The ATP11C Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphocyte leukemia cell line, engineered to disrupt the ATP11C gene. This polyclonal pool provides a heterogeneous loss-of-function model for investigating ATP11C-dependent phospholipid translocation without clonal selection, enabling the study of gene disruption effects across a diverse cellular background.
Jurkat cells are an immortalized human T lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T cell leukemia. Widely employed as a model for T cell signaling, activation, and apoptosis, Jurkat cells retain key characteristics of T lymphoblasts and serve as a robust platform for interrogating immune cell functions in vitro. Their well-characterized signaling networks and ease of genetic manipulation make them particularly suitable for CRISPR-based knockout studies.
ATP11C encodes a P4-ATPase phospholipid flippase that, in complex with its obligatory subunit CDC50A (TMEM30A), actively translocates phosphatidylserine and phosphatidylethanolamine from the exoplasmic to the cytoplasmic leaflet of the plasma membrane, thereby maintaining membrane phospholipid asymmetry. ATP11C activity is regulated by upstream Ca2+ signaling and caspase-mediated cleavage during apoptosis. Disruption of ATP11C leads to aberrant phosphatidylserine exposure on the cell surface, which serves as a downstream signal for apoptotic cell recognition and clearance by phagocytes. This flippase is thus a critical node connecting intracellular calcium dynamics, apoptotic execution, and immune recognition.
In Jurkat T cells, ATP11C-mediated phospholipid asymmetry is intimately linked to T cell receptor signaling, activation-induced phosphatidylserine exposure, and apoptotic cell death. Loss of ATP11C function in these cells models the dysregulated flippase activity observed in certain B-cell immunodeficiencies and autoimmune disorders. The polyclonal knockout population captures a range of editing outcomes, reflecting the heterogeneous response of T lymphoblasts to ATP11C disruption and facilitating the study of phenotype variability in cell signaling and apoptosis pathways.
This knockout product is ideally suited for applications exploring phospholipid asymmetry in T cell signaling, mechanistic apoptosis research, and immune deficiency modeling. Researchers can employ flow cytometry with Annexin V staining to quantify phosphatidylserine exposure, perform flippase activity assays to measure ATP11C function, and validate gene disruption via western blotting or RT-qPCR. Apoptosis assays using inducers such as Fas ligand or etoposide can further dissect the role of ATP11C in programmed cell death. For additional technical specifications and ordering details, please contact Ascent Research.
