The ABCF3 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line, in which the gene encoding the cytosolic ATP-binding cassette protein ABCF3 has been disrupted. This knockout model provides a loss-of-function system for investigating ABCF3-dependent innate immune signaling and translational regulation.
The SK-HEP-1 parental cell line, originally isolated from the ascites of a male patient with liver adenocarcinoma, serves as an established model for hepatocellular carcinoma research. SK-HEP-1 cells display characteristics of epithelial hepatic adenocarcinoma and are widely utilized to study liver cancer biology, immune responses, and host-pathogen interactions.
ABCF3 is a cytosolic ATP-binding cassette protein that functions as a modulator of the RIG-I-like receptor (RLR) signaling pathway. It is activated by upstream viral RNA sensors, including RIG-I and MDA5, and interacts with the mitochondrial antiviral signaling protein MAVS at the ribosome interface. ABCF3 facilitates signal transduction to TBK1 and IRF3, promoting the phosphorylation and nuclear translocation of IRF3, which in turn drives the transcription of type-I interferons such as IFNB1 and downstream interferon-stimulated genes (ISGs). Additionally, ABCF3 may influence NF-??B pathway components, contributing to a broader antiviral and pro-inflammatory response. The protein also associates with ribosomes and other ABCF family members, suggesting roles in translational control during innate immune activation.
Disruption of ABCF3 in SK-HEP-1 cells is anticipated to impair RIG-I-dependent antiviral signaling and interferon production, thereby attenuating the cellular response to viral infection. Given the role of innate immunity in tumor surveillance, this knockout model is particularly relevant for deciphering immune evasion mechanisms in hepatocellular carcinoma. It enables the dissection of how hepatic adenocarcinoma cells modulate interferon responses and may reveal vulnerabilities in viral infection contexts or immune-based therapeutic strategies.
Researchers can employ this polyclonal knockout population in a variety of assays to probe ABCF3 function, including RT-qPCR for IFNB1 and ISG expression, interferon-beta luciferase reporter assays, western blotting for IRF3 phosphorylation, and viral infection challenges. Co-immunoprecipitation studies can assess ABCF3 interactions with MAVS, while transcriptomic analyses via RNA-seq can elucidate global expression changes. This model supports investigations into innate immune signaling, antiviral defense, host-pathogen interactions, and immune disorders. For additional information, please contact Ascent Research.
