Abcam, ab258017, Human KHK (ketohexokinase) knockout HEK-293T cell lysate

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KHK KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon5.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon5.

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 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-KHK, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, 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.
Ketohexokinase also known as KHK or fructokinase is an enzyme that catalyzes the phosphorylation of fructose to fructose-1-phosphate utilizing ATP in the process. This enzyme has two isoforms: KHK-C and KHK-A with the cytosolic form (KHK-C) being approximately 35 kDa in mass. KHK is expressed at high levels in the liver kidney cortex and small intestine showing its importance for fructose metabolism in these tissues. The liver in particular exhibits extensive expression which facilitates the initial step in fructose metabolism.
Biological function summary
Ketohexokinase plays a significant role in the initial stage of fructose metabolism by converting fructose to fructose-1-phosphate. This reaction is a part of the fructose metabolic pathway enabling the use of fructose as an energy source especially in hepatocytes. KHK operates as a monomer and does not form part of any larger protein complex. The enzyme importantly controls the rate of fructose utilization preventing accumulation of free fructose which could lead to metabolic issues.
Pathways
Ketohexokinase belongs to the fructose metabolism pathway which is a subset of the larger carbohydrate metabolism. This enzyme's product fructose-1-phosphate subsequently interacts with aldolase B which is involved in further steps of the glycolysis and gluconeogenesis pathways. Besides aldolase B ketohexokinase's activity influences the balance between fructose and glucose metabolism connecting fructolysis with glycolytic and gluconeogenic pathways.
Dysfunction of ketohexokinase has been linked to hereditary fructose intolerance a condition resulting from a deficiency of aldolase B where the accumulation of fructose-1-phosphate can cause liver damage and hypoglycemia. KHK has also been implicated in metabolic syndrome where excessive fructose consumption exacerbates conditions like insulin resistance and fatty liver disease. The relationship of KHK with metabolic syndrome highlights its interaction with insulin pathways which involves proteins such as insulin receptor substrates that are affected by altered fructose metabolism.