Description
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 exon3 and 1 bp insertion in exon3.,
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, 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-SLC25A13, 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.
The SLC25A13 protein also known as Citrin is a member of the solute carrier family 25 involved in transporting solutes across the mitochondrial membrane. Citrin functions as a calcium-dependent aspartate/glutamate carrier. It is around 67 kDa in mass. Citrin is primarily expressed in the liver heart and pancreas where it facilitates the exchange of metabolites necessary for cellular metabolism. The protein is localized to the inner mitochondrial membrane where it takes part in important cellular processes.
Biological function summary
Citrin plays an important role in the urea cycle gluconeogenesis and lipid metabolism by facilitating the exchange of cytosolic glutamate for mitochondrial aspartate. It operates independently not as part of a larger protein complex. By ensuring the appropriate balance of amino acids and metabolites Citrin contributes to maintaining metabolic homeostasis. The protein's activity supports the liver's function and influences energy production efficiency especially under anabolic conditions.
Pathways
Citrin is integral to the malate-aspartate shuttle and the urea cycle. The malate-aspartate shuttle is involved in transferring reducing equivalents across the mitochondrial membrane which is essential for efficient ATP production. Citrin interacts closely with mitochondrial enzymes like carbamoyl phosphate synthetase I in the urea cycle emphasizing its link to ammonia detoxification. Citrin's transport activity indirectly supports the function of other mitochondrial carriers including SLC25A12 and SLC25A11 by maintaining the requisite balance of substrates required for their processes.
Citrin deficiency is associated with two genetic conditions: Citrullinemia Type II and Neonatal Intrahepatic Cholestasis caused by Citrin Deficiency (NICCD). Both disorders arise from mutations in the SLC25A13 gene and disrupt normal urea cycle function leading to the accumulation of toxic substances like ammonia. Citrin's interaction with proteins involved in amino acid metabolism including SLC25A15 (ornithine transporter) highlights its role in maintaining nitrogen balance. Understanding Citrin's activity can aid in diagnosing and treating metabolic disorders linked to urea cycle dysfunction.
