ABHD17B Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-mediated loss-of-function model of the ABHD17B gene in a human hepatic adenocarcinoma background. The product comprises a polyclonal population of edited SK-HEP-1 cells, each harboring distinct gene disruptions that collectively reduce ABHD17B expression and activity. This format avoids clonal selection artifacts, offering a more representative tool for studying depalmitoylase function in liver cancer. The cells are suitable for a wide range of biochemical, imaging, and functional assays, enabling rigorous investigation of ABHD17B-dependent pathways.
SK-HEP-1 is a widely employed hepatic adenocarcinoma cell line originally derived from the ascites of a 52-year-old male patient. It exhibits both endothelial and epithelial characteristics and is frequently used as a model for hepatocellular carcinoma, liver metastasis, and tumor signaling studies. In this context, the ABHD17B knockout allows direct assessment of how depalmitoylation dynamics influence oncogenic processes in hepatic malignancy.
ABHD17B functions as a protein depalmitoylase that hydrolyzes palmitate thioesters on cysteine residues of substrate proteins, regulating their membrane localization and signaling. It is activated downstream of NMDA receptor-mediated glutamatergic signaling and calcium influx. Key substrates include the synaptic scaffold PSD-95 (DLG4) and Ras GTPases; ABHD17B interacts with PSD-95 and zDHHC palmitoyltransferases in dynamic acylation cycles. In neurons, activity-dependent depalmitoylation of PSD-95 controls synaptic strength, while in cancer cells, ABHD17B-mediated depalmitoylation of Ras modulates its membrane microdomain partitioning and downstream MAPK and PI3K cascades. Thus, ABHD17B sits at a critical intersection between synaptic plasticity and oncogenic Ras signaling.
In the SK-HEP-1 background, ABHD17B knockout provides a powerful tool to probe how depalmitoylation controls Ras trafficking and oncogenic signaling in hepatic adenocarcinoma. Aberrant Ras palmitoylation alters its distribution between plasma membrane and endomembranes, influencing proliferation, migration, and survival. Disruption of ABHD17B allows examination of impaired depalmitoylation effects on Ras localization, phospho-signaling networks, and cellular metabolism. This model is therefore ideally suited for studying depalmitoylase inhibitors as potential therapies for Ras-driven liver malignancies and for elucidating resistance mechanisms to membrane-targeted agents.
Typical applications include immunofluorescence microscopy for Ras subcellular localization, Western blotting for palmitoylation levels and downstream effector phosphorylation, and functional assays for migration, invasion, and metabolism. Co-immunoprecipitation and acyl-biotin exchange methods enable protein interaction mapping and global palmitoylation profiling, while RNA-seq and phospho-signaling arrays reveal transcriptomic and kinomic changes. These polyclonal cells are also amenable to high-throughput screening for palmitoylation cycle modulators. For further information, please contact Ascent Research.
