EC Number   |
General Information |
Reference |
|---|
    3.3.2.10 | 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 |
754331 |
| 3.3.2.10 | 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 |
-, 708017 |
| 3.3.2.10 | 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 |
709564 |
| 3.3.2.10 | 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 |
708238 |
| 3.3.2.10 | malfunction |
beneficial effects of several potent soluble epoxide hydrolase inhibitors in cardiac hypertrophy |
709563 |
| 3.3.2.10 | 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 |
709248 |
| 3.3.2.10 | 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 |
-, 755285 |
| 3.3.2.10 | malfunction |
diabetes is one of the main factors responsible for end-stage renal disease caused by impaired endothelium |
708324 |
| 3.3.2.10 | malfunction |
enzyme knockdown in zebrafish causes defects in the caudal vein plexus |
732817 |
| 3.3.2.10 | malfunction |
enzyme knockout mice are more susceptible to seizures than wild type mice |
731562 |
