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 and glutathione must be evaluated simultaneously

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

4 CYP2E1 expression induced ERK1/2 activation through incr

5 CYP2E1 is degraded by the ubiquitin-proteasome pathway,

6 CYP2E1 is recognized as the most important enzyme for in

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

8 CYP2E1 overexpression in a hepatocyte cell line decrease

9 CYP2E1 overexpression was also associated with increased

10 CYP2E1 protein and activity were elevated in acetone- or

11 CYP2E1 substrate complexation converts it into a stable

12 CYP2E1 thus exhibits biphasic turnover in the mammalian

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

14 CYP2E1-dependent RIP3 expression induces hepatocyte necr

15 CYP2E1-knockout mice exhibited only minor liver injury a

16 CYP2E1-overexpressing cells were resistant to menadione

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

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

19 .9, 95% confidence interval (CI): 1.4, 6.1), CYP2E1 -332T>A AT/AA genotypes (OR = 2.0, 95% CI: 1.2, 3

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

21 pression of the cytochrome P450 isoform 2E1 (CYP2E1) has been implicated in hepatocyte injury and dea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 Although CYP2E1 is predominantly found in the endoplasmic reticul

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

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

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

52 0 (CYP) protein expression and activity, and CYP2E1 may play a role in the pathogenesis of NAFLD and

53 hich express alcohol dehydrogenase (ADH) and CYP2E1.

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

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

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

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

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

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

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

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

62 THMs, including factors affecting CYP2D6 and CYP2E1 activity.

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

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

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

66 c activity and mRNA expression of CYP3A2 and CYP2E1.

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

68 CYP3A4 and CYP2E1 mRNA levels were not significantly different betw

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

70 sed protein expression of CYP1A2, CYP3A4 and CYP2E1.

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

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

73 affect highly studied genes such as GBA and CYP2E1.

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

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

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

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

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

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

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

81 ) mRNA (P < 0.001), which was accompanied by CYP2E1 induction (P < 0.001) and oxidative stress with i

82 onse to increased oxidative stress caused by CYP2E1 was studied.

83 against increased oxidative stress caused by CYP2E1.

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

85 uggesting that chronic oxidant generation by CYP2E1 may regulate cellular responses through these sig

86 Nrf2 induction by CYP2E1 and its importance in the adaptive response to in

87 atotoxicity of drugs that are metabolized by CYP2E1.

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

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

90 In conclusion, chronic CYP2E1 overexpression leads to sustained ERK1/2 activati

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

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

93 Consequent CYP2E1 gain of function accelerates reactive O2 species

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

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

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

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

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

99 50 isoforms CYP3A4, CYP2D6, CYP2C9, CYP2C19, CYP2E1, and CYP1A2 are responsible for the oxidative met

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

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

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

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

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

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

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

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

108 The cytochrome P450 enzyme CYP2E1 defluorinates many drugs.

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

110 t toxicity in HepG2 E47 cells, which express CYP2E1 and in hepatocytes from pyrazole-treated rats.

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

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

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

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

115 nexplained substrate inhibition observed for CYP2E1.

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

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

118 Depletion of glutathione (GSH) from CYP2E1-expressing cells by treatment with l-buthionine s

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

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

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

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

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

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

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

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

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

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

129 However, CYP2E1-overexpressing cells were sensitized to necrotic

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

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

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

133 mechanism adds to the complexities of human CYP2E1 regulation.

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

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

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

137 ecretion were all significantly decreased in CYP2E1 overexpressing cells.

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

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

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

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

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

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

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

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

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

147 e activation of p38 MAPK by BSO treatment in CYP2E1-expressing liver cells cause a loss in NF-kappaB-

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

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

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

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

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

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

154 raperitoneally with pyrazole (Pyr) to induce CYP2E1.

155 nitric oxide synthase, and ethanol-inducible CYP2E1.

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

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

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

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

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

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

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

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

164 nes expressing predominantly mt CYP2E1 or mc CYP2E1.

165 onsumption induced rat hepatic mitochondrial CYP2E1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

186 The effect of CYP2E1 overexpression on MAPK activation and their funct

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 ally active NH2-terminally truncated form of CYP2E1 (mtCYP2E1) was detected in the mitochondrial comp

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

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

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

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

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

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

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

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

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

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

208 as was found in mice with elevated levels of CYP2E1.

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

210 osure and is correlated with the presence of CYP2E1.

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

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

213 heir function in altering death responses of CYP2E1-overexpressing hepatocytes were investigated.

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

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

222 Either LPS or CYP2E1 are considered independent risk factors involved

223 of ERK1/2 in hepatocytes that overexpressed CYP2E1.

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 these rats had increased cytochrome P4502E1 (CYP2E1) mRNA (P < 0.001), which was accompanied by CYP2E

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

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

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

232 O); indeed a NO donor decreased the BSO plus CYP2E1-dependent toxicity, whereas inhibition of inducib

233 580 afforded protection against the BSO plus CYP2E1-dependent toxicity.

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

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

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

237 Inhibition of EGFR signaling reversed CYP2E1-induced resistance to menadione and sensitization

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

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

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

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

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

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

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

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

246 which is augmented by mitochondrion-targeted CYP2E1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

276 This loss, coupled to CYP2E1-generated oxidant stress, synergize to promote ce

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

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

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

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

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 liver injury involves ethanol metabolism via CYP2E1 and consequent oxidant stress, as well as potenti

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

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

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

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

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

295 However, the mechanism by which CYP2E1 overexpression may promote cell death is unknown.

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

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

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

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