Abcam, ab266558, Human APEX2 knockout HEK-293T cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
APEX2 KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 17 bp deletion in exon 1. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 17 bp deletion in exon 1

Product details:
We will provide viable cells that proliferate on revival.
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-APEX2, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
APEX2 also known as apurinic/apyrimidinic endodeoxyribonuclease 2 is a protein that plays a critical role in DNA repair and maintenance. Weighing approximately 60 kDa APEX2 functions by resolving abasic sites in DNA which are common lesions that occur spontaneously or due to oxidative stress. This process is essential to prevent DNA strand breaks and maintain genomic stability. APEX2 is expressed ubiquitously in human tissues with a higher concentration noted in immune cells which suggests its involvement in regulating cellular responses under oxidative stress conditions.
Biological function summary
APEX2 maintains genomic integrity by participating in the base excision repair (BER) pathway where it acts on AP sites facilitating proper DNA repair. It does not function alone but often interacts with other proteins involved in this pathway forming a highly efficient complex. These interactions ensure the correct processing of damaged DNA allowing cells to preserve their genomic content effectively. APEX2's mediation of DNA repair contributes significantly to cell survival and response to DNA-damaging agents.
Pathways
APEX2 finds important roles in the DNA damage response mechanism and oxidative stress response pathways. It collaborates with proteins like XRCC1 and DNA polymerase beta in the BER pathway to safeguard genetic information. These interactions underline its importance in the repair mechanism ensuring accuracy and efficiency in correcting DNA errors. This coordination of pathways highlights APEX2's function in controlling cellular oxidative stress response and maintaining cellular homeostasis.
Defects or dysregulation in APEX2 activity have associations with cancer and neurodegenerative disorders. Altered APEX2 levels can lead to inadequate DNA repair resulting in increased mutations that contribute to oncogenesis. Additionally proteins like p53 which regulate cell cycle and apoptosis also interact with APEX2 highlighting its role in tumor suppression. Furthermore impaired DNA repair due to APEX2 dysregulation can escalate oxidative damage in neurons exacerbating conditions like Alzheimer's disease. Understanding these connections is important for exploring potential therapeutic approaches targeting the DNA repair machinery.