The KATNAL1 Knockout SK-HEP-1 Polyclonal Cells are a genetically engineered cell population generated by CRISPR/Cas9-mediated disruption of the KATNAL1 gene. This product provides a heterogeneous pool of SK-HEP-1 cells with targeted gene disruption, avoiding clonal selection artifacts. As a polyclonal knockout model, it facilitates the study of katanin p60-dependent mechanisms in a liver adenocarcinoma context. Researchers can use these cells to explore microtubule dynamics, cell cycle regulation, and ciliary biology without the confounding effects of single-clone variability.
The parental SK-HEP-1 cell line is an epithelial line derived from the ascites of a patient with liver adenocarcinoma. SK-HEP-1 cells are widely used in hepatocellular carcinoma research for their robust growth and well-characterized cytoskeletal features. They exhibit a mesenchymal-like phenotype, making them suitable for investigating processes such as migration and invasion. Their hepatic origin and disease relevance provide a relevant backdrop for examining microtubule-severing enzymes in cancer progression.
KATNAL1 encodes the p60 catalytic subunit of katanin, an ATP-dependent microtubule-severing enzyme. The protein assembles into a functional complex with the regulatory subunit KATNB1 (p80) and directly interacts with tubulin and microtubule-associated proteins. KATNAL1 activity is activated by cell cycle kinases CDK1 and Aurora A, which phosphorylate the p60 subunit to regulate severing during mitosis. Downstream, KATNAL1-mediated severing controls mitotic spindle disassembly, ciliary resorption, and intracellular transport, thereby impacting cell division, ciliogenesis, and cytoplasmic organization.
In SK-HEP-1 adenocarcinoma cells, loss of KATNAL1 disrupts normal microtubule turnover, likely leading to hyperstable filaments that impair mitotic spindle assembly and chromosome segregation. Given the role of microtubule dynamics in cancer cell motility and proliferation, this knockout model enables precise dissection of katanin-dependent processes in liver cancer. It allows investigation of how KATNAL1 deficiency influences cellular responses to chemotherapeutic agents and the crosstalk between microtubule severing and oncogenic signaling pathways.
Experimental applications include immunofluorescence microscopy to visualize microtubule network reorganization, western blotting to confirm KATNAL1 ablation and assess tubulin modifications, and flow cytometry for cell cycle profiling. Time-lapse imaging captures real-time mitotic defects, while migration/invasion assays and ciliogenesis induction protocols evaluate functional outcomes. These approaches support drug target screening for microtubule-related disorders and mechanistic studies into katanin biology. For further information, please contact Ascent Research.
