EC Number |
General Information |
Reference |
---|
5.3.99.5 | malfunction |
enzyme inhibition induces cell death in vitro. Selective TXS inhibition significantly reduces tumour cell growth and increases apoptosis, while TXS overexpression stimulates cell proliferation and invasiveness, and is protective against apoptosis, quantification of multi-parameter apoptosis signalling, overview |
728292 |
5.3.99.5 | malfunction |
inhibition of thromboxane synthase induces lung cancer cell death via increasing the nuclear p27 |
703584 |
5.3.99.5 | more |
role of membranes in modulating the thermodynamics and kinetics of enzyme substrate binding, redox potential of enzyme incorporated into lipid bilayers of nanodiscs, overview. Binding of substrate to the enzyme can induce conformational changes in the protein that block small-molecule ligand egress |
727320 |
5.3.99.5 | more |
the adaptive active site in the enzyme might be capable of binding multiple ligands simultaneously because of its large size and flexibility. Ligand and substrate binding structure, competitive binding experiments with Nile Red, a fluorescence dye, and 2-p-toluidinylnaphthalene-6-sulfonic acid, and the computer-simulated TXAS structure with clotrimazole as a heme ligand, molecular dynamics simulations of clotrimazole and 2-p-toluidinylnaphthalene-6-sulfonic acid-docking enzyme, overview |
727012 |
5.3.99.5 | physiological function |
the enzyme is a membrane-associated cytochrome P450 that metabolizes the cyclooxygenase product prostaglandin into thromboxane A2, a potent inducer of vasoconstriction and platelet aggregation |
727320 |
5.3.99.5 | physiological function |
thromboxane synthase metabolises prostaglandin H2 into thromboxanes, which are biologically active on cancer cells. TXS overexpression occurs in a range of cancers, and associated with a poor prognosis, although in non-small lung cancer cells, no significant correlation with patient survival is observed |
728292 |