1.14.15.3 (E)-N'-(4-butyl-2-methylphenyl)-N-hydroxyformimidamide HET0016, almost completely abolishes hypotonic solutions- or 2,4,6-trinitrophenol-induced enhancement of receptor-activated cationic current I(TRPC6) 26997 1.14.15.3 (E)-N'-(4-butyl-2-methylphenyl)-N-hydroxyformimidamide HET0016, diminishes TRPC6-like channel activity in myocytes 26997 1.14.15.3 1,1-dichloroethene 50% of BMO activity is irreversibly lost after oxidation of approximately 25 nmol/mg protein 135253 1.14.15.3 1,2-cis-dichloroethene 50% of BMO activity is lost after oxidation of 120 nmol/mg protein 135251 1.14.15.3 1,2-trans-dichloroethene 50% of BMO activity is lost after oxidation of 20 nmol/mg protein 135252 1.14.15.3 1,7-octadiyne inhibits oxidation of methyl tert-butyl ether; putative mechanism-based inactivator, strongly inhibitory at 0.1% (v/v) 56837 1.14.15.3 1-octyne acts as a mechanism-based inhibitor of AlkB 174800 1.14.15.3 1-octyne irreversible inhibition, oxidation product hexylketene or its equivalent, covalently binds to AlkB 174800 1.14.15.3 11-dodecynoic acid completely inhibited lauric acid omega-hydroxylation 32016 1.14.15.3 17-octadecynoic acid almost completely abolishes hypotonic solutions- or 2,4,6-trinitrophenol-induced enhancement of receptor-activated cationic current I(TRPC6) 39698 1.14.15.3 17-octadecynoic acid irreversible CYP omega-hydroxylase inhibitor, significantly inhibits myocardial apoptosis 39698 1.14.15.3 8-hydroxyquinoline 1 mM, 2 min 100% inhibition 321 1.14.15.3 8-hydroxyquinoline no inhibition 321 1.14.15.3 Ca2+ - 15 1.14.15.3 CO 50 : 50 100% inhibition, 10 : 90 91% inhibition 176 1.14.15.3 CO - 176 1.14.15.3 Co2+ - 23 1.14.15.3 Cu2+ 0.1 mM concentration, 100% inhibition 19 1.14.15.3 Cu2+ - 19 1.14.15.3 diethyldithiocarbamate reduces activity to 88% 373 1.14.15.3 EDTA - 21 1.14.15.3 Fe2+ in 0.5 mM concentration, 100% inhibition 25 1.14.15.3 Hg2+ 0.1 mM concentration, 100% inhibition 33 1.14.15.3 KCN 1 mM, 2 min 32% inhibition 161 1.14.15.3 KCN reversible inhibitor 161 1.14.15.3 KCN - 161 1.14.15.3 menadione - 240 1.14.15.3 Mg2+ - 6 1.14.15.3 Mn2+ - 11 1.14.15.3 additional information no effect: FAD and FMN 2 1.14.15.3 additional information no inhibition by metyrapone 2 1.14.15.3 n-alkanes C5-C10 inhibits oxidation of methyl tert-butyl ether, weaker inhibition at longer chain length 124965 1.14.15.3 n-butane inhibits oxidation of methyl tert-butyl ether 13739 1.14.15.3 n-decane 0.1% (v/v) 138675 1.14.15.3 n-decyl-beta-D-maltopyranoside - 174801 1.14.15.3 n-dodecane 0.1% (v/v) 34753 1.14.15.3 n-dodecyl-beta-D-maltopyranoside - 174802 1.14.15.3 n-dodecyl-N,N-dimethylamine-n-oxide - 36294 1.14.15.3 n-heptane 0.1% (v/v) 17952 1.14.15.3 n-hexane 0.1% (v/v) 14171 1.14.15.3 N-hydroxy-N'-(4-n-butyl-2-methylphenyl)formamidine HET0016, a potent and selective inhibitor of CYP omega-hydroxylase, significantly inhibits myocardial apoptosis. Pretreatment with PD98059, the inhibitor of ERK1/2, but not SB203580 or SP600125, almost completely blocks the effect exerted by HET0016. Exogenous 20-hydroxyeicosatetraenoic acid administration exerts opposite effects 155127 1.14.15.3 N-methylsulfonyl-12, 12-dibromododec-11-enamide a selective CYP omega-hydroxylase inhibitor, significantly inhibits myocardial apoptosis 155126 1.14.15.3 N-methylsulfonyl-12,12-dibromododec-11-enamide 0.4 mg/kg, significant inhibition 62193 1.14.15.3 N-methylsulfonyl-12,12-dibromododec-11-enamide specific inhibitor, results in an increased phenylephrine-induced tension 62193 1.14.15.3 n-nonane 0.1% (v/v) 138674 1.14.15.3 n-octane 0.1% (v/v) 32341 1.14.15.3 n-pentane 0.1% (v/v) 138673 1.14.15.3 Ni2+ - 38 1.14.15.3 octyl glucose neopentyl glycol - 161709 1.14.15.3 p-chloromercuribenzoate 0.1 mM concentration, 51% inhibition 43 1.14.15.3 Pb2+ - 139 1.14.15.3 propane inhibits oxidation of methyl tert-butyl ether 7275 1.14.15.3 propionate 0.01 mM, strong inhibition 312 1.14.15.3 retinoic acid 0.005 mM, 56% reduction of activity 2354 1.14.15.3 Zn2+ - 14