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BRAND / VENDOR: Abcam

Abcam, ab258282, Human VKORC1 knockout HEK-293T cell lysate

CATALOG NUMBER: ab258282
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Product Description

Size: 1Kit
VKORC1 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1 and 20 bp deletion in exon1.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp insertion in exon1 and 20 bp deletion in exon1.

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-VKORC1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Vitamin K epoxide reductase complex subunit 1 (VKORC1) also known as VKOR is an enzyme that plays an important role in the vitamin K cycle. This enzyme has a molecular mass of approximately 18 kDa. VKORC1 helps in reducing vitamin K 23-epoxide to its active hydroquinone form which is necessary for the gamma-carboxylation of vitamin K-dependent proteins. These proteins are mainly responsible for blood coagulation. VKORC1 expression is high in the liver where much of the synthesis of clotting factors occurs.
Biological function summary
VKORC1 is integral to the vitamin K cycle an essential process for activating vitamin K-dependent clotting factors. It operates within a complex with its protein partner VKORC1-like 1 (VKORC1L1). This partnership is important for maintaining effective blood coagulation. The active form of vitamin K produced by VKORC1 ensures the activity of several blood clotting factors especially factors II VII IX and X. Without proper function of VKORC1 these factors would remain inactive.
Pathways
The vitamin K cycle is where VKORC1 makes a significant impact and this cycle is vital for blood coagulation processes. Specifically VKORC1 reduces vitamin K epoxide working closely with gamma-glutamyl carboxylase (GGCX) another enzyme that modifies the glutamic acid residues on clotting factors. This modification is important for their proper functioning within the coagulation cascade. The interplay between VKORC1 and GGCX directly connects to the synthesis of active blood coagulation proteins.
VKORC1 mutations are notably linked to warfarin resistance and susceptibility to bleeding disorders. Warfarin is an anticoagulant that targets VKORC1 to prevent clot formation and variations in this protein can lead to altered drug response. Furthermore any dysfunction in VKORC1 may result in vitamin K epoxide reductase deficiency affecting coagulation and leading to increased bleeding risk. Mutations could also affect partner proteins like coagulation factors II and VII leading to disorders related to abnormal blood clotting processes.


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