Abcam, ab264785, Human VKORC1 knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
VKORC1 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 16 bp deletion in exon 1. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 16 bp deletion in exon 1,
Disease:Adenocarcinoma

Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant 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, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°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.