A1, UGT1A6, IL6, and SAA1.

280 To understand the functional significance of CYP1B1 up-regulation in endometrial cancers with regard

281 In conclusion, our data suggest that CYP1B1 up-regulation plays a crucial role in endometrial

282 sensitive piezoimmunosensor for detection of CYP1B1 using single-chain fragment variable antibodies (

283 We genotyped three SNPs in CYP19A1 and CYP1B1 using TaqMan and imputed SNPs in estrogen recepto

284 DD on mammary gland expression of Cyp1A1 and Cyp1B1 vary over time and are significantly greater duri

285 CYP1B1 was also associated with these mutations categori

286 The role of mitochondrial CYP1B1 was assessed using A549 lung epithelial cells sta

287 ermeability for small molecular tracers, and Cyp1b1 was downregulated in glioma vessels in which BBB

288 , no change in gene expression of CYP1A1 and CYP1B1 was observed when the cells were exposed to DBP.

289 An additive induction of CYP1A1 and CYP1B1 was observed with cotreatment of SRM 1649a and BP

290 ore, we showed that expression of CYP1A1 and CYP1B1 was reduced significantly in an independent cohor

291 unorubicin sensitivity and the expression of CYP1B1 was significantly correlated with sensitivity to

292 sis, we show that the cytochrome P450 enzyme Cyp1b1 was significantly decreased in beta-catenin-defic

293 ing of the primary congenital glaucoma gene, CYP1B1, was performed on 47 proband deoxyribonucleic aci

294 The mRNA expression of CYP1A1 and CYP1B1 were both increased approximately 20-fold after 2

295 zed AhR-regulated genes including Cyp1a1 and Cyp1b1 were corroborated.

296 he tamoxifen-metabolizing enzymes CYP1A1 and CYP1B1 were detected by immunohistochemistry in and arou

297 CYP1B1 were quantitatively detected in normal and malign

298 adjustment for multiple comparisons, SNPs in CYP1B1 were strongly associated with KIT exon 11 codon 5

299 urified phase I enzyme, cytochrome P450 1B1 (CYP1B1), which is expressed in breast tissue, to oxidize

300 However, incubation of GSH and CYP1B1 with 2-OHE(2) resulted in nearly linear conjugati