The BAX Knockout Ca Ski Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Ca Ski cervical carcinoma line, in which the pro-apoptotic BAX gene has been disrupted. This heterogeneous pool of BAX-deficient cells provides a robust loss-of-function model for investigating apoptosis regulation and therapeutic resistance mechanisms without clonal selection. As a polyclonal population, it captures a diversity of editing events, offering a more averaged biological response suitable for population-level assays and drug screening.
Ca Ski is an epithelial cell line originally isolated from a cervical squamous cell carcinoma metastasis and is characterized by stable integration of the human papillomavirus type-16 (HPV-16) genome. The presence of HPV-16 oncoproteins E6 and E7 leads to functional inactivation of p53 and Rb, respectively, mimicking common features of high-risk HPV-associated malignancies. This genetic background makes Ca Ski an ideal host for studying BAX-dependent apoptotic pathways in the context of viral oncogenesis and the interplay between viral proteins and host apoptotic machinery.
BAX is a core pro-apoptotic member of the Bcl-2 family that resides in the cytosol and, upon activation by cellular stress, undergoes conformational change and translocates to the mitochondrial outer membrane. Upstream regulators such as p53, JNK, and p38 MAPK, along with BH3-only proteins BIM, PUMA, and NOXA, promote BAX activation, whereas anti-apoptotic factors BCL-2, BCL-xL, and MCL-1 bind and sequester BAX to prevent its oligomerization. Once activated, BAX interacts with BAK and VDAC, forming pores that permeabilize the outer membrane, facilitating the release of cytochrome c. This triggers APAF-1-mediated caspase-9 cleavage, which then activates caspase-3, executing the intrinsic apoptotic cascade.
In the Ca Ski cellular environment, BAX knockout abrogates a critical node in mitochondrial apoptosis, potentially conferring resistance to apoptotic stimuli such as chemotherapy or radiation. This model enables dissection of the contributions of BAX versus other apoptotic effectors in a background where p53 is suppressed by HPV-16 E6. It is particularly valuable for examining how viral oncoproteins rewire apoptotic thresholds and for evaluating BH3 mimetics that target anti-apoptotic proteins, as the absence of BAX may reveal alternative death pathways or compensatory mechanisms.
Researchers can employ this cell model for a broad range of functional studies, including apoptosis profiling via Annexin V/PI staining, caspase-3/9 activity assays, and mitochondrial membrane potential measurements. It is suitable for co-immunoprecipitation experiments to probe BCL-2 family interactions, cytochrome c release assays, and drug sensitivity screens for agents like navitoclax or venetoclax. Additional uses include investigating DNA damage response pathways, ischemia-reperfusion injury models, and the role of BAX in neurodegenerative disease mechanisms. For detailed technical specifications or assistance with experimental design, please contact Ascent Research.
