Results 11 to 20 of about 101,558 (168)
The crystal structure of mycobacterial epoxide hydrolase A [PDF]
Scientific Reports, 2020 AbstractThe human pathogen Mycobacterium tuberculosis is the causative agent of tuberculosis resulting in over 1 million fatalities every year, despite decades of research into the development of new anti-TB compounds. Unlike most other organisms M. tuberculosis has six putative genes for epoxide hydrolases (EH) of the α/β-hydrolase family with little ...
Boris Krichel +9 more
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Cholesterol epoxide hydrolase and cancer
Current Opinion in Pharmacology, 2012 Cholesterol epoxide hydrolase (ChEH) catalyzes the hydration of cholesterol-5,6-epoxides (5,6-EC) into cholestane-3β,5α,6β-triol. ChEH is a hetero-oligomeric complex called the anti-estrogen binding site (AEBS) comprising 3β-hydroxysterol-Δ(8)-Δ(7)-isomerase (D8D7I) and 3β-hydroxysterol-Δ(7)-reductase (DHCR7).
Silvente-Poirot, Sandrine, Poirot, Marc
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Microsomal epoxide hydrolase polymorphisms
Molecular Medicine Reports, 2010 Microsomal epoxide hydrolase plays a dual role in the activation and detoxification of carcinogenic compounds. Two polymorphic sites have been described in exons 3 and 4 of the microsomal epoxide hydrolase gene that change tyrosine residue 113 to histidine (Tyr113His) and histidine 139 to arginine (His139Arg), respectively.
Pinarbasi, Hatice +2 more
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Epoxides and Soluble Epoxide Hydrolase in Cardiovascular Physiology [PDF]
Physiological Reviews, 2012 Epoxyeicosatrienoic acids (EETs) are arachidonic acid metabolites that importantly contribute to vascular and cardiac physiology. The contribution of EETs to vascular and cardiac function is further influenced by soluble epoxide hydrolase (sEH) that degrades EETs to diols. Vascular actions of EETs include dilation and angiogenesis.
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Visualization of a Covalent Intermediate between Microsomal Epoxide Hydrolase, but not Cholesterol Epoxide Hydrolase, and their Substrates [PDF]
European Journal of Biochemistry, 1997 Mammalian soluble and microsomal epoxide hydrolases have been proposed to belong to the family of αlβ‐hydrolase‐fold enzymes. These enzymes hydrolyse their substrates by a catalytic triad, with the first step of the enzymatic reaction being the formation of a covalent enzyme‐substrate ester. In the present paper, we describe the direct visualization of
Müller, F +10 more
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Catalysis of potato epoxide hydrolase, StEH1 [PDF]
Biochemical Journal, 2005 The kinetic mechanism of epoxide hydrolase (EC 3.3.2.3) from potato, StEH1 (Solanum tuberosum epoxide hydrolase 1), was studied by presteady-state and steady-state kinetics as well as by pH dependence of activity. The specific activities towards the different enantiomers of TSO (trans-stilbene oxide) as substrate were 43 and 3 μmol·min−1·mg−1 with the ...
Mikael Widersten, Lisa T. Elfström
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Asian Journal of Pharmaceutical Research and DevelopmentEpoxyeicosatrienoic acids (EETs) have numerous cardiovascular benefits, including vasodilation, anti-inflammatory actions, and anti-migratory effects on vascular smooth muscle cells.
Pooja M. Sontakke +4 more
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Genetic deletion of soluble epoxide hydrolase delays the progression of Alzheimer’s disease
Journal of Neuroinflammation, 2019 Soluble epoxide hydrolase (sEH) is a bifunctional enzyme with COOH-terminal hydrolase and NH2-terminal lipid phosphatase activities. It is expressed in various cell types in the brain and is involved in the pathogenesis of inflammatory and ...
Hsueh-Te Lee +3 more
semanticscholar +1 more source
Role of Soluble Epoxide Hydrolase in Metabolism of PUFAs in Psychiatric and Neurological Disorders
Frontiers in Pharmacology, 2019 Inflammation plays a key role in the pathogenesis of a number of psychiatric and neurological disorders. Soluble epoxide hydrolases (sEH), enzymes present in all living organisms, metabolize epoxy fatty acids (EpFAs) to corresponding 1,2-diols by the ...
K. Hashimoto
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Pharmaceutical Effects of Inhibiting the Soluble Epoxide Hydrolase in Canine Osteoarthritis
Frontiers in Pharmacology, 2019 Osteoarthritis (OA) is a degenerative joint disease that causes pain and bone deterioration driven by an increase in prostaglandins (PGs) and inflammatory cytokines.
C. McReynolds +8 more
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