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Vitamin K is essential for blood clotting but must be enzymatically activated. Additionally we are shipping VKORC1 Kits (8) and VKORC1 Proteins (4) and many more products for this protein.
Showing 10 out of 27 products:
Human Polyclonal VKORC1 Primary Antibody for EIA, IHC (fro) - ABIN493558
Li, Chang, Jin, Lin, Khvorova, Stafford: Identification of the gene for vitamin K epoxide reductase. in Nature 2004
Show all 3 references for ABIN493558
Human Polyclonal VKORC1 Primary Antibody for EIA, IF - ABIN1450145
Oldenburg, Bevans, Müller, Watzka: Vitamin K epoxide reductase complex subunit 1 (VKORC1): the key protein of the vitamin K cycle. in Antioxidants & redox signaling 2006
Possession of CYP2C9 (show CYP2C9 Antibodies)*2 and/or CYP2C9 (show CYP2C9 Antibodies)*3 allele variants is associated with lower time of international normalized ratio (INR (show INSR Antibodies)) in the therapeutic range (TTR (show TTR Antibodies)) values and warfarin dose variations in aortic valve replacement patients, the latter affected also by VKORC1 c.-1693G>A polymorphism
Three SNPs (CYP2C9 (show CYP2C9 Antibodies) *2, *3 and VKORC1 c.-1639G > A) were genotyped by electrochemical detection using a sandwich-type format that included a 3' short thiol capture probe and a 5' ferrocene-labeled signal probe.
Our results show that anticoagulated patients have a high risk of adverse events if they are carriers of 1 or more genetic polymorphisms in the VKORC1 (rs9923231) and CYP2C9 (show CYP2C9 Antibodies) (rs1799853 and rs1057910) genes.
The VKORC1 (-1693 G>A) AA genotype was associated with fewer cases of DVT (odds ratio = 0.435; 95% confidence interval 0.205-0.991; P = .031).
This study provides data on VKORC1 and CYP4F2 (show CYP4F2 Antibodies) 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 Antibodies) interaction can affect warfarin stable dosage.
VKORC1S1639 GG and the wild type CYP2C9 (show CYP2C9 Antibodies)*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
quantified mRNA levels for VKORC1, VKORC1L1, GGCX (show GGCX Antibodies), and NQO1 (show NQO1 Antibodies) and measured VKOR enzymatic activities in 29 different tissues
OCN is gamma-carboxylated by the gamma-carboxylase (GGCX (show GGCX Antibodies)) 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