Abcam, ab258272, Human UNG knockout HeLa cell lysate

Size: 1Kit
UNG KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon1 and Insertion of the selection cassette in exon1.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 2 bp deletion in exon1 and Insertion of the selection cassette 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, 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-UNG, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, 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.
UNG which stands for Uracil-DNA glycosylase is an enzyme that functions mechanically to remove uracil from DNA. This preventive action is necessary because uracil can result from the deamination of cytosine or due to misincorporation during DNA replication. UNG exhibits a mass of approximately 33 kDa and shows expression in various tissues underlining its importance across different cellular environments. UNG is ubiquitously expressed but displays higher activity in proliferating cells making it integral during cell division.
Biological function summary
URACIL-DNA glycosylase engages in base excision repair (BER) an important DNA repair process. This enzyme initiates the repair by excising uracil bases creating an abasic site subsequently processed by other repair proteins. UNG actively functions within single-enzymatic action but also associates with various DNA repair complexes highlighting its multifaceted role in genome maintenance. It guards against mutations by maintaining DNA integrity reducing the risk errors pose to genetic stability.
Pathways
UNG plays a role in DNA repair and cell cycle pathways contributing essential actions to genomic stability and cell proliferation. Specifically it integrates into the base excision repair pathway working alongside other proteins like APEX1 and DNA polymerase beta to ensure proper repair of damaged DNA. These related proteins cooperate to fix abasic sites that arise after UNG's glycosylase activity ensuring that genetic information remains accurate and undamaged as cells replicate.
Mutations in UNG can present increased susceptibility to immunodeficiency and cancer. One such disorder includes hyper-IgM syndrome a condition where BER defects lead to an impaired immune response. Proteins like CD40 and CD40L intersect with UNG-related pathways impacting germinal center reactions and immunoglobulin isotype switching. The enzyme's dysfunction potentially contributes to the accumulation of genetic errors fostering oncogenesis in several cancers by allowing abnormal cells to escape normal regulatory mechanisms.