The IFI16 Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population carrying a disrupted IFI16 gene in the SK-HEP-1 human hepatic adenocarcinoma cell line. This loss-of-function model facilitates investigation of IFI16-dependent innate immune signaling, DNA sensing, and p53-mediated transcriptional control without clonal bias. The polyclonal format maintains the diversity of edited alleles, providing a robust population-level tool for functional studies.
SK-HEP-1 cells were originally derived from ascites of a liver adenocarcinoma patient and display endothelial-like morphology. They are extensively used as a model for hepatocellular carcinoma and endothelial cell biology, offering a relevant host for examining tumor?Cimmune interactions and hepatic innate immunity.
IFI16 is a pattern recognition receptor that senses cytoplasmic and nuclear double-stranded DNA, triggering innate immune responses. Upon ligand engagement, IFI16 recruits and activates the adaptor STING, which then signals through TBK1 to phosphorylate IRF3, promoting its nuclear translocation and induction of type I interferons including IFN-??. Concurrently, STING activates NF-??B to drive pro-inflammatory cytokine expression. IFI16 also binds the tumor suppressor p53, enhancing p53 transcriptional activity on targets such as p21, thereby governing cell cycle arrest and apoptosis. Its activity is modulated by upstream cues like interferon-??, interferon-??, cytosolic DNA, and DNA damage. IFI16 interacts with STING, p53, BRCA1, ASC, and AIM2, placing it at the intersection of DNA sensing, inflammation, and genome stability.
Within SK-HEP-1 hepatic adenocarcinoma cells, knockout of IFI16 enables dissection of its dual roles in innate immunity and tumor suppression. This model is especially suited for studying how cytosolic DNA recognition influences inflammatory microenvironments in liver cancer, with relevance to hepatocellular carcinoma, viral hepatitis, and autoimmune disorders such as systemic lupus erythematosus and Sj?gren??s syndrome. The endothelial-like phenotype of SK-HEP-1 provides additional opportunities to explore IFI16 involvement in angiogenic signaling or vascular mimicry.
Researchers can employ these knockout cells to analyze STING-TBK1-IRF3 cascade kinetics using IFN-?? luciferase reporter assays, examine protein complexes via co-immunoprecipitation of IFI16 partners like STING or p53, and measure apoptosis or cell cycle changes by flow cytometry. Transcriptional responses can be quantified by RT-qPCR and subcellular localization assessed with immunofluorescence microscopy. The IFI16 Knockout SK-HEP-1 Polyclonal Cells thus support a wide range of mechanistic and translational studies in innate immunity and cancer biology. For additional product details or ordering assistance, contact Ascent Research.
