ライフサイエンスコーパス: CYP2E1

1 CYP2E1 activity and protein levels were higher in the Py

2 CYP2E1 but also CYP2A5 were increased by the pyrazole/LP

3 CYP2E1 is degraded by the ubiquitin-proteasome pathway,

4 CYP2E1 is recognized as the most important enzyme for in

5 CYP2E1 is the first P450 shown to be an hsp90 "client" p

6 CYP2E1 overexpression in a hepatocyte cell line decrease

7 CYP2E1 overexpression was also associated with increased

8 CYP2E1 protein and activity were elevated in acetone- or

9 CYP2E1 substrate complexation converts it into a stable

10 CYP2E1 thus exhibits biphasic turnover in the mammalian

11 CYP2E1 was induced by ethanol in wild-type mice, and oxi

12 CYP2E1-dependent RIP3 expression induces hepatocyte necr

13 CYP2E1-knockout mice exhibited only minor liver injury a

14 ining (35 +/- 18% vs. 23 +/- 14%; P = 0.02), CYP2E1 protein content (68 +/- 9% vs. 56 +/- 11%; P < 0.

15 tochrome P450 family 2 subfamily E member 1 (CYP2E1) and cytochrome P450 family 1 subfamily A member

16 .9, 95% confidence interval (CI): 1.4, 6.1), CYP2E1 -332T>A AT/AA genotypes (OR = 2.0, 95% CI: 1.2, 3

17 Human microsomal cytochrome P-450 2E1 (CYP2E1) monooxygenates > 70 low molecular weight xenobio

18 Cytochrome P450 2E1 (CYP2E1) activates several hepatotoxins and contributes t

19 ein and/or constitutive cytochrome P450 2E1 (CYP2E1) and as purified components in a cell-free system

20 otein coding regions of cytochrome P450 2E1 (CYP2E1) are known to be associated with several diseases

21 ing globulin (TBG), and cytochrome P450 2E1 (CYP2E1) by measuring the expression of alpha1-antitrypsi

22 esistance and increased cytochrome P450 2E1 (CYP2E1) expression are both associated with and mechanis

23 Alcohol-inducible cytochrome P450 2E1 (CYP2E1) has the most rapid turnover of any member of thi

24 Cytochrome P450 2E1 (CYP2E1) induction and tumor necrosis factor alpha (TNF-a

25 The ethanol-inducible cytochrome P450 2E1 (CYP2E1) is also induced under different pathological and

26 Cytochrome P450 2E1 (CYP2E1) is suggested to play a role in alcoholic liver d

27 Cytochrome P450 2E1 (CYP2E1) may be a central pathway in generating oxidative

28 Increased levels of cytochrome P450 2E1 (CYP2E1) protein expression and activities, which resulte

29 used to covalently link cytochrome P450 2E1 (CYP2E1) with cytochrome b(5) (b(5)) through the formatio

30 ave increased levels of cytochrome P450 2E1 (CYP2E1), but the underlying mechanisms are unknown.

31 e RIP3 in the livers of cytochrome P450 2E1 (CYP2E1)-deficient mice, indicating CYP2E1-mediated ethan

32 tosis, and induction of cytochrome P450 2E1 (CYP2E1).

33 Cytochrome P450-2E1 (CYP2E1) increases oxidative stress.

34 of two intermolecular cross-links, Lys(428)(CYP2E1)-Asp(53)(b(5)) and Lys(434)(CYP2E1)-Glu(56)(b(5))

35 Lys(428)(CYP2E1)-Asp(53)(b(5)) and Lys(434)(CYP2E1)-Glu(56)(b(5)), which provides the first direct e

36 in on CYP1A2, CYP2B1/6, CYP2C9/11, CYP2D1/6, CYP2E1 and CYP3A2/4 activities in human and rat liver an

37 Here we have identified a CYP2E1/Bid/C1q-dependent pathway that is activated in re

38 Based on the characterized cross-links, a CYP2E1-b(5) complex model was constructed, leading to im

39 In addition CYP2E1 oxidizes much larger C9-C20 fatty acids that can

40 Neither SP600125 nor SB203580 affected CYP2E1 activity or protein levels.

41 chrome P450 (CYP)2E1 Abs, 14 had Abs against CYP2E1 modified by INH, 14 had anti-CYP3A4 antibodies, a

42 The protective effects of Nrf2 against CYP2E1-dependent toxicity can be blocked by l-buthionine

43 The ability of Nrf2 to protect against CYP2E1-dependent AA toxicity and its possible mechanism

44 and increase of GSH levels, protects against CYP2E1-dependent AA toxicity.

45 Although CYP2E1 is predominantly found in the endoplasmic reticul

46 In contrast, CYP+5/1A1 and CYP2E1 were able to bypass TOM20 and TOM22 but required

47 termediates by cytochrome p450 (CYP) 2D6 and CYP2E1 enzymes.

48 0 (CYP) protein expression and activity, and CYP2E1 may play a role in the pathogenesis of NAFLD and

49 hich express alcohol dehydrogenase (ADH) and CYP2E1.

50 ells) were exposed to ethanol, both ADH- and CYP2E1-generated products reduced STAT1 phosphorylation.

51 tes to be much higher than by PGK, apoE, and CYP2E1 promoters, and the fragment of -435bp to -26bp fr

52 served at 37 degrees C and 30 degrees C, and CYP2E1 enzyme capacity (maximum velocity) was not altere

53 n of two cytochrome P450 enzymes, CYP1A2 and CYP2E1, was almost completely abolished in livers from h

54 vious study, we hypothesized that CYP2A6 and CYP2E1 accommodate multiple xylene ligands.

55 ymes bound to either b5 alpha4-5 (CYP2A6 and CYP2E1) or this region and alpha2-3 (CYP2D6 and CYP3A4)

56 mpetitive inhibition for CYP2B1, CYP2C11 and CYP2E1 with Ki values less than 9.93 muM were observed.

57 n stimulated these activities of CYP2C19 and CYP2E1 equivalent to wild-type b(5).

58 THMs, including factors affecting CYP2D6 and CYP2E1 activity.

59 ethiazole (CMZ), an inhibitor of CYP2E1, and CYP2E1-knockout mice.

60 At 24 hrs after CA a decrease in CYP3A2 and CYP2E1 activity was observed, 55.7% +/- 12.8% and 46.8%

61 CA-mediated inhibition of CYP3A2 and CYP2E1 was attenuated by hypothermia, as was the increas

62 c activity and mRNA expression of CYP3A2 and CYP2E1.

63 or) as a relevant E3 in CYP3A4, CYP3A23, and CYP2E1 UPD.

64 CYP1A2, CYP3A4 and CYP2E1 mRNA levels were decreased, while miRNAs were inc

65 CYP3A4 and CYP2E1 mRNA levels were not significantly different betw

66 latory response to modify CYP1A2, CYP3A4 and CYP2E1 translation due to cellular stress and injury.

67 sed protein expression of CYP1A2, CYP3A4 and CYP2E1.

68 oligomerization of human CYP3A4, CYP3A5, and CYP2E1 in microsomal membranes.

69 esults in CYP2E1(Delta3-29) degradation, and CYP2E1(Delta3-29) co-immunoadsorbs with myc-CHIP from cy

70 affect highly studied genes such as GBA and CYP2E1.

71 abolic zonation was lost, as shown by GS and CYP2E1, in 71% and 88%, respectively, with normalization

72 Elevations in hepatic lipid peroxidation and CYP2E1 expression that are seen in NAFLD improve signifi

73 as distinct factors, insulin resistance and CYP2E1 expression may be interrelated through the abilit

74 n of CYP1A1 and CYP1A2 are cell specific and CYP2E1 and GSTM1 may not play a significant role in lung

75 alidation pertaining to other genes, such as CYP2E1 or DRD2, is necessary.

76 activation of other P450 reactions, such as CYP2E1-catalyzed oxygenations, which are insensitive to

77 ASD DMRs at CYP2E1 and IRS2 reached genome-wide significance, replic

78 Methylation at CYP2E1 associated with both ASD diagnosis and genotype w

79 t via C1q provided the critical link between CYP2E1/Bid-dependent apoptosis and onset of adipose tiss

80 me-induced toxicity was reduced/abolished by CYP2E1 siRNA.

81 against increased oxidative stress caused by CYP2E1.

82 Overall, the oxidative stress elicited by CYP2E1-mediated APAP metabolism might significantly cont

83 atotoxicity of drugs that are metabolized by CYP2E1.

84 exosomes are mediated, at least in part, by CYP2E1 enzyme.

85 This inhibition of insulin signaling by CYP2E1 overexpression was partially c-Jun N-terminal kin

86 Arachidonic acid (AA) causes CYP2E1-dependent toxicity in HepG2 cells.

87 Cellular CYP2E1 is well-known to mediate alcohol- (ALC) and aceta

88 ies of fatty acid analogs by cocrystallizing CYP2E1 with omega-imidazolyl-octanoic fatty acid, omega-

89 th small molecules revealed a small, compact CYP2E1 active site, which would be insufficient to accom

90 Consequent CYP2E1 gain of function accelerates reactive O2 species

91 observed that the plasma exosomes containing CYP2E1 cargo further exacerbate ALC- and APAP-induced to

92 e used to make adenovirus vectors containing CYP2E1 promoter-driven luciferase reporters for analyses

93 a gene-signature (CAV1, CD36, MLXIPL, CPT1C, CYP2E1) that strongly associated with epithelial-mesench

94 These mice exhibited increased CYP1A1, CYP2E1, and CYP2U1 expression and abundant levels of the

95 nes (such as CYP3A4, CYP2D6, CYP2C9, CYP1A2, CYP2E1 and UGT1A4) in THLE-2 cell microarrays.

96 d States and is primarily caused by CYP1A2-, CYP2E1-, and CYP3A4-driven conversion of APAP into hepat

97 suggested a role of CYP1A2, CYP2A6, CYP2B6, CYP2E1, and CYP3A4 in the metabolism of chiral PCBs.

98 ho were homozygous wild-type for the CYP2C9, CYP2E1, or GSTM3 polymorphisms, women carrying 1 or 2 co

99 ne by human CYP1A2, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4 occurs with up to 80% C-4 methyl inve

100 es (CYP1A2, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A5).

101 a mixed inhibitor of CYP2B6, CYP2C9, CYP2D6, CYP2E1 and CYP3A4, but also a non-competitive inhibitor

102 of mixed oligomers in CYP3A4/CYP3A5, CYP3A4/CYP2E1, and CYP3A5/CYP2E1 pairs and demonstrated that th

103 in CYP3A4/CYP3A5, CYP3A4/CYP2E1, and CYP3A5/CYP2E1 pairs and demonstrated that the association of ei

104 ed rats or mice, conditions known to elevate CYP2E1.

105 CMZ decreased the elevated CYP2E1 activity by 90%, but CYP2A5 activity was also low

106 The cytochrome P450 enzyme CYP2E1 defluorinates many drugs.

107 Every P450 tested except CYP2E1 was capable of raloxifene bioactivation, based on

108 terms of understanding the role of exosomal CYP2E1 in cell-cell interactions, and their effects on d

109 results showed an important role of exosomal CYP2E1 in exacerbating ALC- and APAP-induced toxicity.

110 igated the potential role of plasma exosomal CYP2E1 in mediating ALC- and APAP-induced toxicity.

111 significant induction of the plasma exosomal CYP2E1 level in a binge drinking murine model.

112 Purified, bacterially expressed CYP2E1(Delta3-29) is ubiquitylated in a CHIP-dependent m

113 HepG2 cells expressing CYP2E1 (E47 cells) showed increased Nrf2 mRNA and protei

114 med human skin fibroblasts stably expressing CYP2E1 with the hsp90 inhibitor radicicol results in CYP

115 with CYP2E1 was direct, and this facilitated CYP2E1 methylation at R379, leading to its degradation t

116 al docking studies with a homology model for CYP2E1, the two sites for monocyclic molecules, pNP and

117 nexplained substrate inhibition observed for CYP2E1.

118 patic retinoid uptake, as well as a role for CYP2E1 in the catabolism of hepatic retinoid.

119 oduct ratios, and ( k H/ k D) obs values for CYP2E1 and CYP2A6 oxidation of m-xylene-alpha- (2)H 3 an

120 Increased oxidative stress from CYP2E1 induction by pyrazole in vivo sensitizes the live

121 omes contain substantial level of functional CYP2E1.

122 or rs2070673 in the cytochrome P4502E1 gene, CYP2E1 (dichloromethane: OR = 4.42, 95% CI: 2.03, 9.62;

123 ound in the order CYP1B1 > CYP1A2 > CYP1A1 > CYP2E1 > myoglobin, the same as the order of their metab

124 or CA supplementation did not affect hepatic CYP2E1 levels or glutathione depletion after APAP treatm

125 we assessed the relationship between hepatic CYP2E1 and CYP3A activities and their messenger RNA (mRN

126 pid peroxidation levels and elevated hepatic CYP2E1 activity, but hepatic CYP3A4/5 activity is decrea

127 cohol consumption is known to induce hepatic CYP2E1 activity, but its effect on hepatic and intestina

128 findings indicate that increased hepatocyte CYP2E1 expression and the presence of steatohepatitis re

129 Indeed, in cultured human hepatocytes, CYP2E1 is detectably ubiquitinated, and this is enhanced

130 In the current work we have determined how CYP2E1 can accommodate a series of fatty acid analogs by

131 d by transfecting a plasmid containing human CYP2E1 cDNA lacking the hydrophobic endoplasmic reticulu

132 Structures of human CYP2E1 have been solved to 2.2 angstroms for an indazole

133 w show upon heterologous expression of human CYP2E1 in Saccharomyces cerevisiae that its autophagic l

134 mechanism adds to the complexities of human CYP2E1 regulation.

135 molecular weight substrates, the hydrophobic CYP2E1 active site is the smallest yet observed for a hu

136 was independently associated with changes in CYP2E1 protein expression after bariatric surgery (r = 0

137 al changes in association with a decrease in CYP2E1 protein and activity.

138 ecretion were all significantly decreased in CYP2E1 overexpressing cells.

139 re-negative cells and was enhanced 3-fold in CYP2E1-expressing L14 cells.

140 t, free fatty acids (FFAs) were increased in CYP2E1-knockout mice but not in wild-type mice.

141 decreased by ethanol in wild-type but not in CYP2E1-knockout mice.

142 r were observed in wild-type mice but not in CYP2E1-knockout mice.

143 AA activates Nrf2 in CYP2E1-expressing HepG2 cells (E47 cells), increasing Nr

144 of fatty acid oxidation, was up-regulated in CYP2E1-knockout mice fed ethanol but not in wild-type mi

145 ith the hsp90 inhibitor radicicol results in CYP2E1 degradation that is inhibited by the proteasome i

146 ependent E3 ubiquitin ligase CHIP results in CYP2E1(Delta3-29) degradation, and CYP2E1(Delta3-29) co-

147 ethanol was higher in wild-type mice than in CYP2E1-knockout mice.

148 ssive smoke exposure and genetic variants in CYP2E1, NAT2, and UGT1A7.

149 resulting in 20-fold or greater variation in CYP2E1 expression.

150 ominance of mitochondrial proteins including CYP2E1.

151 Ethanol exposure to VL-17A cells increased CYP2E1 and decreased proteasome peptidase activities.

152 KT cell-deficient mice resulted in increased CYP2E1-mediated APAP biotransformation and susceptibilit

153 In summary, chronic ethanol increases CYP2E1 activity in adipose, leading to Bid-mediated apop

154 P450 2E1 (CYP2E1)-deficient mice, indicating CYP2E1-mediated ethanol metabolism is critical for RIP3

155 raperitoneally with pyrazole (Pyr) to induce CYP2E1.

156 nitric oxide synthase, and ethanol-inducible CYP2E1.

157 ation by ethanol is suppressed by inhibiting CYP2E1 or aldehyde dehydrogenase and requires an elevate

158 development of ethanol-induced liver injury, CYP2E1 is required for the induction of oxidative stress

159 hibition of PKA or PKC blocked intracellular CYP2E1 ubiquitination and turnover.

160 this we used the mouse hepatocyte cell line (CYP2E1/ADH-transfected HepB5 cells) or primary mouse hep

161 interactions in the chemically cross-linked CYP2E1-b5 complex.

162 Human liver CYP2E1 is a monotopic, endoplasmic reticulum-anchored cy

163 Lymphocyte CYP2E1 and CYP3A4 mRNA levels did not correlate with CYP

164 h the endoplasmic reticulum (microsomes) (mc CYP2E1) and mitochondria (mt CYP2E1).

165 nes expressing predominantly mt CYP2E1 or mc CYP2E1.

166 onsumption induced rat hepatic mitochondrial CYP2E1.

167 Moreover, CYP2E1 induction was accompanied by an increase in its m

168 ria from ethanol-fed rats containing high mt CYP2E1 showed higher levels of F(2)-isoprostane producti

169 microsomes) (mc CYP2E1) and mitochondria (mt CYP2E1).

170 table cell lines expressing predominantly mt CYP2E1 or mc CYP2E1.

171 These results strongly suggest that mt CYP2E1 induces oxidative stress and augments alcohol-med

172 redominantly mitochondrion-targeted (Mt(++)) CYP2E1 and livers from alcohol-treated rats showed loss

173 Notably, expression of Mt++ CYP2E1 protein in yeast cells caused more severe mitocho

174 Neither CYP2E1 levels nor covalent binding of [14C] CCl4-derived

175 While no CYP2E1 was present in the CYP2E1 knockout mice, CYP2A5 a

176 CA decreased CYP3A2 mRNA (p < 0.05), but not CYP2E1 mRNA.

177 he nitroxidative stress marker iNOS, but not CYP2E1, was significantly elevated only in FF-fed WT.

178 uctures provide insights into the ability of CYP2E1 to effectively bind and metabolize both small mol

179 This study evaluated the ability of CYP2E1 to potentiate or synergize the hepatotoxicity of

180 n may be interrelated through the ability of CYP2E1-induced oxidant stress to impair hepatic insulin

181 The accumulation of CYP2E1 in hepatic mitochondria induced by ethanol consum

182 nt study, the possible synergistic action of CYP2E1 and LPS in liver injury was investigated by evalu

183 Neither the expression or activity of CYP2E1, required for bio-activation of CCl4, nor AST and

184 ted CYP2E1(Delta3-29) yields coadsorption of CYP2E1(Delta3-29).

185 and serum revealed that the contribution of CYP2E1 to APAP metabolism decreased with increasing APAP

186 ations affecting subcellular distribution of CYP2E1 with alcohol-induced toxicity.

187 Ethanol feeding increased the expression of CYP2E1 in adipocytes, but not stromal vascular cells, in

188 pathway activation induces the expression of CYP2E1, CYP1A2, and aryl hydrocarbon receptor, but not o

189 tion of VPA and APAP increased expression of CYP2E1, formation of NAPQI-protein adducts, and depletio

190 aluating the effects of pyrazole (inducer of CYP2E1), Chlormethiazole (CMZ), an inhibitor of CYP2E1,

191 Induction of CYP2E1 by ethanol is one mechanism by which ethanol caus

192 Induction of CYP2E1 by ethanol is one pathway through which ethanol g

193 r acetone- or pyrazole-mediated induction of CYP2E1 can potentiate liver injury in obesity.

194 tress and liver injury and that induction of CYP2E1 enhances these effects.

195 In conclusion, induction of CYP2E1 plays an important role in the enhancement of LPS

196 rosative stress elicited by the induction of CYP2E1.

197 mans were mediated entirely by inhibition of CYP2E1.

198 educed/abolished by a selective inhibitor of CYP2E1 enzyme activity (diallyl ether).

199 2E1), Chlormethiazole (CMZ), an inhibitor of CYP2E1, and CYP2E1-knockout mice.

200 usly showed that miconazole, an inhibitor of CYP2E1, blocks defluorination of FCWAY in rats.

201 Chlormethiazole, an inhibitor of CYP2E1, lowered macrovesicular fat accumulation, inhibit

202 stration of chlormethiazole, an inhibitor of CYP2E1, to the Pyr/Jo2-treated mice caused a significant

203 rotein and mRNA are blocked by inhibitors of CYP2E1 activity and a reactive oxygen species (ROS) scav

204 as ethanol, can regulate the interaction of CYP2E1 with the chaperones hsp90 and hsp70 to profoundly

205 The introduction of CYP2E1 to CYP2E1-knockout mice via an adenovirus restore

206 e elevated the activity and protein level of CYP2E1 in all mice.

207 e stress (as reflected in elevated levels of CYP2E1 and protein carbonyls).

208 that naturally express comparable levels of CYP2E1 as human liver to demonstrate that ethanol, at su

209 hese exosomes containing increased levels of CYP2E1 caused significant toxicity in monocytic cells co

210 We speculate that overexpression of CYP2E1 might synergize and increase the susceptibility t

211 osure and is correlated with the presence of CYP2E1.

212 ent, involving a shift in regionalisation of CYP2E1, which may prevent toxicity thresholds being reac

213 the N-terminal protein targeting regions of CYP2E1 that markedly affect subcellular localization of

214 he small molecule metabolome and the role of CYP2E1 in ethanol-induced hepatotoxicity were investigat

215 Thus, we aimed to study the role of CYP2E1 in promoting liver fibrosis by high cholesterol-c

216 and D65 are essential for the stimulation of CYP2E1 and CYP2C19 activities and that the phospholipid

217 Previously structures of CYP2E1 with small molecules revealed a small, compact CY

218 l respiratory chain, is a critical target of CYP2E1-mediated alcohol toxicity.

219 CYP2A6, CYP2C19, and CYP17A1 but not that of CYP2E1 or CYP2D6, suggesting that the b(5) interaction v

220 unction is largely mediated by its effect on CYP2E1 expression.

221 nvestigation of the effect of hypothermia on CYP2E1-mediated metabolism.

222 cells expressing either ADH (VA-13 cells) or CYP2E1 (E-47 cells) were exposed to ethanol, both ADH- a

223 Either LPS or CYP2E1 are considered independent risk factors involved

224 to mitochondria, HepG2 lines overexpressing CYP2E1 in mitochondria (mE10 and mE27 cells) were establ

225 uitin-ligase impairs hepatic cytochrome P450 CYP2E1 degradation.

226 ucleotide phosphate oxidase, cytochrome P450 CYP2E1, or both are responsible for the production of DN

227 n the in vivo kinetics of a cytochrome P450 (CYP2E1) probe drug, chlorzoxazone, and to investigate th

228 protein kinase (MAPK) in cytochrome P4502E1 (CYP2E1) potentiation of lipopolysaccharide or tumor necr

229 ne synthetase (GS), anti-cytochrome P4502E1 (CYP2E1), anti-CD34, and anti alpha-smooth muscle actin (

230 DA) levels (a marker of lipid peroxidation), CYP2E1 and CYP3A4/5 protein expression, and steatosis, a

231 In the process, CYP2E1 can generate toxic or carcinogenic compounds, as

232 y observed catalytic activity of recombinant CYP2E1 in dependence on the total concentration of the a

233 increase of ketone bodies, which up-regulate CYP2E1 through protein stabilization.

234 alpha1 and elucidate how MATalpha1 regulates CYP2E1 expression.

235 We found that MATalpha1 negatively regulates CYP2E1 at mRNA and protein levels, with the latter being

236 rs402710, CXCR2 rs1126579, CYP1A1 rs4646903, CYP2E1 rs6413432, ERCC1 rs11615, ERCC2 rs13181, FGFR4 rs

237 e (IND) inhibited catalysis through a single CYP2E1 site (K(i) = 0.12 microM).

238 ass spectrometric analyses, we identify some CYP2E1 phosphorylation/ubiquitination sites in spatially

239 , totally abolished the ability to stimulate CYP2E1-catalyzed chlorzoxazone 6-hydroxylation.

240 leakage than the wild-type mice, suggesting CYP2E1 contributes to ethanol-induced toxicity.

241 lating mitochondrial function by suppressing CYP2E1 expression at multiple levels.

242 eting, indicating that mitochondria-targeted CYP2E1 plays an important role in alcohol liver toxicity

243 To study the role of mitochondrial targeted CYP2E1 in generating oxidative stress and causing damage

244 ently, we showed that mitochondrion-targeted CYP2E1 augments alcohol-mediated toxicity, causing an in

245 which is augmented by mitochondrion-targeted CYP2E1.

246 recognition particle, preferentially targets CYP2E1 to the endoplasmic reticulum.

247 These results demonstrate that CYP2E1 is important in fast food-mediated liver fibrosis

248 Pulse-chase studies found that CYP2E1 protein level is upregulated in LKO hepatocytes.

249 These results indicate that CYP2E1 contributes to experimental alcoholic fatty liver

250 These results revealed that CYP2E1 in the mitochondrial compartment could induce oxi

251 Thus, the diverse roles that CYP2E1 has in normal physiology, toxicity, and drug meta

252 These results show that CYP2E1 sensitizes liver hepatocytes to LPS or TNF-alpha

253 Control experiments show that CYP2E1, which has an omega-1 regiospecificity, primarily

254 Studies including ours have shown that CYP2E1 is bimodally targeted to both the endoplasmic ret

255 c fatty liver in this model and suggest that CYP2E1-derived oxidative stress may inhibit oxidation of

256 pecifically, we show for the first time that CYP2E1 is transcriptionally regulated by the WNT/beta-ca

257 The CYP2E1 active site also has two adjacent voids: one encl

258 The CYP2E1 inhibitor chlormethiazole and iNOS inhibitor N-(3

259 sphonium conjugated carboxyl proxyl, and the CYP2E1 inhibitor diallyl sulfide prevented the loss of C

260 We have conducted a study to compare the CYP2E1 and CYP3A activities in 20 individuals with moder

261 ical importance of the two ion pairs for the CYP2E1-b(5) interaction, and the stimulatory effect of b

262 PBC were compared according to genotype, the CYP2E1 c2 allele was associated with signs of more sever

263 al chlorinated ethene removal was 87% in the CYP2E1 bed, 85% in the WT bed, and 34% in the unplanted

264 Instead of the BM3-like binding mode in the CYP2E1 channel, these structures reveal interactions bet

265 ts from hypothermia-induced decreases in the CYP2E1 enzyme affinity for the substrate chlorzoxazone.

266 While no CYP2E1 was present in the CYP2E1 knockout mice, CYP2A5 activity was also lower.

267 A 1.2-kilobase pair portion of the CYP2E1 promoter was associated with 5- to 10-fold greate

268 edly decreased the systemic clearance of the CYP2E1 substrate, chlorzoxazone, when compared with norm

269 to glutathione ethyl ester, catalase, or the CYP2E1 inhibitor diallyl sulfide partially reversed the

270 interfering RNA (siRNA)-Nrf2 potentiates the CYP2E1-dependent AA toxicity.

271 hepatocytes to LPS or TNF-alpha and that the CYP2E1-enhanced LPS or TNF-alpha injury, oxidant stress,

272 oorly with wild-type b(5) for binding to the CYP2E1.POR complex yet accepts electrons from POR at a s

273 We propose that these CYP2E1 phosphorylation clusters may serve to engage each

274 ally decreased as a second molecule bound to CYP2E1 through an effector site (K(ss) = 260 microm), wh

275 The introduction of CYP2E1 to CYP2E1-knockout mice via an adenovirus restored macroves

276 ited high selectivity for CYP2A6 relative to CYP2E1, -3A4, -2B6, -2C9, -2C19, and -2D6.

277 quitin-conjugating E2 enzymes as relevant to CYP2E1 UPD.

278 of either two 4MP or one IND molecule(s) to CYP2E1, respectively.

279 1a KO livers have a reduced methylated/total CYP2E1 ratio.

280 a1 levels and a decrease in methylated/total CYP2E1 ratio.

281 gulatory elements controlling transcription, CYP2E1 promoter constructs were used to make adenovirus

282 oth transcriptional and post-transcriptional CYP2E1 regulatory mechanisms are known, resulting in 20-

283 contrast to wild-type SV 129 mice, treating CYP2E1 knockout mice with PY plus TNF-alpha did not indu

284 fection of HEK cells with both the truncated CYP2E1 and the hsp70-dependent E3 ubiquitin ligase CHIP

285 ytosol of HEK cells expressing the truncated CYP2E1(Delta3-29) yields coadsorption of CYP2E1(Delta3-2

286 xation/withdrawal results in a fast turnover CYP2E1 species, putatively generated through its futile

287 uitin ligases were capable of ubiquitinating CYP2E1, a process enhanced by protein kinase (PK) A and/

288 radioligands that undergo defluorination via CYP2E1.

289 Z) oral clearance was used to assess in vivo CYP2E1 activity.

290 ibility, the effects of in vitro and in vivo CYP2E1 overexpression on hepatocyte insulin signaling we

291 evels of protein and mRNA are increased when CYP2E1 is elevated.

292 ation by this pathway, we have asked whether CYP2E1 is regulated by the chaperone machinery.

293 In this study, we investigated whether CYP2E1 plays a role in experimental alcoholic fatty live

294 INH was found to form covalent adducts with CYP2E1, CYP3A4, and CYP2C9.

295 nd CYP3A4 mRNA levels did not correlate with CYP2E1 and CYP3A activities.

296 association of either CYP3A4 or CYP3A5 with CYP2E1 causes activation of the latter enzyme.

297 etabolites were detected in incubations with CYP2E1.

298 Interaction of MATalpha1 with CYP2E1 was direct, and this facilitated CYP2E1 methylati

299 ent diet mouse model of steatohepatitis with CYP2E1 overexpression, insulin-induced IRS-1, IRS-2, and

300 (++) cells in comparison with wild type (WT) CYP2E1-expressing or ER(+) (mostly microsome-targeted) c