Enables vitamin-K-epoxide reductase (warfarin-insensitive) activity. Contributes to vitamin-K-epoxide reductase (warfarin-sensitive) activity. Involved in regulation of blood coagulation and response to organic cyclic compound. Predicted to be located in endoplasmic reticulum. Predicted to be active in endoplasmic reticulum membrane. Used to study warfarin sensitivity. Human ortholog(s) of this gene implicated in combined deficiency of vitamin K-dependent clotting factors 2 and warfarin resistance. Orthologous to human VKORC1 (vitamin K epoxide reductase complex subunit 1); PARTICIPATES IN acenocoumarol pharmacodynamics pathway; alteplase pharmacodynamics pathway; aminocaproic acid pharmacodynamics pathway; INTERACTS WITH (+)-schisandrin B; 17alpha-ethynylestradiol; 2,3,7,8-tetrachlorodibenzodioxine.
[VKORC1 protein results in increased reduction of vitamin K1 oxide] which results in increased carboxylation of and results in increased activity of F9 protein more ...
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in increased expression of VKORC1 mRNA and [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of VKORC1 mRNA
VKORC1 promoter polymorphism results in decreased susceptibility to Acenocoumarol and VKORC1 protein polymorphism results in decreased susceptibility to Acenocoumarol
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in increased expression of VKORC1 mRNA
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of VKORC1 mRNA
coumachlor inhibits the reaction [VKORC1 protein results in increased reduction of Vitamin K 1] and coumachlor inhibits the reaction [VKORC1 protein results in increased reduction of vitamin K1 oxide]
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in increased expression of VKORC1 mRNA and [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of VKORC1 mRNA
VKORC1 protein mutant form results in decreased susceptibility to difenacoum and VKORC1 protein polymorphism results in decreased susceptibility to difenacoum
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of VKORC1 mRNA
fluindione inhibits the reaction [VKORC1 protein results in increased reduction of Vitamin K 1] and fluindione inhibits the reaction [VKORC1 protein results in increased reduction of vitamin K1 oxide]
[INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol A] results in increased expression of VKORC1 mRNA and [INS protein co-treated with Dexamethasone co-treated with 1-Methyl-3-isobutylxanthine co-treated with Indomethacin co-treated with bisphenol F] results in increased expression of VKORC1 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of VKORC1 mRNA
[NOG protein co-treated with Valproic Acid co-treated with dorsomorphin co-treated with 4-(5-benzo(1 and 3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide] results in increased expression of VKORC1 mRNA
[VKORC1 protein results in increased reduction of vitamin K1 oxide] which results in increased carboxylation of and results in increased activity of F9 protein more ...
VKORC1 gene mutant form results in decreased susceptibility to Warfarin and VKORC1 protein polymorphism results in decreased susceptibility to Warfarin
VKORC1 gene mutant form results in decreased susceptibility to Warfarin and VKORC1 protein polymorphism results in decreased susceptibility to Warfarin
The inhibitory effect of calumenin on the vitamin K-dependent gamma-carboxylation system. Characterization of the system in normal and warfarin-resistant rats.
Engineering of a recombinant vitamin K-dependent gamma-carboxylation system with enhanced gamma-carboxyglutamic acid forming capacity: evidence for a functional CXXC redox center in the system.
mutations of the human homolog are detected in individuals with combined deficiency of Vitamin K-dependent clotting factors type 2 (VKCFD2) and warfarin resistance (WR)
