The ASCC3 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, engineered to disrupt the ASCC3 gene. This product provides a loss-of-function model for investigating the roles of ASCC3 in DNA repair, transcription regulation, and cellular responses to genotoxic stress. The polyclonal format represents a heterogeneous pool of edited cells, offering a robust system for functional studies without clonal selection biases.
HeLa cells are an immortalized human epithelial cell line originating from a cervical adenocarcinoma associated with human papillomavirus 18 (HPV18). These cells exhibit rapid proliferation and have been instrumental in numerous areas of biomedical research, including cancer biology, virology, and DNA damage response. Their well-characterized genetic background and susceptibility to various stressors make them an ideal host for generating ASCC3 knockout models to study DNA repair pathways in a cancer-relevant context.
ASCC3 encodes a DNA helicase that functions as a core component of the Activating Signal Co-integrator Complex (ASCC), which includes ASCC1, ASCC2, and TRIP4. This complex is activated by DNA damage signals and ATM/ATR kinases, and it plays a critical role in transcription-coupled nucleotide excision repair and the resolution of alkylation damage. ASCC3 unwinds DNA at sites of transcription-blocking lesions, facilitating repair completion and subsequent transcription resumption. The ASCC complex interacts with RNA polymerase II and components of the ubiquitin system, linking DNA repair to RNA processing. Dysregulation of ASCC3 can lead to persistent DNA damage, increased sensitivity to alkylating agents, and may contribute to neurodegenerative disorders and cancer progression.
In the HeLa cell background, which retains HPV18 E6/E7 oncoproteins that impair p53 and Rb pathways, ablation of ASCC3 may exacerbate genomic instability and alter chemosensitivity. This model provides a powerful tool to dissect the interplay between viral oncogenesis and DNA repair deficiencies. By studying ASCC3 knockout in this system, researchers can gain insights into how cervical adenocarcinoma cells cope with alkylation damage and how the ASCC complex maintains transcriptional integrity under genotoxic stress, potentially informing therapeutic strategies for HPV-associated cancers.
These polyclonal knockout cells are suitable for a wide range of experimental approaches, including Western blotting and RT-qPCR to confirm ASCC3 disruption and downstream effects, immunofluorescence to visualize DNA damage markers such as ??H2AX foci, and comet assays to assess DNA fragmentation. Cell viability assays with alkylating agents can evaluate chemosensitivity, while co-immunoprecipitation studies can explore protein interactions within the ASCC complex. This model also enables functional investigations into transcription-coupled repair mechanisms and the role of the ASCC complex in neurodegenerative disease pathways. For further details or to discuss your specific research needs, please contact Ascent Research.
