APEX2 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 17 bp deletion in exon 1.
AP endonuclease 2, AP endonuclease XTH2, APE 2, APEX L2, APEX nuclease (apurinic/apyrimidinic endonuclease) 2, APEX nuclease 2, APEX nuclease-like 2, APEX2_HUMAN, Apurinic-apyrimidinic endonuclease 2, Apurinic/apyrimidinic endonuclease 2, Apurinic/apyrimidinic endonuclease like 2, C430040P13Rik, DNA apurinic or apyrimidinic site lyase 2, DNA-(apurinic or apyrimidinic site) lyase 2, EC 4.2.99.18, OTTHUMP00000023390, OTTHUMP00000061908, XTH 2, ZGRF2, Zinc finger GRF type containing 2
APEX2 KO cell line available to order. Free of charge wild type control provided. Knockout achieved by using CRISPR/Cas9, Homozygous: 17 bp deletion in exon 1.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
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 and patent pages.
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.
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.
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.
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Homozygous: 17 bp deletion in exon 1
Sequencing chromatogram displaying sequence edit in exon 1
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