The ATP1B1 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous population of SK-HEP-1 cells carrying targeted disruption of the ATP1B1 gene. This polyclonal knockout model is designed to abolish expression of the beta-1 subunit of the Na+/K+-ATPase, enabling loss-of-function studies without clonal selection. The product provides a versatile tool for investigating the role of ATP1B1 in ion homeostasis, cell volume regulation, and epithelial polarity within a hepatic adenocarcinoma context.
SK-HEP-1 is a human hepatic adenocarcinoma epithelial cell line originally derived from the ascites of a patient with liver adenocarcinoma. This cell line retains key hepatic characteristics, including drug-metabolizing enzymes and functional bile acid transporters, making it a valuable model for studying liver cancer biology and hepatocyte function. Its epithelial origin and tumorigenic properties also make it suitable for investigating epithelial-mesenchymal transition (EMT) and metastasis.
ATP1B1 encodes the beta-1 subunit of the Na+/K+-ATPase, an integral membrane protein that assembles with the catalytic alpha subunit (ATP1A1) to form the active ion pump. This pump generates and maintains transmembrane Na? and K? electrochemical gradients, which are indispensable for driving secondary active transporters such as SGLT1, NHE1, and NCX1, regulating cell volume, and establishing epithelial polarity. ATP1B1 expression is regulated by aldosterone, thyroid hormone (T3), and transcription factors Sp1 and AP-1, and is responsive to osmotic stress and hypoxia. The beta-1 subunit interacts with FXYD1, ankyrin, adducin, and occludin, linking the pump to the cytoskeleton and tight junction complexes. Disruption of ATP1B1 abolishes these critical interactions, impairing ion homeostasis and downstream Wnt signaling.
In the SK-HEP-1 hepatic adenocarcinoma model, loss of ATP1B1 disrupts Na?/K? gradients, potentially altering cell volume, membrane potential, and secondary active transport processes that are vital for nutrient uptake and drug metabolism. This knockout can be exploited to study the contribution of Na+/K+-ATPase to liver cancer cell physiology, including EMT, migration, and invasion. Moreover, since ATP1B1 mutations are linked to Charcot-Marie-Tooth disease and hypertension, these polyclonal knockout cells provide a platform for examining the molecular mechanisms underlying these pathologies in a cancer-relevant lineage.
This polyclonal knockout product is suitable for ion transport studies using Na+/K+-ATPase activity assays or intracellular ion measurement, cancer cell biology investigations via Transwell migration and TEER assays, and EMT research. Additional applications include drug uptake assays, Na+/K+-ATPase structure-function analysis, and Charcot-Marie-Tooth disease modeling. Standard validation methods include Western blotting, RT-qPCR, immunofluorescence, and co-immunoprecipitation. For further information, please contact Ascent Research.
