Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary extracted from

  • Lee, C.J.; Goncalves, L.L.; Wells, P.G.
    Embryopathic effects of thalidomide and its hydrolysis products in rabbit embryo culture: evidence for a prostaglandin H synthase (PHS)-dependent, reactive oxygen species (ROS)-mediated mechanism (2011), FASEB J., 25, 2468-2483.
    View publication on PubMed

Inhibitors

EC Number Inhibitors Comment Organism Structure
1.14.99.1 5,8,11,14-Eicosatetraynoic acid
-
Oryctolagus cuniculus
1.14.99.1 Acetylsalicylic acid irreversible inhibitor Oryctolagus cuniculus

Organism

EC Number Organism UniProt Comment Textmining
1.14.99.1 Oryctolagus cuniculus
-
isozymes PHS-1 and PHS-2
-

Source Tissue

EC Number Source Tissue Comment Organism Textmining
1.14.99.1 embryo
-
Oryctolagus cuniculus
-

Synonyms

EC Number Synonyms Comment Organism
1.14.99.1 PHS
-
Oryctolagus cuniculus
1.14.99.1 prostaglandin H synthase
-
Oryctolagus cuniculus

General Information

EC Number General Information Comment Organism
1.14.99.1 additional information PHS is involved in the mechanism of thalidomide to cause increased embryonic DNA oxidation measured as 8-oxoguanine leading to embryopathies, phenotype, overview. A prostaglandin H synthase-dependent, reactive oxygen species-mediated mechanism. Thalidomide teratogenicity was blocked by maternal pretreatment with acetylsalicylic acid, an irreversible inhibitor of prostaglandin H synthase Oryctolagus cuniculus