3.3.2.9: microsomal epoxide hydrolase
This is an abbreviated version!
For detailed information about microsomal epoxide hydrolase, go to the full flat file.
Word Map on EC 3.3.2.9
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3.3.2.9
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phenobarbital
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cholesterol
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phospholipid
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hepatocytes
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monooxygenase
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hydroxylase
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triglyceride
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xenobiotics
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steroid
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nadph-cytochrome
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thyroid
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isozymes
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lipoprotein
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s-transferase
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testosterone
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aniline
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benzoapyrene
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phosphatidylcholine
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glucuronidation
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3-methylcholanthrene
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bile
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drug-metabolizing
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arachidonic
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prostaglandin
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acyltransferase
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heme
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hepatotoxicity
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nadph-dependent
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cyp2e1
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gsh
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autoimmune
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apolipoprotein
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cyp1a2
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autoantibody
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biphenyls
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polycyclic
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udp-glucuronosyltransferase
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monoxide
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glucose-6-phosphatase
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tetrachloride
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polychlorinated
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thyroglobulin
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ketoconazole
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demethylase
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ccl4
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desaturation
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n-oxide
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androstenedione
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beta-hydroxysteroid
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21-hydroxylase
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synthesis
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medicine
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drug development
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analysis
- 3.3.2.9
- phenobarbital
- cholesterol
- phospholipid
- hepatocytes
- monooxygenase
- hydroxylase
- triglyceride
- xenobiotics
- steroid
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nadph-cytochrome
- thyroid
- isozymes
- lipoprotein
- s-transferase
- testosterone
- aniline
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benzoapyrene
- phosphatidylcholine
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glucuronidation
- 3-methylcholanthrene
- bile
-
drug-metabolizing
-
arachidonic
- prostaglandin
- acyltransferase
- heme
-
hepatotoxicity
-
nadph-dependent
- cyp2e1
- gsh
- autoimmune
-
apolipoprotein
- cyp1a2
- autoantibody
- biphenyls
-
polycyclic
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udp-glucuronosyltransferase
- monoxide
- glucose-6-phosphatase
-
tetrachloride
-
polychlorinated
- thyroglobulin
- ketoconazole
- demethylase
- ccl4
-
desaturation
- n-oxide
- androstenedione
-
beta-hydroxysteroid
- 21-hydroxylase
- synthesis
- medicine
- drug development
- analysis
Reaction
Synonyms
alpha,beta fold epoxide hydrolase, alpha,beta-fold type EH, E1-b', EC 3.3.2.3, EC 4.2.1.63, EC 4.2.1.64, EH1, EH2, Eha, EHb, EPHX, EPHX 1, EPHX1, EPOX, epoxide hydrolase, HYL1, JH epoxide hydrolase, JHEH, juvenile hormone epoxide hydrolase, mEH, mEH-like protein, mEH1, mEPHX, microsomal, microsomal EH, microsomal EPHX1, Microsomal epoxide hydrolase, microsomal epoxide hydrolase 1, microsomal epoxide hydrolase-like protein, microsomal xenobiotic epoxide hydrolase, More, PNSO hydrolase, SEH, styrene-epoxide hydrolase, Tcjheh-r1, Tcjheh-r3, XEHase, xenobiotic epoxide hydrolase
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PROTEIN VARIANTS 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
A139G
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a naturally occuring polymorphism, leads to reduced EPHX1 activity, but is not involved in pathogeneiss of asthma and COPD
E404D
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mutation of the catalytic triad residue leads to increased activity compared to the wild-type enzyme
H139R
R43T
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mutant shows reduced activity compared to the wild-type enzyme, molecular modelling
T113C
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a naturally occuring polymorphism, leads to reduced EPHX1 activity, but is not involved in pathogeneiss of asthma and COPD
T275A
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mutant shows similar activity compared to the wild-type enzyme, molecular modelling
Y113H
Y133H
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naturally occuring mutation, frequencies in hepatocellular carcinoma, controls, and the chronic viral hepatitis subjects, respectively, overview
E404D
catalytic triad mutation, enzymatic activity of mEH can be greatly increased by a point mutation, leading to an E404D amino acid exchange in its catalytic triad, the mutation improves metabolic detoxification but impairs cerebral blood flow regulation. In liver microsomes from mutant mice, turnover of the xenobiotic compound phenanthrene-9,10-oxide is four times faster compared to wild-type liver microsomes. Hemodynamics are assessed in mEH E404D mutant and WT cerebral cortex and hippocampus using cerebral blood volume (CBV)-based functional magnetic resonance imaging (fMRI). Basal CBV0 levels are similar between mEH E404D and control mice in both brain areas. But vascular reactivity and vasodilation in response to the vasodilatory drug acetazolamide are reduced in mEH E404D forebrain compared to WT controls by factor 3 and 2.6, respectively. Role of mEH E404D in acetazolamide-induced vasodilation in cerebral cortex and hippocampus
additional information
H139R
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mutant shows increased activity compared to the wild-type enzyme, molecular modelling
H139R
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natural genotype, frequency of the polymorphism, the mutant enzyme shows 25% increased activity compared to the wild-type enzyme
H139R
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natural genotype, frequency of the polymorphism, the mutant enzyme shows increased activity compared to the wild-type enzyme
H139R
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the mutation is a genetic contributor to chronic obstructive pulmonary disease susceptibility
H139R
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there is a significant association between early-onset lung cancer and the presence of EPHX1 exon 4 variant H139R
H139R
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the naturally occuring mutation is a risk factor for hepatocellular carcinoma with both control and chronic hepatitis-infected individuals, association of GSTT1 and GSTM1 null genotypes and mEPHX polymorphisms with hepatitis virus-related HCC risk in an Indian population. Frequencies in hepatocellular carcinoma, controls, and the chronic viral hepatitis subjects, respectively, overview
H139R
naturally occuring enzyme mutation, a polymorphism in exon 4, involved in development of esophageal squamous cell carcinoma
H139R
rs2234922, A416>G, naturally occuring mutation, used as marker to predict EPHX1 activity
Y113H
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mutant shows similar activity compared to the wild-type enzyme, molecular modelling
Y113H
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natural genotype, frequency of the polymorphism, the mutant enzyme shows 40% reduced activity compared to the wild-type enzyme
Y113H
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natural genotype, frequency of the polymorphism, the mutant enzyme shows reduced activity compared to the wild-type enzyme
Y113H
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the mutant is associated with 40-50% decrease in microsomal epoxide hydrolase activity
Y113H
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the mutation is a genetic contributor to chronic obstructive pulmonary disease susceptibility
Y113H
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the mutation is associated with higher risk of squamous cell esophageal cancer
Y113H
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the mutation leads to altered enzyme activity, but is not associated with pancreatic diseases
Y113H
naturally occuring enzyme mutation, a polymorphism in exon 3, involved in development of esophageal squamous cell carcinoma (ESCC), exon 3 slow genotype predicts low mEH activity associated with the ESCC risk. Elevated ESCC risk estimates are seen in smokers independent of genotypes but the association is stronger among smokers with exon 3 variant
Y113H
rs1051740, T337>C, naturally occuring mutation, used as marker to predict EPHX1 activity
additional information
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genotyping of 3553 humans, enzyme polymorphisms are not associated with colon cancer
additional information
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genotyping of 497 humans, enzyme polymorphisms are associated with esophageal squamous-cell-carcinoma, ESCC, and smoking or areca chewing, higher enzyme activity can contribute to lower the risk of cancer development, overview
additional information
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naturally occurring genetic polymorphisms of the enzyme are responsible for varying susceptibility of cigarette smoking humans to chronic obstructive pulmonary disease, COPD
additional information
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genotyping and identifcation of single nucleotide polymorphisms c416A/G, rs2234922, and c337T/C, role of the mutations in carbamazepine treatement of epilepsy, overview
additional information
genotype analysis of the EPHX1 intron 1 polymorphism in the Lancaster County Old Order Amish population, identification of heterozygous mutations in human EPHX1 that result in a 95% decrease in mEH expression levels. EPHX1 transcription is significantly inhibited by two heterozygous mutations observed in the Old Order Amish population that present numerous hypercholanemic subjects in the absence of liver damage suggesting a defect in bile acid transport into the hepatocyte. The identity of the regulatory proteins binding to these sites, established using biotinylated oligonucleotides in conjunction with mass spectrometry is poly(ADP-ribose)polymerase-1 (PARP-1) (bound to the EPHX1 proximal promoter) and a linker histone complex, H1.2/Aly (bound to a regulatory intron 1 site). High frequency of the H1.2 site polymorphism in the Amish population results in a potential genetic predisposition to hypercholanemia
additional information
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genotype analysis of the EPHX1 intron 1 polymorphism in the Lancaster County Old Order Amish population, identification of heterozygous mutations in human EPHX1 that result in a 95% decrease in mEH expression levels. EPHX1 transcription is significantly inhibited by two heterozygous mutations observed in the Old Order Amish population that present numerous hypercholanemic subjects in the absence of liver damage suggesting a defect in bile acid transport into the hepatocyte. The identity of the regulatory proteins binding to these sites, established using biotinylated oligonucleotides in conjunction with mass spectrometry is poly(ADP-ribose)polymerase-1 (PARP-1) (bound to the EPHX1 proximal promoter) and a linker histone complex, H1.2/Aly (bound to a regulatory intron 1 site). High frequency of the H1.2 site polymorphism in the Amish population results in a potential genetic predisposition to hypercholanemia
additional information
identification of two heterozygous mutations in gene EPHX1 intron-1, heterozygous polymorphism phenotype, overview. EPHX1 intron-1 heterozygous polymorphism are previously described in a high percentage of the Lancaster County Old Order Amish population that present numerous hypercholanemic subjects without liver injury, suggesting the loss of transport capacity. No mutations have been detected in the NTCP gene from this population
additional information
significant interaction is seen between mEH exon 3 and exon 4 genotypes and between predicted mEH activity and positive family history of cancer suggesting an association of ESCC risk with mEH polymorphisms which get modified by tobacco smoking and positive family history of cancer
additional information
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significant interaction is seen between mEH exon 3 and exon 4 genotypes and between predicted mEH activity and positive family history of cancer suggesting an association of ESCC risk with mEH polymorphisms which get modified by tobacco smoking and positive family history of cancer
additional information
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mEH knockout mice are less sensitive to the carcinogenic activity of 7,12-dimethylbenz[a]anthracene compared to wild-type mice, but show no altered phenotype
additional information
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significant difference in extracellular dopamine uptake is observed between mEH-/- and wild-type mice
