The EIF2AK2 Knockout SK-HEP-1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal population with functional disruption of the EIF2AK2 gene, which encodes the interferon-inducible double-stranded RNA-activated protein kinase PKR. This product is supplied as a mixed pool of edited cells, not a monoclonal line, providing a knockout model for interrogating PKR-dependent biology. The SK-HEP-1 hepatic adenocarcinoma host ensures an epithelial context relevant to liver cancer.
SK-HEP-1 is a human hepatic adenocarcinoma cell line originally mischaracterized as endothelial but later confirmed to be of hepatocyte origin. It co-expresses epithelial and endothelial markers, is tumorigenic in xenograft models, and serves as a tractable system for studying hepatocellular carcinoma pathobiology. This unique dual phenotype facilitates investigation of the interplay between hepatic epithelial identity and mesenchymal features during tumor progression.
PKR is a key innate immune sensor and stress kinase activated by dsRNA, interferons (IFN-??, IFN-??, IFN-??), and stimuli such as oxidative or ER stress. Upon activation, PKR phosphorylates eIF2?? to suppress translation and triggers downstream signaling through NF-??B, JNK, p38 MAPK, and the FADD/caspase-8 apoptotic cascade. Its activity is regulated by interactions with PACT, TRBP, and the inhibitor P58IPK, and it integrates with eIF2?? kinases PERK, GCN2, and HRI to coordinate stress responses.
Knocking out EIF2AK2 in SK-HEP-1 cells abrogates PKR-mediated eIF2?? phosphorylation and downstream signaling, enabling dissection of PKR??s contributions to hepatocellular carcinoma biology. The model is particularly suited to study how loss of PKR alters responses to interferon, dsRNA, ER stress, and TNF-??, and how it impacts NF-??B-driven inflammation or apoptosis regulation in a liver cancer context. The hepatic adenocarcinoma background also permits investigation of PKR??s role in tumorigenesis and drug resistance.
Experimental applications include western blotting for PKR and phospho-eIF2??, RT-qPCR for interferon-stimulated genes, RNA-seq transcriptomics, Annexin V/PI apoptosis assays, NF-??B luciferase reporting, and viral infection challenge. This polyclonal knockout model supports research in innate immunity, antiviral signaling, stress pathways, hepatocellular carcinoma, apoptosis, and drug resistance. For further information or technical assistance, please contact Ascent Research.
