Abcam, ab257221, Human IDH1 knockout HeLa cell lysate

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IDH1 KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: Insertion of the selection cassette in exon 4.
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, Homozygous: Insertion of the selection cassette in exon 4.,
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-IDH1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, 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.
IDH1 also known as isocitrate dehydrogenase 1 is an enzyme with a molecular weight of approximately 45 kDa. It participates in the citric acid cycle aiding the conversion of isocitrate to alpha-ketoglutarate while producing NADPH. IDH1 resides primarily in the cytoplasm and peroxisomes of cells. It finds expression in various tissues most notably the liver and brain where metabolic processes are highly active.
Biological function summary
Isocitrate dehydrogenase 1 plays an important role in cellular metabolism by helping to maintain the NADP+/NADPH balance important for redox reactions. This enzyme operates mainly as a homodimer meaning two identical subunits form a complex for functional activity. It contributes significantly to lipid and glucose metabolism due to its production of NADPH which the cells use for biosynthetic pathways and detoxification.
Pathways
The involvement of IDH1 in the citric acid cycle highlights its importance in energy production and metabolic regulation. This enzyme closely associates with other metabolic enzymes such as IDH2 another member of the isocitrate dehydrogenase family found in mitochondria suggesting a coordinated function between cytoplasmic and mitochondrial metabolism. Beyond its role in the citric acid cycle IDH1 also relates to the pentose phosphate pathway an alternative glucose metabolism route providing reducing equivalents and ribose 5-phosphate for nucleotide synthesis.
IDH1 mutations particularly the IDH1 R132H variant frequently appear in certain cancers like gliomas and acute myeloid leukemia (AML). These mutations lead to a neomorphic enzyme function producing 2-hydroxyglutarate instead of alpha-ketoglutarate disrupting normal cellular metabolism and aiding tumorigenesis. The mutated IDH1 also affects the TET2 protein which involves in DNA demethylation potentially altering gene expression and contributing to oncogenic pathways.