The KHNYN Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. These cells feature targeted disruption of the KHNYN gene, leading to loss of KHNYN protein function. The polyclonal format provides a heterogeneous knockout background suitable for studying gene ablation effects without clonal selection artifacts. This product offers a genetically defined model for investigating KHNYN-dependent pathways in a liver-derived epithelial context.
The SK-HEP-1 parental line was established from ascites of a male patient with liver adenocarcinoma and displays adherent, epithelial-like morphology with both endothelial and epithelial traits. This cell line serves as a robust hepatocellular carcinoma model, widely employed in liver cancer biology research including tumorigenesis and host?Cpathogen interactions. Its susceptibility to viral infection makes it particularly relevant for examining hepatic antiviral innate immunity, providing a clinically pertinent setting to explore KHNYN function.
KHNYN encodes an RNA-binding protein that functions as an essential cofactor for the zinc-finger antiviral protein ZAP (ZC3HAV1). Upon interferon stimulation, ZAP binds CpG-rich viral RNA and recruits KHNYN to assemble a complex with the RNA exosome and the exonuclease XRN1, promoting degradation of retroviral transcripts. KHNYN expression is induced via type I interferon signaling through STAT1/STAT2/IRF9, downstream of sensors such as RIG-I and MDA5. Thus, KHNYN operates at the interface of interferon signaling and RNA decay to execute retrovirus restriction. Key interacting factors include ZC3HAV1, RNA exosome components, and XRN1.
In SK-HEP-1 cells, knockout of KHNYN provides a specific tool to dissect the ZAP?CKHNYN antiviral axis in a hepatic adenocarcinoma background. The liver is a frequent site of viral infection and hepatocellular carcinoma often develops from chronic hepatitis, underscoring the relevance of antiviral restriction factors in this tissue. This knockout model allows researchers to evaluate how loss of KHNYN impacts retroviral replication, interferon responsiveness, and the stability of viral RNAs. Comparative analysis with wild-type cells can delineate KHNYN-dependent contributions to innate immunity.
This polyclonal knockout population is ideal for retrovirus replication assays (e.g., HIV-1, MLV), interferon treatment experiments, RT-qPCR analysis of ISGs, and RNA immunoprecipitation to characterize KHNYN?CRNA interactions. Western blotting can assess protein expression, while immunofluorescence tracks ZAP localization. RNA decay assays using transcriptional inhibitors measure transcript half-lives. The model also enables CRISPR knockout validation and studies of viral-host interplay in hepatic cells. For further details, please contact Ascent Research.
