3.3.2.10: soluble epoxide hydrolase
This is an abbreviated version!
For detailed information about soluble epoxide hydrolase, go to the full flat file.
Word Map on EC 3.3.2.10
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3.3.2.10
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epoxyeicosatrienoic
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arachidonic
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diol
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s-transferase
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hydrolases
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hypertension
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benzoapyrene
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epoxygenase
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styrene
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dihydroxyeicosatrienoic
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enantioselectivity
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phenobarbital
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dhets
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trans-stilbene
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leukotriene
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eicosanoids
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drug-metabolizing
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cyp1a1
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3-methylcholanthrene
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o-deethylase
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oxylipins
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xenobiotic-metabolizing
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dihydrodiols
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enantiopure
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ethoxyresorufin
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lta4
-
glycidyl
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arene
-
urea-based
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cyclohexene
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ethoxycoumarin
-
medicine
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beta-naphthoflavone
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oxirane
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20-hydroxyeicosatetraenoic
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udp-glucuronyltransferase
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20-hete
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cyp2j2
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udp-glucuronosyl
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1-naphthol
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aminopyrine
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edhfs
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analysis
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radiobacter
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3-methylcholanthrene-treated
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butadiene
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udpgt
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hydroxyeicosatetraenoic
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epichlorohydrin
-
aldrin
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synthesis
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pentoxyresorufin
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drug development
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agriculture
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adamantyl
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pharmacology
- 3.3.2.10
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epoxyeicosatrienoic
-
arachidonic
- diol
- s-transferase
- hydrolases
- hypertension
-
benzoapyrene
- epoxygenase
- styrene
-
dihydroxyeicosatrienoic
-
enantioselectivity
- phenobarbital
-
dhets
- trans-stilbene
-
leukotriene
-
eicosanoids
-
drug-metabolizing
- cyp1a1
- 3-methylcholanthrene
-
o-deethylase
- oxylipins
-
xenobiotic-metabolizing
-
dihydrodiols
-
enantiopure
-
ethoxyresorufin
- lta4
-
glycidyl
- arene
-
urea-based
- cyclohexene
-
ethoxycoumarin
- medicine
- beta-naphthoflavone
-
oxirane
-
20-hydroxyeicosatetraenoic
-
udp-glucuronyltransferase
- 20-hete
- cyp2j2
-
udp-glucuronosyl
- 1-naphthol
- aminopyrine
-
edhfs
- analysis
- radiobacter
-
3-methylcholanthrene-treated
- butadiene
-
udpgt
-
hydroxyeicosatetraenoic
- epichlorohydrin
- aldrin
- synthesis
-
pentoxyresorufin
- drug development
- agriculture
-
adamantyl
- pharmacology
Reaction
Synonyms
AnEH, BNSEH1, CEH, Cterm-EH, Cytosolic epoxide hydrolase, EC 3.1.3.76, EC 3.3.2.3, EC 4.2.1.63, EC 4.2.1.64, EET-metabolizing enzyme, EH, EH3, EPHX2, EPHX3, epoxide hydrolase 1, epoxide hydrolase 2, epoxide hydrolase-3, epoxyeicosatrienonic acid-metabolizing enzyme, EPXH1, EPXH2, EPXH2B, hepoxilin hydrolase, hsEH, mEH, More, PNSO hydrolase, PsEH, s-EH, SEH, soluble epoxide hydrolase, soluble-type epoxide hydrolase, SPEH1, SPEH2, TESO hydrolase, TSO hydrolase
ECTree
3.3.2.10 soluble epoxide hydrolaseAdvanced search results
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General Information on EC 3.3.2.10 - soluble epoxide hydrolase
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
evolution
the structure of sEH from Danio rerio is compared to sEHs from mammalia, most of EHs possess the catalytic triad consisting of an acidic nucleophile and a basic charge relay system, two tyrosine residues in the cap domain and the characteristic oxyanion hole are also highly conserved
malfunction
metabolism
physiological function
additional information
malfunction
acute hypoxic vasoconstriction in sEH-/- mice is insensitive to sEH inhibition but inhibited by the epoxyeicosatrienoic acid antagonist, and chronic hypoxia induces an exaggerated pulmonary vascular remodelling. In wild-type mice, chronic sEH inhibition increases serum epoxyeicosatrienoic acid levels but fails to affect acute hypoxic vasoconstriction, right ventricle weight, pulmonary artery muscularization, or voluntary running distance
malfunction
administration of an sEH inhibitor significantly attenuates LPS-mediated induction of hepatic COX-2 expression and circulating PGE2 levels in mice. Inhibition of sEH-mediated EET hydrolysis has also significantly reduced cerebral infarct volume in rodents after middle cerebral artery occlusion. sEHI treatment downregulates proinflammatory gene expression in the aorta and circulating levels in serum, and reduces inflammatory cell infiltration into the vascular wall
malfunction
association of sEH gene Ephx2 polymorphisms with increased risk of atherosclerosis and cardiovascular diseases, role of epoxyeicosatrienoic acids, EETs, and sEH in the pathogenesis of atherosclerosis, overview
malfunction
association of sEH gene Ephx2 polymorphisms with increased risk of atherosclerosis and cardiovascular diseases, role of epoxyeicosatrienoic acids, EETs, and sEH in the pathogenesis of atherosclerosis, overview
malfunction
association of sEH gene Ephx2 polymorphisms with increased risk of atherosclerosis and cardiovascular diseases, role of epoxyeicosatrienoic acids, EETs, and sEH in the pathogenesis of atherosclerosis, overview
malfunction
beneficial effects of several potent soluble epoxide hydrolase inhibitors in cardiac hypertrophy
malfunction
blood flow during middle cerebral artery occlusion is higher and infarct size is smaller in wild-type female compared with male mice, overview. Sex differences in cerebral blood flow and ischemic damage are abolished after ovariectomy and are absent in sEH knockout mice
malfunction
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diabetes is one of the main factors responsible for end-stage renal disease caused by impaired endothelium
malfunction
diabetes is one of the main factors responsible for end-stage renal disease caused by impaired endothelium
malfunction
in vivo, streptozotocin-induced diabetes results in the tyrosine nitration of the sEH in murine lungs and a significant decrease in its activity. Inhibition of sEH has beneficial effects on vascular inflammation and hypertension
malfunction
inhibition of sEH has beneficial effects on vascular inflammation and hypertension
malfunction
polymorphimsm in gene EPHX2 are associated with ischemic stroke risk. sEH inhibition and gene deletion reduce infarct size after focal cerebral ischemia in mice
malfunction
polymorphimsm in gene EPHX2 are associated with ischemic stroke risk. sEH inhibition and gene deletion reduce infarct size after focal cerebral ischemia in mice
malfunction
polymorphimsm in gene EPHX2 are associated with ischemic stroke risk. sEH inhibition and gene deletion reduce infarct size after focal cerebral ischemia in mice
malfunction
sEH expression is absent in samples from patients with pulmonary hypertension. As sEH inhibitors do not promote the development of pulmonary hypertension it seems likely that the N-terminal lipid phosphatase may play a role in the development of this disease
malfunction
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sEH inhibitor treatment is effectively preventing pressure overload- and angiotensin II-induced cardiac hypertrophy and reverses the pre-established cardiac hypertrophy caused by chronic pressure overload, overview
malfunction
sEH knockout and its inhibition prevent hyperglycemia in diabetes, and sEH knockoit also enhances islet GSIS through the amplifying pathway and decreases islet cell apoptosis in diabetes, overview
malfunction
soluble epoxide hydrolase deficiency attenuates neointima formation in the femoral cuff model of hyperlipidemic mice
malfunction
the enzyme and vascular remodeling are associated with cardiovascular disease. Inhibition of SEH prevents smooth muscle cell proliferation in vitro and affects vascular remodeling in vivo, but induces cell proliferation in the left carotid of spontaneously hypertensive stroke-prone rats
malfunction
treatment of apolipoprotein E-deficient mice with sEH inhibitors significantly attenuates atherosclerosis development and abdominal aortic aneurysm formation
malfunction
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enzyme knockdown in zebrafish causes defects in the caudal vein plexus
malfunction
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enzyme knockout mice are more susceptible to seizures than wild type mice
malfunction
enzyme single nucleotide polymorphisms are associated with cardiovascular disease
malfunction
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the increased epoxyeicosatrienoic acid bioavailability, as a function of deficiency/inhibition of soluble epoxide hydrolase, potentiates vasodilator responses that counteract pressure-induced vasoconstriction to lower blood pressure
malfunction
deletion of sEH decreases expression of HMG-CoA reductase, fatty acid synthase, and low density lipoprotein receptor. Sterol regulatory element binding proteins (SREBPs) regulate the expression of all three enzymes and SREBP activation is attenuated in the absence of sEH. The effect is attributed to the AMPK-activated protein kinase (AMPK) which is activated in the absence of sEH. Livers from wild-type versus sEH-/- littermates contain significantly higher levels of the sEH substrate 12,13-epoxyoctadecenoic acid, which elicits dAMPK activation, while the corresponding sEH product is inactive. Thus, AMPK activation and subsequent inhibition of SREBP can account for the altered expression of lipid metabolizing enzymes in sEH-/- mice
malfunction
expression of sEH is significantly increased on day 7, 14, 21 and 28 after pilocarpine-induced status epilepticus (SE). Administration with sEH inhibitors attenuates the SE-induced up-regulation of interleukin-1beta (IL-1beta) and interleukin-6 (IL-6), the degradation of epoxyeicosatrienoic acids, as well as IkappaB phosphorylation. Following treatment with inhibitor AUDA, the frequency and duration of spontaneous motor seizures in the pilocarpine-SE mice are decreased and the seizure-induction threshold of the fully kindled mice is increased. Upregulation of hippocampal IL-1beta and IL-6 is found in both wild-type and sEH knockout mice after successful induction of SE. sEH KO mice are more susceptible to seizures than wild-type mice. Seizure related neuroinflammation and ictogenesis are attenuated by pharmacological inhibition of sEH enzymatic activity but not by sEH genetic deletion. Behavior monitoring of convulsive spontaneous recurrent seizures in the pilocarpine-induced SE model
malfunction
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sEH knockout and its inhibition prevent hyperglycemia in diabetes, and sEH knockoit also enhances islet GSIS through the amplifying pathway and decreases islet cell apoptosis in diabetes, overview
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malfunction
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expression of sEH is significantly increased on day 7, 14, 21 and 28 after pilocarpine-induced status epilepticus (SE). Administration with sEH inhibitors attenuates the SE-induced up-regulation of interleukin-1beta (IL-1beta) and interleukin-6 (IL-6), the degradation of epoxyeicosatrienoic acids, as well as IkappaB phosphorylation. Following treatment with inhibitor AUDA, the frequency and duration of spontaneous motor seizures in the pilocarpine-SE mice are decreased and the seizure-induction threshold of the fully kindled mice is increased. Upregulation of hippocampal IL-1beta and IL-6 is found in both wild-type and sEH knockout mice after successful induction of SE. sEH KO mice are more susceptible to seizures than wild-type mice. Seizure related neuroinflammation and ictogenesis are attenuated by pharmacological inhibition of sEH enzymatic activity but not by sEH genetic deletion. Behavior monitoring of convulsive spontaneous recurrent seizures in the pilocarpine-induced SE model
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malfunction
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deletion of sEH decreases expression of HMG-CoA reductase, fatty acid synthase, and low density lipoprotein receptor. Sterol regulatory element binding proteins (SREBPs) regulate the expression of all three enzymes and SREBP activation is attenuated in the absence of sEH. The effect is attributed to the AMPK-activated protein kinase (AMPK) which is activated in the absence of sEH. Livers from wild-type versus sEH-/- littermates contain significantly higher levels of the sEH substrate 12,13-epoxyoctadecenoic acid, which elicits dAMPK activation, while the corresponding sEH product is inactive. Thus, AMPK activation and subsequent inhibition of SREBP can account for the altered expression of lipid metabolizing enzymes in sEH-/- mice
-
malfunction
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acute hypoxic vasoconstriction in sEH-/- mice is insensitive to sEH inhibition but inhibited by the epoxyeicosatrienoic acid antagonist, and chronic hypoxia induces an exaggerated pulmonary vascular remodelling. In wild-type mice, chronic sEH inhibition increases serum epoxyeicosatrienoic acid levels but fails to affect acute hypoxic vasoconstriction, right ventricle weight, pulmonary artery muscularization, or voluntary running distance
-
malfunction
-
in vivo, streptozotocin-induced diabetes results in the tyrosine nitration of the sEH in murine lungs and a significant decrease in its activity. Inhibition of sEH has beneficial effects on vascular inflammation and hypertension
-
metabolism
epoxide hydrolases comprise a family of enzymes important in detoxification and conversion of lipid signaling molecules, namely epoxyeicosatrienoic acids. Soluble epoxide hydrolase mediates the bulk of the cerebral epoxyeicosatrienoic acid metabolism, overview
metabolism
soluble epoxide hydrolase is a key enzyme in the metabolism of vasodilator eicosanoids called epoxyeicosatrienoic acids, EETs
metabolism
soluble epoxide hydrolase is the major enzyme responsible for the metabolism and inactivation of epoxyeicosatrienoic acids, EETs
metabolism
the enzyme is involved in the arachidonate cascade, pathways overview
metabolism
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epoxide hydrolases comprise a family of enzymes important in detoxification and conversion of lipid signaling molecules, namely epoxyeicosatrienoic acids. Soluble epoxide hydrolase mediates the bulk of the cerebral epoxyeicosatrienoic acid metabolism, overview
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physiological function
conversion of epoxyeicosatrienoic acids to their corresponding diols, dihydroxyeicosatrienoic acids, DHETS, by sEH is responsible for decreasing EET levels and thereby diminishing their beneficial cardiovascular properties, detailed overview
physiological function
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sEH is a xenobiotic-metabolizing enzyme that metabolizes epoxides to produce vicinal diols. Epoxyeicosatrienoic acids are substrates of sEH and have important roles in renal function such as ion transport and the proliferation of cells and the action of epoxyeicosatrienoic acids is important for maintaining renal and vascular homeostasis
physiological function
sEH is a xenobiotic-metabolizing enzyme that metabolizes epoxides to produce vicinal diols. Epoxyeicosatrienoic acids are substrates of sEH and have important roles in renal function such as ion transport and the proliferation of cells and the action of epoxyeicosatrienoic acids is important for maintaining renal and vascular homeostasis
physiological function
sEH is an enzyme involved in the metabolism of endogenous inflammatory and antiapoptotic mediators
physiological function
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sEH is not essentially involved in the metabolization and clearance of carcinogenic xenobiotics. But sEH is involved in inflammation
physiological function
sEH is responsible for renal protection with DOCA-salt hypertension
physiological function
sEH plays an important role in the physiology of cells including proliferation. The epoxide hydrolase and phosphatase domains of sEH have different biological functions
physiological function
soluble epoxide hydrolase is a key enzyme in the metabolic conversion and degradation of P450 eicosanoids called epoxyeicosatrienoic acids, EETs
physiological function
soluble epoxide hydrolase is a key enzyme in the metabolic conversion and degradation of P450 eicosanoids called epoxyeicosatrienoic acids, EETs
physiological function
soluble epoxide hydrolase is a key enzyme in the metabolic conversion and degradation of P450 eicosanoids called epoxyeicosatrienoic acids, EETs
physiological function
soluble epoxide hydrolase is a key enzyme in the metabolism of vasodilator eicosanoids called epoxyeicosatrienoic acids, EETs, and is sexually dimorphic and suppressed by estrogen
physiological function
soluble epoxide hydrolase is a key enzyme involved in the metabolism of epoxy fatty acid mediators such as epoxyeicosatrienoic acids with emerging roles in the regulations of hypertension and inflammation
physiological function
soluble epoxide hydrolase is the major enzyme responsible for the metabolism and inactivation of epoxyeicosatrienoic acids, EETs. In the central nervous system, EETs are thought to play a role in the regulation of local blood flow, protection from ischemic injury, inhibition of inflammation, the release of peptide hormones and modulation of fever
physiological function
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hepoxilin hydrolase activity is abolished in liver preparations from sEH-/- mice, and liver homogenates of sEH-/- mice show elevated basal levels of hepoxilins but lowered levels of trioxilins compared with wild-type animals
physiological function
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soluble epoxide hydrolase activity determines the severity of ischemia-reperfusion injury in kidney
physiological function
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soluble epoxide hydrolase regulates hematopoietic progenitor cell function via generation of fatty acid diols
physiological function
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the enzyme plays an important role in the generation of epilepsy
physiological function
through its metabolism of the epoxyeicosatrienoic acids and other lipid mediators, the enzyme contributes to the regulation of vascular tone, nociception, angiogenesis and the inflammatory response. The enzyme plays a role in either the initiation of corpus luteum formation, and/or in the regression of the structure. The enzyme is implicated in the pathology of pulmonary hypertension
physiological function
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transgenic enzyme expression in endothelium results in impaired endothelium-dependent vasodilation in the cerebral circulation. Females are more susceptible to enhanced ischemic damage as a result of increased endothelial soluble epoxide hydrolase than males, especially in end-arteriolar striatal region
physiological function
activities of EPHX2 and EPHX3 in production of the linoleate triols detected as end products of the 12R-lipoxygenase pathway in the epidermis and functioning in formation of the mammalian water permeability barrier
physiological function
activities of EPHX2 and EPHX3 in production of the linoleate triols detected as end products of the 12R-lipoxygenase pathway in the epidermis and functioning in formation of the mammalian water permeability barrier
physiological function
activities of EPHX2 and EPHX3 in production of the linoleate triols detected as end products of the 12R-LOX pathway in the epidermis and functioning in formation of the mammalian water permeability barrier
physiological function
mammalian soluble epoxide hydrolase (sEH) is involved in mediating the metabolism of the endogenous lipid epoxides such as epoxyeicosatrienoic acids (EETs) that are derived from arachidonic acid. The sEH converts epoxide-containing substrates into the corresponding more polar and less potent vicinal diols. EETs are vasodilation mediators through the activation of the Ca2+-activated K+-channels in endothelial cells which benefit many renal and cardiovascular diseases. EETs are reported to be involved in the cell angiogenesis and proliferation which may offer a protective role in ischemic and reperfusion injury. Furthermore, the EETs are anti-inflammatory mediators in endothelial cells by inhibiting the expression of the proatherogenic mediator vascular cell adhesion molecule-1 that is induced by tumor necrosis factor-alpha (TNF-alpha). In addition, EETs suppress the NF-kappaB-mediated expression of cytokines by activating PPARgamma
physiological function
mammalian soluble epoxide hydrolase (sEH) is involved in mediating the metabolism of the endogenous lipids epoxides such as epoxyeicosatrienoic acids (EETs) that are derived from arachidonic acid. The sEH converts epoxide-containing substrates into the corresponding more polar and less potent vicinal diols. EETs are vasodilation mediators through the activation of the Ca2+-activated K+-channels in endothelial cells which benefit many renal and cardiovascular diseases. EETs are reported to be involved in the cell angiogenesis and proliferation which may offer a protective role in ischemic and reperfusion injury. Furthermore, the EETs are anti-inflammatory mediators in endothelial cells by inhibiting the expression of the proatherogenic mediator vascular cell adhesion molecule-1 that is induced by tumor necrosis factor-alpha (TNF-alpha). In addition, EETs suppress the NF-kappaB-mediated expression of cytokines by activating PPARgamma
physiological function
mammalian soluble epoxide hydrolase (sEH) is involved in mediating the metabolism of the endogenous lipids epoxides such as epoxyeicosatrienoic acids (EETs) that are derived from arachidonic acid. The sEH converts epoxide-containing substrates into the corresponding more polar and less potent vicinal diols. EETs are vasodilation mediators through the activation of the Ca2+-activated K+-channels in endothelial cells which benefit many renal and cardiovascular diseases. EETs are reported to be involved in the cell angiogenesis and proliferation which may offer a protective role in ischemic and reperfusion injury. Furthermore, the EETs are anti-inflammatory mediators in endothelial cells by inhibiting the expression of the proatherogenic mediator vascular cell adhesion molecule-1 that is induced by tumor necrosis factor-alpha (TNF-alpha). In addition, EETs suppress the NF-kappaB-mediated expression of cytokines by activating PPARgamma
physiological function
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soluble epoxide hydrolase (sEH) hydrolyzes epoxyeicosatrienoic acids (EETs) in the metabolic pathway of arachidonic acid
physiological function
soluble epoxide hydrolase (sEH) is a key enzyme in the metabolic conversion of epoxyeicosatrienoic acids into their less active form, dihydroxyeicosatrienoic acids (DHET). Enzyme sEH may play an important role in the generation of epilepsy. It may have clinical therapeutic implication for epilepsy in the future, particularly when treating temporal lobe epilepsy
physiological function
the human soluble Epoxide Hydrolase (hsEH) is an enzyme involved in the hydrolysis of endogenous anti-inflammatory and cardio-protective signalling mediators known as epoxyeicosatrienoic acids (EETs). EETs' conversion into the corresponding diols by hsEH generates non-bioactive molecules, thereby the enzyme inhibition is be expected to enhance the EETs bioavailability, and their beneficial properties
physiological function
the role of the C-terminal (epoxide hydrolase) domain is confirmed by its participation in the metabolism of epoxy fatty acids to vicinal diols that are endogenous mediators of various undesirable physiological processes. Inhibition of sEH is efficient in inflammatory and neuropathic pains
physiological function
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sEH is an enzyme involved in the metabolism of endogenous inflammatory and antiapoptotic mediators
-
physiological function
-
soluble epoxide hydrolase (sEH) is a key enzyme in the metabolic conversion of epoxyeicosatrienoic acids into their less active form, dihydroxyeicosatrienoic acids (DHET). Enzyme sEH may play an important role in the generation of epilepsy. It may have clinical therapeutic implication for epilepsy in the future, particularly when treating temporal lobe epilepsy
-
physiological function
-
mammalian soluble epoxide hydrolase (sEH) is involved in mediating the metabolism of the endogenous lipids epoxides such as epoxyeicosatrienoic acids (EETs) that are derived from arachidonic acid. The sEH converts epoxide-containing substrates into the corresponding more polar and less potent vicinal diols. EETs are vasodilation mediators through the activation of the Ca2+-activated K+-channels in endothelial cells which benefit many renal and cardiovascular diseases. EETs are reported to be involved in the cell angiogenesis and proliferation which may offer a protective role in ischemic and reperfusion injury. Furthermore, the EETs are anti-inflammatory mediators in endothelial cells by inhibiting the expression of the proatherogenic mediator vascular cell adhesion molecule-1 that is induced by tumor necrosis factor-alpha (TNF-alpha). In addition, EETs suppress the NF-kappaB-mediated expression of cytokines by activating PPARgamma
-
physiological function
-
mammalian soluble epoxide hydrolase (sEH) is involved in mediating the metabolism of the endogenous lipid epoxides such as epoxyeicosatrienoic acids (EETs) that are derived from arachidonic acid. The sEH converts epoxide-containing substrates into the corresponding more polar and less potent vicinal diols. EETs are vasodilation mediators through the activation of the Ca2+-activated K+-channels in endothelial cells which benefit many renal and cardiovascular diseases. EETs are reported to be involved in the cell angiogenesis and proliferation which may offer a protective role in ischemic and reperfusion injury. Furthermore, the EETs are anti-inflammatory mediators in endothelial cells by inhibiting the expression of the proatherogenic mediator vascular cell adhesion molecule-1 that is induced by tumor necrosis factor-alpha (TNF-alpha). In addition, EETs suppress the NF-kappaB-mediated expression of cytokines by activating PPARgamma
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additional information
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cardioprotective roles of sEH inhibition in myocardial ischemia-reperfusion injury
additional information
cardioprotective roles of sEH inhibition in myocardial ischemia-reperfusion injury
additional information
enzyme inhibition protects against ischemic stroke, mechanism and cytoprotective, anti-inflammatory, and other effects, overview
additional information
enzyme inhibition protects against ischemic stroke, mechanism and cytoprotective, anti-inflammatory, and other effects, overview
additional information
inhibition of sEH leads to an increase in epoxyeicosatrienoic acids resulting in the potentiation of their anti-inflammatory and vasodilatory effects
additional information
inhibition of soluble epoxide hydrolase attenuated atherosclerosis, abdominal aortic aneurysm formation, and dyslipidemia
additional information
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inhibition of soluble epoxide hydrolase attenuated atherosclerosis, abdominal aortic aneurysm formation, and dyslipidemia
additional information
inhibition of soluble epoxide hydrolase enhances the anti-inflammatory effects of aspirin and 5-lipoxygenase activation protein inhibitor in a murine model, detailed overview
additional information
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inhibition of soluble epoxide hydrolase enhances the anti-inflammatory effects of aspirin and 5-lipoxygenase activation protein inhibitor in a murine model, detailed overview
additional information
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sEh inhibition reduces inflammation. In several mouse models, sEH inhibition reduces atherosclerosis and aortic aneurysm formation. The anti-proliferative effect of urea-based sEH inhibitors is probably caused by PPARa activation and consecutive inhibition of cyclin D1 expression. And sEH inhibition affects renal fucntions, overview
additional information
treatment with sEH inhibitors reduces blood pressure in several animal models of hypertension
additional information
treatment with sEH inhibitors reduces blood pressure in several animal models of hypertension
additional information
catalytically important and highly conserved amino acids are Asp331, Tyr379, Tyr460, Asp496 and His524. Proposed active site of Danio rerio sEH based on homology structural modelling
additional information
evaluation of different epoxide hydrolase (EH) enzymes in the hydrolysis of skin-relevant fatty acid epoxides and comparison to the products to those of acid-catalyzed hydrolysis
additional information
evaluation of different epoxide hydrolase (EH) enzymes in the hydrolysis of skin-relevant fatty acid epoxides and comparison to the products to those of acid-catalyzed hydrolysis
additional information
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evaluation of different epoxide hydrolase (EH) enzymes in the hydrolysis of skin-relevant fatty acid epoxides and comparison to the products to those of acid-catalyzed hydrolysis
additional information
evaluation of different epoxide hydrolase (EH) enzymes in the hydrolysis of skin-relevant fatty acid epoxides and comparison to the products to those of acid-catalyzed hydrolysis
additional information
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evaluation of different epoxide hydrolase (EH) enzymes in the hydrolysis of skin-relevant fatty acid epoxides and comparison to the products to those of acid-catalyzed hydrolysis
additional information
the enzyme is bifunctional possessing C-terminal epoxide hydrolase and N-terminal phosphatase activities
additional information
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transition state of epoxide ring opening catalyzed by sEH, and binding mode of urea which mimic the transition state
