The ATP11B Knockout Jurkat Polyclonal Cells comprise a heterogeneous population of human T lymphocytes derived from the Jurkat cell line, genetically engineered via CRISPR/Cas9-mediated disruption of the ATP11B gene. This polyclonal knockout model provides a powerful tool for studying the loss-of-function effects of ATP11B in a well-characterized immortalized T cell background. The polyclonal format ensures a diverse representation of knockout genotypes without clonal selection, offering a robust representation of the knockout phenotype for bulk population analyses.
The Jurkat cell line was originally established from the peripheral blood of a 14-year-old male with acute lymphoblastic leukemia (ALL). As an immortalized T lymphocyte line, Jurkat cells are widely employed in biomedical research to investigate T cell receptor signaling, apoptosis, and leukemia biology. Their well-documented responsiveness to apoptotic stimuli, such as Fas ligand and staurosporine, makes them an ideal host for studying flippase-mediated regulation of phosphatidylserine externalization.
ATP11B encodes a P4-ATPase phospholipid flippase that actively translocates phosphatidylserine (PS) and phosphatidylethanolamine from the outer to the inner leaflet of the plasma membrane, thereby maintaining membrane lipid asymmetry. The flippase function of ATP11B requires its obligate chaperone and beta subunit, CDC50A (also known as TMEM30A). During apoptosis, activated caspase-3 and caspase-7 cleave ATP11B, inactivating its flippase activity. This cleavage event disrupts PS asymmetry, leading to the exposure of PS on the cell surface, where it serves as an “eat-me” signal recognized by phagocytic receptors such as TIM4 and BAI1. In this signaling network, ATP11B functions downstream of cellular stress signals and upstream of PS-dependent phagocytosis pathways.
In the Jurkat T cell model, disruption of ATP11B is expected to compromise the maintenance of membrane phospholipid asymmetry, resulting in aberrant PS exposure and potentially altered apoptotic signaling. This knockout cell population enables researchers to mechanistically dissect the caspase-flippase signaling axis in lymphocytes. Given the role of membrane asymmetry in immune recognition and T cell homeostasis, the ATP11B knockout Jurkat cells provide a physiologically relevant system to explore how lipid flippase dysfunction contributes to T cell apoptosis, immune clearance, and pathologies including leukemia and neurological disorders.
This polyclonal knockout product is suitable for a range of advanced research applications, including quantitative assessment of PS externalization via Annexin V binding assays and flow cytometry, analysis of ATP11B protein levels and caspase-3 cleavage by Western blotting, and investigation of flippase modulator effects in drug screening campaigns. Additionally, the cells support co-immunoprecipitation studies of the ATP11B?CCDC50A interaction and functional apoptosis induction assays using staurosporine or Fas ligand. For more information or to discuss your specific experimental needs, please contact Ascent Research.
