The APOBEC3A Knockout Ca Ski Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human cervical carcinoma Ca Ski cell line. This product provides a loss-of-function model for APOBEC3A, generated via CRISPR/Cas9-mediated gene disruption, enabling detailed investigation of innate antiviral immunity and viral restriction mechanisms without altering the host cell’s HPV-related background.
The Ca Ski cell line, isolated from a metastatic cervical carcinoma, serves as a well-established model for HPV-associated cervical cancer. These epithelial cells harbor an integrated HPV-16 genome and constitutively express the viral oncoproteins E6 and E7, alongside wild-type p53, providing a physiologically relevant context to investigate viral oncogenesis, host-virus interactions, and tumor suppressor pathways.
APOBEC3A encodes a cytidine deaminase that catalyzes deamination of cytosine to uracil in single-stranded DNA, playing dual roles in antiviral innate immunity and somatic hypermutation. Its expression is potently upregulated by interferon-alpha and interferon-gamma through JAK-STAT signaling downstream of TLR activation. APOBEC3A acts on viral cDNA and host genomic DNA, contributing to viral restriction and mutagenesis. It interacts with APOBEC3G and is targeted by HIV-1 Vif, and its enzymatic activity triggers DNA damage response pathways, linking to the cGAS-STING-TBK1-IRF3 axis and subsequent induction of interferon-stimulated genes (ISGs).
In Ca Ski cells, APOBEC3A knockout disrupts the innate immune response to HPV infection by attenuating interferon-mediated signaling and reducing cytidine deaminase activity. This loss impairs the restriction of viral nucleic acids and diminishes APOBEC3A-driven somatic mutations, potentially altering the DNA damage response landscape. Consequently, the knockout model enables elucidation of APOBEC3A’s contribution to HPV oncogene-driven transformation and the interplay between viral persistence and host genome instability.
This knockout cell population is suitable for diverse experimental applications, including dissecting the role of APOBEC3A in innate antiviral signaling through western blotting, RT-qPCR, and interferon signaling reporter assays. It facilitates investigation of mutation signatures and DNA damage responses using mutation analysis and DNA damage assays. Furthermore, the model supports cancer immunotherapy research by enabling co-culture and flow cytometry-based immune cell activation studies, and allows examination of APOBEC3A interactions via co-immunoprecipitation. For technical inquiries, please contact Ascent Research.
