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Vitamin K is essential for blood clotting but must be enzymatically activated. Additionally we are shipping VKORC1 Antibodies (27) and VKORC1 Kits (7) and many more products for this protein.
Showing 4 out of 4 products:
This study provides data on VKORC1 and CYP4F2 variants among an indigenous Ghanaian population. In a multivariate analysis, duration of Ghanaian patients on warfarin therapy and VKORC1 gene was associated with warfarin dose classification.
Obtained results suggested that VKORC1 -1639A allele can be a possible genetic risk factor for IS in Ukrainian population.
VKORC1-CYP2C9 (show CYP2C9 Proteins) interaction can affect warfarin stable dosage.
VKORC1S1639 GG and the wild type CYP2C9 (show CYP2C9 Proteins)*1*1genotypes are associated with the high-dose requirement for warfarin therapy.
A protein homology model of human VKORC1 was constructed to elucidate the binding modes of vitamin K 2,3-epoxide, R-warfarin, & S-warfarin in wild-type & mutant VKORC1 enzymes. Structural analysis of each model in conjunction with automated in-silico docking, provided a mechanism that explains warfarin resistance associated with the Val66Met & other VKORC1 polymorphisms.
This study explored the correlations of VKORC1-1639 G/A, 1173 C/T and 497 T/G genetic polymorphisms with warfarin maintenance dose requirement in patients undergoing cardiac valve
we identified differences in the frequency distribution in the Tibetan population located in the ALOX5 (show ALOX5 Proteins) , VKORC1 and PTGS2 (show PTGS2 Proteins) genes
Our meta-analysis provides strong evidence that two SNPs in the VKORC1 gene, rs2359612 and rs9923231, contribute to the risk of cardiovascular and cerebrovascular diseases.
ESR1 (show ESR1 Proteins) and VKORC1 single nucleotide polymorphisms were used to determine the vitamin K dosage in patients with ulcer-related hemorrhage.
In this study, we investigated two VKORC1 gene polymorphisms, -1639G/A and 1173C/T, for effects on warfarin maintenance dosage in valvular heart disease (VHD) patients
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