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Vitamin K is essential for blood clotting but must be enzymatically activated. Additionally we are shipping VKORC1 Antibodies (28) and VKORC1 Kits (14) and many more products for this protein.
Showing 4 out of 4 products:
results suggest that the VKORC1 gene rs7294 polymorphism is important for the development of essential hypertension
both vIL-6 and VKORC1v2 interact with calnexin cycle proteins UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1), which catalyzes monoglucosylation of N-glycans, and oppositely acting glucosidase II (GlucII), and that vIL-6 can promote protein folding.
Patients with non-variceal upper gastrointestinal bleeding caused by the use of NSAID or low dose aspirin are more frequent carriers of the VKORC1-1639 G>A polymorphism.
Our results supported an enzyme activating role for rs56314408C of VKORC1 while rs9923231G>A had no evidence of being functional
Polymorphisms in VKORC1 partially affected daily warfarin dosage requirements. VKORC1 genotype and height are the primary determinants influencing warfarin dosage in Japanese pediatric patients.
VKORC polymorphism affects PC dosage in the initiation as well as the maintenance phase. High rates of bleeding complications and thromboembolic events were found at the beginning of PC therapy in VAD (show KCTD1 Proteins) patients.
Genetic variants of CYP2C9 (show CYP2C9 Proteins)/VKORC1 and age are significant determinants of the maintenance dose of warfarin in patients with atrial fibrillation/valve replacement.
The Arg98Trp mutation disrupts an ER retention motif of VKORC1 leading to mislocalisation of the protein to outside the endoplasmatic reticulum. In this review, we summarize the clinical data, diagnosis, therapy and molecular pathomechanism of VKCFD2.
Possession of CYP2C9 (show CYP2C9 Proteins)*2 and/or CYP2C9 (show CYP2C9 Proteins)*3 allele variants is associated with lower time of international normalized ratio (INR (show INSR Proteins)) in the therapeutic range (TTR (show TTR Proteins)) 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 Proteins) *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.
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