ATP11C Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. These cells harbor a targeted disruption of the ATP11C gene, resulting in loss of ATP11C protein function. As a polyclonal product, the population contains diverse edit-induced genotypes, providing a biologically relevant model for studying gene disruption effects without clonal selection.
The A-549 cell line, originally from a 58-year-old Caucasian male with lung adenocarcinoma, serves as a classic alveolar type II epithelial model used in cancer and respiratory research. Its epithelial phenotype and genetic background make it suitable for investigating membrane biology, apoptosis, and tumor signaling. The knockout was engineered to ablate ATP11C expression, enabling dissection of flippase-mediated lipid dynamics in this widely used cancer cell context.
ATP11C encodes a P4-ATPase flippase that, together with its obligate beta-subunits TMEM30A/B, actively transports phosphatidylserine from the outer to the inner plasma membrane leaflet, preserving lipid asymmetry. In B cells, ATP11C is regulated by the transcription factor Pax5 and functions upstream of phosphatidylserine internalization, preventing externalization that would trigger phagocytosis and modulating B cell receptor signaling via the NF-??B pathway. Knockout leads to constitutive phosphatidylserine exposure, disrupting membrane organization and immune signaling.
In A-549 cells, loss of ATP11C allows researchers to examine how phosphatidylserine asymmetry affects cancer cell behavior. Altered lipid distribution may influence plasma membrane properties, receptor signaling platforms, and interactions with immune components. This model is valuable for studying tumor immune evasion, as exposed phosphatidylserine can inhibit immune attack and promote survival, and for investigating apoptosis resistance and drug susceptibility in lung adenocarcinoma.
Applications include Annexin V staining and flow cytometry to quantify phosphatidylserine externalization, RT-qPCR and western blotting for gene and protein analysis, and functional assays such as apoptosis, viability, and migration tests. The model enables exploration of signaling crosstalk and screens for modulators of flippase activity. For further information, please contact Ascent Research.
