The ATP11A Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited population of human SK-HEP-1 liver sinusoidal endothelial-like cells with targeted disruption of the ATP11A gene. This polyclonal knockout format yields a heterogeneous mixture of cells carrying diverse loss-of-function mutations, avoiding clonal selection biases and enabling robust assessment of ATP11A-dependent phenotypes at the population level. The product is designed for advanced biomedical studies requiring a genetically defined loss-of-function model in an endothelial context.
SK-HEP-1 cells, derived from a human hepatic adenocarcinoma, are extensively employed as a model for liver sinusoidal endothelial cells (LSECs) due to their expression of endothelial markers such as factor VIII-related antigen and their functional capability for endocytosis and tube formation. These cells recapitulate key attributes of LSECs involved in hepatic filtration, waste clearance, and immune surveillance, offering a physiologically pertinent system for dissecting endothelial cell biology and liver pathophysiology.
ATP11A is a P4-ATPase phospholipid flippase that, heterodimerized with the CDC50A (TMEM30A) subunit, translocates phosphatidylserine and phosphatidylethanolamine from the exoplasmic to the cytoplasmic plasma membrane leaflet, preserving lipid asymmetry. The flippase is regulated by PKC signaling and opposes scramblase activity, thereby controlling phosphatidylserine surface exposure, apoptotic cell clearance, and membrane protein sorting. ATP11A operates within networks involving lipid kinases and membrane trafficking factors, impacting phospholipid transport, apoptosis signaling, and membrane dynamics.
Disruption of ATP11A in the SK-HEP-1 background compromises flippase-mediated lipid asymmetry maintenance in an endothelial-like model, with implications for barrier integrity, apoptotic cell clearance, and signaling relevant to cancer metastasis and neurological disorders. The polyclonal nature captures heterogeneous cellular adaptations, making this model valuable for investigating ATP11A’s role in tumor microenvironment interactions and drug resistance mechanisms.
Researchers can employ this knockout product in Western blotting, RT-qPCR, Annexin V flow cytometry for phosphatidylserine exposure, flippase activity assays, apoptosis assays, and endothelial barrier integrity tests. These methods facilitate exploration of phospholipid flippase function, apoptosis regulation, and lipid asymmetry in endothelial cells, cancer biology, and drug resistance studies. For additional information, please contact Ascent Research.
