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Vitamin K is essential for blood clotting but must be enzymatically activated.
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The final regression models for White and Black patients (Fig. 1) included age, weight, prosthetic valves, amiodarone use, CYP2C9 (show CYP2C9 Proteins)*3, and VKORC1 3673 G>A genotypes as covariates, whereas possession of CYP2C9 (show CYP2C9 Proteins)*2 and simvastatin use were retained in the final model for White, but not Black patients.
No relationship between VKORC1 variants and clinical outcomes in elderly patients treated with vitamin K antagonists.
Until the age of 19, weight has a far greater effect on Vitamin K antagonist dosing variation than VKORC1 and CYP2C9 (show CYP2C9 Proteins) polymorphisms. During the age of 20-40years, VKORC1 and CYP2C9 (show CYP2C9 Proteins) polymorphisms play a significant role.
The VKORC1: c.-1639 G>A polymorphism is associated with aneurysms of the ascending aorta.
1639G4A polymorphism of the vitamin K epoxide reductase complex subunit 1 gene (VKORC1) is likely to be a new risk factor of Retinal Vascular Occlusion.
Studied the association of CYP2C9 (show CYP2C9 Proteins)*2 (430C/T), *3 (1075A/C) and VKORC1 (-1639G/A) polymorphisms on warfarin dose requirements in patients post cardiac valve surgery. Found age and presence of CYP2C9 (show CYP2C9 Proteins) *2 allele significantly affect the daily dosage of warfarin during initiation of warfarin therapy after cardiac valve replacement surgery.
The expression of VKOR in benign prostate epithelial cells, along with the association between a functional VKOR SNP and prostate cancer risk, suggests a possible role for VKOR in mediating the effect of warfarin on prostate cancer risk.
analysis of VKORC1 AA-CYP2C9 (show CYP2C9 Proteins)*1*1 genotypes reveals dosing algorithms for vitamin K antagonists
VKORC1 genotype influenced the likelihood of INR (show INSR Proteins) lability during warfarin maintenance in atrial fibrillation patients.
results suggest that the VKORC1 gene rs7294 polymorphism is important for the development of essential hypertension
quantified mRNA levels for VKORC1, VKORC1L1, GGCX (show GGCX Proteins), and NQO1 (show NQO1 Proteins) and measured VKOR enzymatic activities in 29 different tissues
OCN is gamma-carboxylated by the gamma-carboxylase (GGCX (show GGCX Proteins)) on three glutamic acid residues, a cellular process requiring reduction of vitamin K by a second enzyme, VKORC1.
The involvement of VKORC1L1 in VKOR activity partly explains the low susceptibility of some extrahepatic tissues to vitamin K antagonists.
molecular cloning [VKORC1]
The genetic basis for resistance to anticoagulants lies in mutations in Vkorc1.
An analysis of novel mutations show that the VKORC1 gene is the main target for spontaneous mutations conferring warfarin resistance.
Each VKORC1 T-allele present in patients from the Rotterdam anticoagulation therapy study is shown to decrease the required acenocoumarol dosage by 5.1 mg/week.
Vitamin K is essential for blood clotting but must be enzymatically activated. This enzymatically activated form of vitamin K is a reduced form required for the carboxylation of glutamic acid residues in some blood-clotting proteins. The product of this gene encodes the enzyme that is responsible for reducing vitamin K 2,3-epoxide to the enzymatically activated form. Fatal bleeding can be caused by vitamin K deficiency and by the vitamin K antagonist warfarin, and it is the product of this gene that is sensitive to warfarin. In humans, mutations in this gene can be associated with deficiencies in vitamin-K-dependent clotting factors and, in humans and rats, with warfarin resistance. Two pseudogenes have been identified on chromosome 1 and the X chromosome. Two alternatively spliced transcripts encoding different isoforms have been described.
phylloquinone epoxide reductase
, vitamin K1 epoxide reductase (warfarin-sensitive)
, vitamin K epoxide reductase complex, subunit 1
, vitamin K dependent clotting factors deficiency 2
, vitamin K epoxide reductase complex subunit 1
, vitamin K1 2,3-epoxide reductase subunit 1
, Warfarin resistance