The ATE1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the ATE1 gene, facilitating loss-of-function studies without clonal selection biases. The polyclonal format maintains natural genetic variation, yielding a robust model that reflects cellular heterogeneity. CRISPR/Cas9-mediated gene disruption enables interrogation of ATE1 function in a context that preserves both hepatocellular and endothelial-like characteristics.
SK-HEP-1 cells were isolated from the ascitic fluid of a liver adenocarcinoma patient and display a dual phenotype expressing hepatic and endothelial markers. This cell line is widely used for studying liver cancer biology, vascular mimicry, and angiogenesis. The endothelial-like features, including tube formation capability, are crucial for examining tumor-vascular crosstalk. Retention of these traits in ATE1 knockout derivatives allows dissection of how protein arginylation influences endothelial-like behaviors in a cancerous background.
ATE1 encodes arginyltransferase 1, which mediates N-terminal arginylation of aspartate, glutamate, or oxidized cysteine residues on target proteins. This modification is central to the N-end rule pathway, operating upstream of N-recognins, E3 ubiquitin ligases, and the 26S proteasome to promote substrate degradation or alter activity. ATE1 is regulated by ATF4, HIF1??, and oxidative stress, and modifies downstream effectors including RGS4, RGS5, ??-actin, ??-synuclein, and calreticulin. It interacts with arginyl-tRNA synthetase and proteasome components, integrating stress signals with protein quality control and apoptosis.
Disruption of ATE1 in SK-HEP-1 cells creates a valuable model for exploring the N-end rule pathway in hepatocellular carcinoma. Because SK-HEP-1 cells retain endothelial-like properties, this system is suited to study how arginylation affects vascular mimicry, migration, and invasion??processes linked to tumor angiogenesis and metastasis. Aberrant arginylation is implicated in cancer cell survival and drug resistance, so the model supports investigation of ATE1 loss on Wnt/??-catenin signaling and apoptosis. The polyclonal design reduces clonal artifacts, increasing translational relevance.
Typical applications include Western blotting and RT-qPCR to confirm knockout and assess downstream targets, arginylation activity assays, and functional assays such as transwell migration, tube formation, and apoptosis profiling. RNA-seq can reveal transcriptomic changes, and co-immunoprecipitation maps altered protein interactions. These cells are suitable for drug sensitivity screens targeting arginylation and for studying endothelial-mesenchymal transition in liver cancer. For more information, contact Ascent Research.
