The APEX2 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the APEX2 gene in a HeLa host background. This knockout model is provided as a heterogeneous pool of edited cells, enabling interrogation of APEX2 loss within a genetically tractable human cell line. The gene-edited population serves as a versatile tool for base excision repair mechanisms, oxidative stress responses, synthetic lethality interactions, and as a control for APEX2-dependent proximity labeling experiments.
The host HeLa cell line is an HPV18-positive cervical adenocarcinoma epithelial line derived from Henrietta Lacks in 1951. This widely used cell model exhibits high proliferative capacity and metastatic potential, suitable for cancer biology research. HeLa cells maintain active DNA damage response pathways and are commonly employed to study DNA repair, genome instability, and chemotherapeutic sensitivity. Their well-characterized nature and experimental amenability provide a solid foundation for gene disruption and pathway analysis.
APEX2 (apurinic/apyrimidinic endodeoxyribonuclease 2) is a multifunctional enzyme that acts in DNA base excision repair by cleaving at abasic sites, generating 3??-hydroxyl and 5??-deoxyribose phosphate termini. Single-strand breaks are processed by polymerase beta (POLB) and ligated by LIG3/XRCC1. APEX2 also has RNA endonuclease activity and contributes to oxidative DNA damage resistance. The gene is transcriptionally regulated by NRF2 and E2F1, and its protein interacts with XRCC1, POLB, LIG3, PCNA, and PARP1. Within the base excision repair network, APEX2 functions alongside APEX1, OGG1, NEIL1, and TDG to preserve genomic integrity.
Disruption of APEX2 in HeLa cells provides a system to dissect its DNA repair and stress tolerance roles in cervical cancer. Given HeLa??s proliferative and metastatic phenotype, the knockout population can be used to explore APEX2-dependent repair under genotoxins like hydrogen peroxide or methyl methanesulfonate. This model facilitates synthetic lethality screens to identify vulnerabilities upon APEX2 loss, potentially informing therapeutic strategies for DNA repair-defective tumors. The polyclonal population allows assessment of functional consequences without clonal bias.
This polyclonal knockout product suits experimental workflows including western blotting, RT-qPCR, comet and ??H2AX immunofluorescence assays for DNA damage evaluation, and H2O2 or MMS sensitivity assays for oxidative stress. It can also serve as a negative control in APEX2 proximity labeling experiments. Researchers in DNA repair, chemoresistance, or synthetic lethal therapies will find this model robust and cost-effective. For further details or custom inquiries, contact Ascent Research.
