Abcam, ab257197, Human IDE (Insulin degrading enzyme) knockout HeLa cell lysate

Size: 1Kit
IDE KO cell lysate available now. KO validated by Western blot. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, Homozygous: 4 bp deletion in exon 14.
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: 4 bp deletion in exon 14.,
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-IDE, 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.
Insulin degrading enzyme (IDE) also known as insulinase is a zinc metalloprotease involved in the breakdown of small proteins including insulin. IDE has a molecular weight of approximately 110 kDa. It works by cleaving the peptide bonds of its substrate proteins therefore decreasing their molecular integrity. IDE is expressed in several tissues including the liver muscle and kidney where it plays a significant role in regulating metabolic processes. This protein can be found both within cells and in the extracellular space.
Biological function summary
IDE manages the levels of insulin and other peptides by degrading them preventing accumulation and maintaining homeostasis. It is not part of a complex but it acts individually in cellular environments to modulate the concentration of its substrates. IDE is important for controlling insulin availability and turnover which impacts glucose metabolism. By influencing the degradation of insulin IDE aids in balancing metabolic demands with insulin availability.
Pathways
IDE plays a vital role in insulin signaling and glucose metabolic processes. It is directly involved in the insulin signaling pathway by regulating insulin levels which consequently affects cellular responses to insulin. IDE connects with several proteins associated with these pathways including insulin receptor and glucose transporters ensuring proper cell signaling and metabolic functions. By modulating insulin levels IDE helps optimize glucose uptake and storage.
IDE has a relevant connection to Alzheimer's disease and type 2 diabetes. Its role in insulin degradation links it to type 2 diabetes where dysregulation of insulin levels can exacerbate the disease. IDE is also associated with Alzheimer's disease since it degrades amyloid-beta peptides. Any malfunction or altered expression of IDE can lead to accumulation of these peptides contributing to Alzheimer's pathology. In the context of these diseases IDE interacts with amyloid-beta precursor protein and components of insulin signaling pathways highlighting its significance in maintaining health and preventing disease progression.