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BRAND / VENDOR: Abcam

Abcam, ab257180, Human CPT2 knockout HeLa cell lysate

CATALOG NUMBER: ab257180
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Product Description

Size: 1Kit
CPT2 KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon1 and 2 bp deletion in exon1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon1 and 2 bp deletion in exon1.,
Disease:Adenocarcinoma

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-CPT2, 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.
Carnitine palmitoyltransferase 2 (CPT2) also known as CPT-2 is an enzyme located mainly in the mitochondria of liver muscle and heart tissues. This enzyme has a molecular mass of approximately 68 kDa. CPT2 plays a mechanical role in the transfer of long-chain fatty acids from the cytosol into the mitochondrial matrix completing the process initiated by CPT1 on the outer mitochondrial membrane. CPT2 acts on the inner mitochondrial membrane converting acylcarnitine back into acyl-CoA which is an essential step in beta-oxidation. Expression of CPT2 is higher in tissues with elevated fatty acid oxidation rates.
Biological function summary
CPT2 is integral to the mitochondrial pathway of fatty acid metabolism. It functions as part of the carnitine shuttle system a complex important for the conversion of acylcarnitine to acyl-CoA inside the mitochondria. This role is vital for the full oxidation of long-chain fatty acids. Through its action CPT2 aids in maintaining energy homeostasis and producing ketone bodies especially during periods of fasting or strenuous exercise.
Pathways
CPT2 is involved in both the beta-oxidation and the carnitine shuttle pathways. These pathways facilitate the energy production from fatty acids particularly during states of low carbohydrate availability. CPT2 works closely with CPT1 as both enzymes form the gateway for the entry of long-chain fatty acids into mitochondria. Together with enzymes from the tricarboxylic acid cycle CPT2 helps sustain ATP production under such metabolic conditions.
Defects in CPT2 can lead to disorders like CPT2 deficiency which present with symptoms of muscle weakness and recurrent rhabdomyolysis especially during prolonged fasting or significant exercise. This deficiency can also result in hypoketotic hypoglycemia and liver dysfunction. CPT2-related disorders often involve altered interactions with proteins such as the acyl-CoA dehydrogenases impacting the normal fatty acid oxidation process and causing metabolic disturbances.


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