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Vitamin K is essential for blood clotting but must be enzymatically activated. Zusätzlich bieten wir Ihnen VKORC1 Antikörper (28) und VKORC1 Proteine (4) und viele weitere Produktgruppen zu diesem Protein an.
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both vIL (zeige VIL1 ELISA Kits)-6 and VKORC1v2 interact with calnexin (zeige CANX ELISA Kits) cycle proteins UDP-glucose:glycoprotein glucosyltransferase 1 (UGGT1 (zeige UGGT1 ELISA Kits)), which catalyzes monoglucosylation of N-glycans, and oppositely acting glucosidase II (GlucII), and that vIL (zeige VIL1 ELISA Kits)-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 (zeige KCTD1 ELISA Kits) patients.
Genetic variants of CYP2C9 (zeige CYP2C9 ELISA Kits)/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 (zeige CYP2C9 ELISA Kits)*2 and/or CYP2C9 (zeige CYP2C9 ELISA Kits)*3 allele variants is associated with lower time of international normalized ratio (INR (zeige INSR ELISA Kits)) in the therapeutic range (TTR (zeige TTR ELISA Kits)) values and warfarin dose variations in aortic valve replacement patients, the latter affected also by VKORC1 c.-1693G>A polymorphism
Three SNPs (CYP2C9 (zeige CYP2C9 ELISA Kits) *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 (zeige CYP2C9 ELISA Kits) (rs1799853 and rs1057910) genes.
quantified mRNA levels for VKORC1, VKORC1L1, GGCX (zeige GGCX ELISA Kits), and NQO1 (zeige NQO1 ELISA Kits) and measured VKOR enzymatic activities in 29 different tissues
OCN is gamma-carboxylated by the gamma-carboxylase (GGCX (zeige GGCX ELISA Kits)) 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